DNAdam Cancer Research Results

DNAdam, DNA damage: Click to Expand ⟱
Source: HalifaxProj(prevent)
Type:
DNA damage plays a crucial role in the development of cancer. The integrity of DNA is essential for the proper functioning of cells, and when DNA is damaged, it can lead to mutations that may contribute to cancer progression.
Scientific Papers found: Click to Expand⟱
5289- 5-HTP,    5-Hydroxytryptophan (5-HTP): Natural Occurrence, Analysis, Biosynthesis, Biotechnology, Physiology and Toxicology
- Review, AD, NA - Review, Arthritis, NA
*5HT↑, 5-HTP plays a major role both in neurologic and metabolic diseases and its synthesis from tryptophan represents the limiting step in serotonin and melatonin biosynthesis.
*Inflam↓, 5-HTP also suppresses inflammation and arthritis through decreasing the production of pro-inflammatory mediators
*memory↑, figure 10
*Sleep↑, In a group of children with sleep terrors, treatment with 5-HTP was able to modulate the arousal level and to induce a long-term improvement of sleep terrors [1
*Weight↓, The effect of 5-HTP on feeding behavior, mood state, and weight loss was studied. 5-HTP promoted decreased food intake and weight loss as well as typical anorexia-related symptoms without changes in mood state during the period of observation
*DNAdam↓, 5-HTP significantly reduced tert-butylhydroperoxide-induced oxidative damage in human fibroblast cells and protected these cells against oxidative DNA damage
*ROS↓, By acting as a reactive oxygen species (ROS) scavenger, 5-HTP has the potential for use in the treatment of inflammatory diseases and as an analgesic
*toxicity↝, An excess of 5-HTP may be responsible for serotonin syndrome (see Section 8.2.1) and an excessive treatment was found to be associated with severe side effects, including behavioral disturbances, abnormal mental functions, and intolerance.

5352- AL,    Anticancer potential of allicin: A review
- Review, Var, NA
*cardioP↑, Allicin has many health-promoting properties, such as cardioprotective, antimicrobic, cholesterol-lowering, anti-inflammatory, and antitumor.
*Bacteria↓,
*Inflam↓,
AntiTum↑,
*DNAdam↓, DNA damage protection, induction of cell death, inhibition of cell proliferation, and block of angiogenesis and metastasis formation.
TumCP↓,
angioG↓,
TumMeta↓,

3163- Ash,  Rad,    Withaferin A, a steroidal lactone, selectively protects normal lymphocytes against ionizing radiation induced apoptosis and genotoxicity via activation of ERK/Nrf-2/HO-1 axis
*radioP↑, Withaferin A (WA) protected only normal lymphocytes, but not cancer cells, against IR-induced apoptosis
selectivity↑,
*Casp3↓, WA treatment led to significant inhibition of IR-induced caspase-3 activation and decreased IR-induced DNA damage to lymphocytes and bone-marrow cells.
*DNAdam↓,
*ROS↓, WA reduced intracellular ROS and GSH levels
*GSH↓,
*NRF2↑, WA induced pro-survival transcription factor, Nrf-2, and expression of cytoprotective genes HO-1, catalase, SOD, peroxiredoxin-2 via ERK.
*HO-1↑,
*Catalase↑,
*SOD↑,
*Prx↑,
*ERK↑, Activated ERK promotes the nuclear translocation and activity of Nrf2

4825- ASTX,    In vivo protective efficacy of astaxanthin against ionizing radiation-induced DNA damage
- in-vivo, Nor, NA
*DNAdam↓, DNA damage was reduced in the radiation+astaxanthin group compared with the radiation group
*radioP↑,

5365- AV,    Aloe Vera Polysaccharides as Therapeutic Agents: Benefits Versus Side Effects in Biomedical Applications
- Review, Nor, NA - Review, IBD, NA - Review, Diabetic, NA
*Wound Healing↑, Traditionally recognized for its anti-inflammatory and antimicrobial effects, which are very important in wound healing, the Aloe Vera relies on its polysaccharides
*Imm↑, which confer immunomodulatory, antioxidant, and tissue-regenerative properties.
*antiOx↑,
*AntiDiabetic↑, graphical abstract
*AntiCan↑,
*Inflam↓, The anti-inflammatory properties of Aloe Vera polysaccharides are primarily mediated through the inhibition of key inflammatory pathways.
*NF-kB↓, Acemannan and other polysaccharides suppress the activation of nuclear factor-kappa B (NF-κB), a transcription factor that regulates the expression of pro-inflammatory genes.
*COX2/PTGS2↓, By inhibiting NF-κB [48,49], Aloe Vera polysaccharides reduce the production of cyclooxygenase-2 (COX-2) and lipoxygenase (LOX),
*5LO↓,
*IL1β↓, Aloe Vera polysaccharides downregulate the expression of pro-inflammatory cytokines like IL-1β, IL-6, and TNF-α, while upregulating anti-inflammatory cytokines such as IL-10
*IL6↓,
*TNF-α↓,
*IL10↑,
*other↓, This dual action helps to mitigate inflammation in conditions such as arthritis, dermatitis, and inflammatory bowel disease (IBD)
*ROS↓, Aloe Vera polysaccharides exhibit potent antioxidant activity by scavenging reactive oxygen species (ROS) and free radicals,
*SOD↑, The polysaccharides enhance the activity of endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), which neutralize oxidative stress and protect cells from damage [17,63].
*Catalase↑,
*GPx↑,
*lipid-P↓, This property is particularly beneficial in preventing lipid peroxidation, DNA damage, and protein oxidation, processes associated with chronic diseases and aging
*DNAdam↓,
*GutMicro↑, Aloe Vera polysaccharides support gastrointestinal health, acting as prebiotics and promoting the growth of beneficial gut microbiota such as Lactobacillus and Bifidobacterium species [64].
*ZO-1↑, enhance the integrity of the intestinal epithelial barrier by upregulating the expression of tight junction proteins such as occludin and zonula occludens-1 (ZO-1) [51,54].
AntiTum↑, Certain polysaccharides in Aloe Vera, including acemannan, have demonstrated antitumoral effects by inducing apoptosis (programmed cell death) in cancer cells.
Casp3↑, This is achieved through the activation of caspase-3 and caspase-9, key enzymes in the apoptotic pathway [45,48].
Casp9↑,
angioG↓, Aloe Vera polysaccharides also inhibit angiogenesis and metastasis by downregulating matrix metalloproteinases (MMPs) and VEGF [75].
MMPs↓,
VEGF↓,
NK cell↑, Moreover, these polysaccharides enhance the immune system’s ability to recognize and destroy cancer cells through stimulating natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) [43,55].

2623- Ba,    Activation of the Nrf2/HO-1 signaling pathway contributes to the protective effects of baicalein against oxidative stress-induced DNA damage and apoptosis in HEI193 Schwann cells
- in-vitro, Nor, HEI193
*DNAdam↓, Our results showed that baicalein effectively inhibited H2O2-induced cytotoxicity and DNA damage associated with the inhibition of reactive oxygen species (ROS) accumulation.
*ROS↓,
*Bax:Bcl2↓, increased the Bax/Bcl-2 ratio
*p‑NRF2↑, baicalein increased not only the expression but also the phosphorylation of nuclear factor-erythroid 2 related factor 2 (Nrf2) and promoted the expression of heme oxygenase-1 (HO-1)
*HO-1↑, it is well known that the antioxidant efficacy of baicalein is related to the activation of the Nrf2/HO-1 signaling pathway
*neuroP↑, suggested that baicalein may have a beneficial effect on the prevention and treatment of peripheral neuropathy induced by oxidative stress.
*MMP↑, inhibitory effect of baicalein on MMP reduction

2689- BBR,    Berberine protects against glutamate-induced oxidative stress and apoptosis in PC12 and N2a cells
- in-vitro, Nor, PC12 - in-vitro, AD, NA - in-vitro, Stroke, NA
*ROS↓, In both cell lines, pretreatment with berberine (especially at low concentrations) significantly decreased ROS generation, lipid peroxidation, and DNA fragmentation, while improving glutathione content and SOD activity in glutamate-injured cells.
*lipid-P↓,
*DNAdam↓, Berberine significantly diminished glutamate-induced DNA fragmentation
*GSH↑,
*SOD↑,
*eff↑, This is relevant to berberine treatment in neurodegenerative disorders, such as dementia (Alzheimer’s disease), seizures, and stroke.
*cl‑Casp3↓, Berberine significantly decreased cleaved caspase-3 and bax/bcl-2 expressions in the glutamate-injured cells
*BAX↓,
*neuroP↑, the current study demonstrated that berberine exerts neuroprotective effects against glutamate-induced N2a and PC12 cytotoxicity via antioxidant and anti-apoptotic mechanisms
*Dose↝, the protective effect of berberine was more significant at lower concentrations and decreased with increasing concentration.
*Ca+2↓, Nadjafi et al demonstrated that berberine protects OLN-93 oligodendrocytes against ischemic-induced cell death by attenuating the intracellular Ca2+ overload similar to the NMDA or the AMPA/kainate receptors antagonists

3514- Bor,  CUR,    Effects of Curcumin and Boric Acid Against Neurodegenerative Damage Induced by Amyloid Beta
- in-vivo, AD, NA
*DNAdam↓, Co-administration of BA and curcumin on synaptosomes exposed to Aβ1-42 resulted in a significant decrease in DNA fragmentation values, MDA levels, and AChE activities.
*MDA↓,
*AChE↓,
*neuroP↑, BA and curcumin had protective effects on rat brain synaptosomes against Aβ1-42 exposure.
*ROS↓, BA and curcumin treatment can have abilities to prevent the alterations of the cholinergic system and inhibit oxidative stress in the cerebral cortex synapses of Aβ1-42 exposed.
*NO↓, Synaptosomes treated with BA showed a significant reduction in MDA and NO levels

4272- Bor,    Neuroprotective properties of borax against aluminum hydroxide-induced neurotoxicity: Possible role of Nrf-2/BDNF/AChE pathways in fish brain
*NRF2↑, BX clearly activating the Nrf-2/ROS signaling pathway.
*ROS↓,
*antiOx↑, BX supported antioxidant capacity without leading apoptosis, lipid peroxidation, inflammatory response and DNA damage.
*lipid-P↑,
*Inflam↓,
*DNAdam↓,
*BDNF↑, BX also increased the BDNF levels and AChE activity.
*neuroP↑, BX exerted a neuroprotective effect against AH-induced neurotoxicity via down-regulating cytokine-related pathways, minimising DNA damage, apoptosis
*GSH↑, as well as up-regulating GSH, AChE, BDNF and antioxidant enzyme levels.

1425- Bos,    Protective Effect of Boswellic Acids against Doxorubicin-Induced Hepatotoxicity: Impact on Nrf2/HO-1 Defense Pathway
- in-vivo, Nor, NA
*ChemoSen↑, BAs significantly improved the altered liver enzyme activities and oxidative stress markers.
*NRF2↑, BAs increased the Nrf2 and HO-1 expression, which provided protection against DOX-induced oxidative insult
*HO-1↑,
*ROS↓, appear to scavenge ROS and inhibit lipid peroxidation and DNA damage of DOX-induced hepatotoxicity
*lipid-P↓,
*DNAdam↓,

6554- BSB,  doxoR,    α-Bisabolol: A Dietary Sesquiterpene that Attenuates Apoptotic and Nonapoptotic Cell Death Pathways by Regulating the Mitochondrial Biogenesis and Endoplasmic Reticulum Stress–Hippo Signaling Axis in Doxorubicin-Induced Acute Cardiotoxicity in Rats
- in-vivo, Nor, NA
*cardioP↑, results that are currently available unequivocally show the cardioprotective role of BSB in DOX-induced cardiotoxicity.
*chemoP↑, BSB preserves the myocardium and reverses all cellular, molecular, and structural disruptions in the cardiac tissues of rats exposed to DOX-induced toxicity.
*antiOx↑, effect is attributed to BSB’s strong antioxidant, antilipid peroxidative, and antiapoptotic properties
*ROS↓,
*toxicity↓, BSB has been listed by the United States Food and Drug Administration (US FDA) as “generally regarded as safe” (GRAS) owing to its low toxicity.
*DNAdam↓, BSB Prevents DOX-Induced DNA Damage
*lipid-P↓, BSB Inhibits Lipid Peroxidation and Improves Antioxidants, ETC Complex, and TCA Cycle Enzymes
*ER Stress↓, BSB suppressed ER-stress-mediated myocardial Hippo-YAP activation and necroptosis against DOX-induced cardiotoxicity.

5916- Cats,  Chemo,    Uncaria tomentosa—Adjuvant Treatment for Breast Cancer: Clinical Trial
- Trial, BC, NA
*DNAdam↓, Uncaria tomentosa reduced the neutropenia caused by chemotherapy and was also able to restore cellular DNA damage.
Neut↓, A greater reduction in the white blood cell (WBCs) and the neutrophil counts were observed in the Ca group along the treatment, differently from the UtCa group, which remained closely the reference values
eff↑, We concluded that Ut is an effective adjuvant treatment for breast cancer.
Imm↑, Uncaria tomentosa enables the stimulation of the immune system, increasing resistance to diseases
Dose↝, Treatment using a daily dose of 300 mg dry Ut extract was effective in reducing the main chemotherapy effect, which is neutropenia.

6139- CHr,    Chrysin and its nanoformulations in cancer therapy: A systematic review of their radiosensitizing, phototherapy-enhancing potentials
- Review, Var, NA
RadioS↑, CHY and its NPs, when combined with radiotherapy (RT) and phototherapy(PT), generate singlet oxygen (¹O₂) and various reactive oxygen species (ROS), causing photooxidative damage, DNA injury, cell-cycle arrest often at the G1 phase, and apoptotic ce
PhotoS↑,
ROS↑,
DNAdam↑,
TumCCA↑,
TumCD↑,
selectivity↑, Conversely, CHY shows notable protective effects in normal cells by reducing oxidative stress, neuroinflammation, and DNA damage through restoring antioxidant defenses, lowering lipid peroxidation, and maintaining neuronal integrity
*ROS↓,
*Inflam↓,
*DNAdam↓,
*antiOx↑,
*lipid-P↓,
*BioAv↑, new developments in CHY-based nanocarrier systems that enhance bioavailability and treatment accuracy, providing a focused view not found in previous reviews of CHY or flavonoids.
eff↑, CHY-derived copper NPs (CuNPs) enhanced the effects of low-dose γ-irradiation in Swiss albino mice bearing Ehrlich tumors and in MCF-7 breast cancer cells
GSH↓, Combined treatment reduced GSH, catalase (CAT), alanine aminotransferase (ALT), creatinine (Cr), and Ca²⁺ levels while increasing MDA levels, indicating intensified oxidative stress
Catalase↓,
ALAT↓,
Ca+2↓,
MDA↑,

6135- CHr,    Chrysin as a Multifunctional Therapeutic Flavonoid: Emerging Insights in Pathogenesis Management: A Narrative Review
- Review, Var, NA - Review, AD, NA
Inflam↓, various cancers has been demonstrated and it modulates cell signaling pathways, including inflammation, angiogenesis, apoptosis, autophagy, and the cell cycle.
angioG↓,
Apoptosis↑,
TumAuto↑,
TumCCA↑,
BioAv↓, Despite its promising pharmacological activities, the clinical utility of chrysin remains limited due to its poor bioavailability, low solubility, limited permeability, and rapid metabolism.
Half-Life↓,
BioAv↓, The oral bioavailability of chrysin has been reported to range from 0.003% to 0.02%, with a maximum plasma concentration between 12 and 64 nM
*ROS↓, The study reported that chrysin administration protected the kidneys and liver of rats from oxidative damage induced by chronic ethanol consumption
*hepatoP↑, Hepatoprotective Potential
*RenoP↑, The renal protective effect of chrysin was related to increasing the antioxidant enzyme activities and decreasing the regulation of serum renal toxicity markers.
TET1↑, chrysin meaningfully induced the expression of TET1 in GC cells.
MMP9↓, hrysin might contribute to its anticancer effects by regulating MMP-9 expression.
cMyc↓, Both c-Myc and Ki-67 expressions were found to be suppressed in the tumor tissues treated with chrysin and G1-treated tumor tissues
Ki-67↓,
CBR1↓, chrysin directly interacts with CBR1, inhibiting its enzymatic activity at both the molecular and cellular levels.
ROS↑, This inhibition led to elevated intracellular ROS levels, triggering ROS-dependent autophagy
ChemoSen↑, chrysin enhances pancreatic cancer cell sensitivity to gemcitabine by inducing ferroptosis death, both in vitro and in vivo
Bax:Bcl2↑, chrysin increased the Bax/Bcl-2 expression ratio in ATC cells following treatment
PUMA↑, PUMA and Notch-1 were activated, and Slug was inactivated by chrysin treatment
NOTCH1↑,
*AntiDiabetic↑, Anti-Diabetic Potential
*neuroP↑, Neuroprotective Effects
*GABA↑, treatment of chrysin improves levels of GABA, monoamines, glutamic acid, and their metabolites in three brain regions, while also inhibiting DNA fragmentation markers like 8-HdG as well as BDNF.
*DNAdam↓,
*BDNF↑,
*memory↑, protective effects of chrysin against memory impairments associated with hippocampal neurogenesis
*AGEs↓, figure 6
*Aβ↓,
*cardioP↑, Cardioprotective Effects
*AntiArt↑, Anti-Arthritis Potential
eff↑, combination potential was higher than apigenin or chrysin alone.
eff↑, combination of quercetin enhanced the toxic effects of chrysin on the cell lines
*eff↑, neuroprotective synergistic effects of chrysin and kaempferol revealed therapeutic potential in mitigating cerebral ischemi
RadioS↑, study reported that treatment of MDA-MB-231 cells with chrysin in combination with radiation therapy (RT) caused synergistic antitumor properties.
eff↑, the combination of metformin and chrysin demonstrated pronounced synergistic cytotoxic effects on cancer cells
ChemoSen↑, chrysin was combined with a low dose of cisplatin, the resulting growth inhibition was significantly enhanced.
eff↑, demonstrating greater potency than chrysin or silver nanoparticles alone [198].

6631- Cic,    Chicoric acid is a potent anti-atherosclerotic ingredient by anti-oxidant action and anti-inflammation capacity.
- in-vitro, Nor, NA
*MMP↑, chicoric acid mitigates apoptotic features caused by oxLDL, such as the subsequent break down of mitochondrial transmembrane potential and the activation of Bax, which promote DNA strand breaks and activate caspase-3.
*BAX↓,
*DNAdam↓,
*Casp3↓,
*NF-kB↓, attenuated the oxLDL activation of NF-κB,
*antiOx↑, anti-oxidant action and anti-inflammation capacity
*Inflam↓,

6141- Cin,    The role and mechanism of cinnamaldehyde in cancer
- Review, Var, NA
Apoptosis↑, Cinnamaldehyde has diverse anti-cancer mechanisms, including inducing apoptosis by activating caspases and damaging mitochondrial function, inhibiting tumor angiogenesis, anti-proliferation, anti-inflammatory and antioxidant.
Casp↑,
mtDam↑,
angioG↓,
TumCP↓,
*Inflam↓,
*antiOx↑,
*ROS↓, In addition, cinnamaldehyde also acts as a reactive oxygen species scavenger, reducing oxidative stress and preventing DNA damage and genomic instability.
*DNAdam↓,
ROS↑, studies have shown that CA can enhance intracellular reactive oxygen species (ROS) levels by inducing mitochondrial dysfunction
*Bcl-2↑, CA exhibits a noteworthy upregulation of B-cell lymphoma protein 2 (Bcl-2) expression (a marker of antiapoptosis), while simultaneously downregulating Bax expression
*BAX↓,
*NF-kB↓, CA has been found to inhibit the activation of nuclear factor-kappa B (NF-κB)
ChemoSen↑, CA enhances the effectiveness of oxaliplatin by promoting apoptosis both in vitro and in vivo
ICAM-1↓, CA down-regulated the expression of adhesion molecules Intercellular adhesion molecule-1 (ICAM-1) and Vascular cell adhesion molecule-1 (VCAM-1)
VCAM-1↓,
PI3K↓, CA downregulates various components of the p PI3K/AKT/mTOR pathway in oral cancer cell lines
Akt↓,
mTOR↓,
BioAv↝, he estimated oral bioavailability of CA was found to be less than 20% for both the 250 and 500 mg/kg doses

3997- CoQ10,    Coenzyme Q and Its Role in the Dietary Therapy against Aging
- Review, AD, NA
*AntiAge↑, anti-aging potential of CoQ and its possible use in dietary therapies to alleviate the effects of aging.
*Inflam↓, CoQ Exerts Anti-Inflammatory Effects through Its Antioxidant Activity
*antiOx↑,
*Apoptosis↓, protective role of CoQ10 against apoptosis by inducing the inhibition of cell death independently from its free radical scavenging properties or antioxidant effects
*BioAv↑, It has been reported that intestinal absorption is threefold faster if CoQ10 is administrated with food intake in rats
*other↝, Actually, it has been reported that NQO1 expression increases during the initial steps of Alzheimer’s disease, indicating a higher lipid peroxidation coupled to a higher necessity for CoQ-dependent antioxidant activity
*cognitive↑, In older mice with clear cognitive and psychomotor impairments, short-time (15 days) CoQ-supplementation improved spatial learning
*DNAdam↓, dietary CoQ has also been shown to improve DNA repair systems [213,214] and modulate inflammatory signaling cascade as well as to reduce endoplasmic reticulum stress [214].
*ER Stress↓,

6375- CPLE,    Beneficial Role of Carica papaya Extracts and Phytochemicals on Oxidative Stress and Related Diseases: A Mini Review
- Review, Var, NA
*antiOx↑, contains various chemical compounds demonstrate significant antioxidant properties including caffeic acid, myricetin, rutin, quercetin, α-tocopherol, papain, benzyl isothiocyanate (BiTC), and kaempferol
*ROS↓, it can counteract pro-oxidants via a number of signaling pathways that either promote the expression of antioxidant enzymes or reduce ROS production.
*Inflam↓, Anti-inflammation activities of Carica papaya.
*AntiDiabetic↑, Anti-diabetes activities of Carica papaya
*neuroP↑, fermented papaya preparation (FPP) exerted neuroprotective properties against copper induced neurotoxicity in Swedish mutant human APP (APPsw) cells
*Wound Healing↑, Wound healing activities of Carica papaya.
*GSH↑, Carica papaya peel extract significantly increased glutathione (GSH), while decreasing MDA and ROS production. Thus, preventing DNA damage and induction of colonic carcinogenesis
*MDA↓,
*DNAdam↓,

5801- CRMs,  Chemo,    Caloric Restriction Enhances Chemotherapy Efficacy and Reshapes Stress Responses in Sarcoma
- in-vivo, sarcoma, NA
TumCG↓, It was found that this combined approach reduced tumor growth more effectively than chemotherapy alone and helped protect the blood, liver, and DNA from treatment-related damage.
*hepatoP↑,
*ROS↓, It also lowered oxidative stress and improved survival.
*OS↑, Caloric Restriction Combined with Chemotherapy Revealed Increased Survival in Sarcoma-Bearing Animals. Caloric restriction improved survival by approximately 81.82% compared to standard treatment
ChemoSen↑, promising approach to enhance the effects of chemotherapy and mitigate its adverse effects.
chemoPv↑,
selectivity↑, Together, these results indicate that caloric restriction enhances the antitumor effect of doxorubicin while offering protection to healthy tissues.
*DNAdam↓, Caloric restriction combined with chemotherapy (CRDOX) reduced DNA damage in peripheral blood cells.

6315- Cro,    Functional Mechanisms of Dietary Crocin Protection in Cardiovascular Models under Oxidative Stress
- in-vivo, NA, NA
*cardioP↑, it protects cardiac cells and significantly inhibits inflammation via modulating molecular signaling pathways TLR4/PTEN/AKT/mTOR/NF-κB and microRNA (miR-21).
*Inflam↓,
*antiOx↑, crocin not only acts as a direct free radical scavenger but also modifies the gene expression profiles of HUVECs and protects mice hearts with anti-inflammatory action under oxidative stress. The results showed that the antioxidant activity of crocin
*ROS↓, inhibition of excessive ROS by carotenoids and antioxidant-based formulations are interesting approaches for better clinical efficacy and oxidative stress-derived damages.
*AntiCan↑, pharmacological properties of saffron as an antioxidant, anticancer, and memory-enhancing factor have been extensively studied in vitro and in vivo
*memory↑,
*NF-kB↓, downregulation of NF-κB/TLR signaling and an upregulation of Nrf-2 and HO-1 [16].
*TLR1↓,
*NRF2↑,
*HO-1↑,
*lipid-P↓, crocin could decrease lipid peroxidation during ischemia-reperfusion (I/R)-induced oxidative damage in the kidney
*DNAdam↓, Crocin Protection against HUVEC DNA Damage
PTEN↓, Down-regulation of PTEN was observed in crocin-treated cells.
MMP↓, Under oxidative stress, there is a significant loss of ΔΨm concurrent with cell death.

6288- DL,    From Citrus to Clinic: Limonene’s Journey Through Preclinical Research, Clinical Trials, and Formulation Innovations
- Review, Var, NA - Review, AD, NA
other↑, Limonene is an unparalleled terpenoid with numerous therapeutic benefits.
DDS↑, Incorporating it into sophisticated drug delivery systems and medical devices, together with personalised medicine strategies, signifies notable progress in its therapeutic use.
*antiOx↑, graohical abstract
*Inflam↓,
*AntiDiabetic↑,
*neuroP↑,
*Imm↑,
*Wound Healing↑,
*other↑, Limonene can act as a solvent for cholesterol and has, therefore, been used curatively to dissolve gallstones.
*BioAv↑, orally administered D-limonene shows complete absorption from the GI tract of both animals and humans.9
*ROS↓, thereby preventing the further generation of reactive oxygen species (ROS), as depicted in Figure 2
*SOD↑, D-limonene restored the activities of antioxidant enzymes, such as SOD, CAT, GP, and GSH level, further resulting in the reduction of oxidative stress by preventing DNA damage and protein denaturation. T
*Catalase↑,
*GSH↑,
*DNAdam↓,
*AntiDiabetic↑, D-limonene is found to reduce oxidative stress and induce the potentiation of beta cells in the pancreas, thus showing beneficial effects in diabetes mellitus
Casp3↑, D-limonene activates caspases 3 and 9
Casp9↑,
BAX↑, increases the expression of BAX protein, and decreases BCL2 protein expression,
Bcl-2↓,
*AChE↓, Limonene inhibited AChE and BChE activities by 10% and 12%, respectively.
*BChE↓,
*Aβ↓, Limonene decreased Aβ42-induced neuronal cell death and reduced ROS levels, adversely affecting extracellular signal-regulated kinase (ERK) phosphorylation
*ROS↓,
*toxicity?, D-limonene shows low toxicity effects and has not shown much affirmation in animal studies. Some studies have reported that they are non-carcinogenic in humans and do not show much toxicity, even after several years, when administered at low doses.

6353- DRE,  Cisplatin,    Insights Into Protective Mechanisms of Dandelion Leaf Extract Against Cisplatin-Induced Nephrotoxicity in Rats: Role of Inhibitory Effect on Inflammatory and Apoptotic Pathways
- in-vivo, Nor, NA
*antiOx↑, Several studies demonstrated the antioxidant, anti-inflammatory, and antiapoptotic effects of dandelion leaf extract (DLE);
*Inflam↓,
*Apoptosis↓,
*NF-kB↓, DLE reduced nuclear factor-κB and cytochrome c expression, and DNA fragmentation
*Cyt‑c↓,
*DNAdam↓,
*GSH↑, also maintained levels of reduced glutathione, superoxide dismutase, and serum albumin.
*SOD↑,
*Albumin↝,
*creat↓, Treatment with DLE + CP maintained the levels of creatinine at all different DLE doses.
*BUN↓, Treatment with DLE + CP significantly ameliorated the elevated levels of creatinine and BUN.
*RenoP↑, These results demonstrate that DLE administration protected the kidney from renal injury that could occur by CP injection.
*lipid-P↓, The DLE pretreated rats showed a significant decline in LPO levels compared to that observed with CP treatment alone
*TNF-α↓, DLE alone decreased the levels of TNF-α by 15% of control levels. Rats treated with DLE prior to CP exhibited a significant (P < .001) suppression in the levels of TNF-α compared to CP-treated rats.
*Casp3↓, animals treated with DLE prior to CP administration showed significant decrease in caspase-9 and caspase-3 to levels comparable to the control and compared to rats treated with CP alone
*Casp9↓,
*chemoP↑, nephroprotective activity of DLE against CP-induced nephrotoxicity.

1605- EA,    Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence
- Review, Var, NA
*BioAv↓, Within the gastrointestinal tract, EA has restricted bioavailability, primarily due to its hydrophobic nature and very low water solubility.
antiOx↓, strong antioxidant properties [12,13], anti-inflammatory effects
Inflam↓,
TumCP↓, numerous studies indicate that EA possesses properties that can inhibit cell proliferation
TumCCA↑, achieved this by causing cell cycle arrest at the G1 phase
cycD1/CCND1↓, reduction of cyclin D1 and E levels, as well as to the upregulation of p53 and p21 proteins
cycE/CCNE↓,
P53↑,
P21↑,
COX2/PTGS2↓, notable reduction in the protein expression of COX-2 and NF-κB as a result of this treatment
NF-kB↓,
Akt↑, suppressing Akt and Notch signaling pathways
NOTCH↓,
CDK2↓,
CDK6↓,
JAK↓, suppression of the JAK/STAT3 pathway
STAT3↓,
EGFR↓, decreased expression of epidermal growth factor receptor (EGFR)
p‑ERK↓, downregulated the expression of phosphorylated ERK1/2, AKT, and STAT3
p‑Akt↓,
p‑STAT3↓,
TGF-β↓, downregulation of the TGF-β/Smad3
SMAD3↓,
CDK6↓, EA demonstrated the capacity to bind to CDK6 and effectively inhibit its activity
Wnt/(β-catenin)↓, ability of EA to inhibit phosphorylation of EGFR
Myc↓, Myc, cyclin D1, and survivin, exhibited decreased levels
survivin↓,
CDK8↓, diminished CDK8 level
PKCδ↓, EA has demonstrated a notable downregulatory impact on the expression of classical isoenzymes of the PKC family (PKCα, PKCβ, and PKCγ).
tumCV↓, EA decreased cell viability
RadioS↑, further intensified when EA was combined with gamma irradiation.
eff↑, EA additionally potentiated the impact of quercetin in promoting the phosphorylation of p53 at Ser 15 and increasing p21 protein levels in the human leukemia cell line (MOLT-4)
MDM2↓, finding points to the ability of reduced MDM2 levels
XIAP↓, downregulation of X-linked inhibitor of apoptosis protein (XIAP).
p‑RB1↓, EA exerted a decrease in phosphorylation of pRB
PTEN↑, EA enhances the protein phosphatase activity of PTEN in melanoma cells (B16F10)
p‑FAK↓, reduced phosphorylation of focal adhesion kinase (FAK)
Bax:Bcl2↑, EA significantly increases the Bax/Bcl-2 rati
Bcl-xL↓, downregulates Bcl-xL and Mcl-1
Mcl-1↓,
PUMA↑, EA also increases the expression of Bcl-2 inhibitory proapoptotic proteins PUMA and Noxa in prostate cancer cells
NOXA↑,
MMP↓, addition to the reduction in MMP, the release of cytochrome c into the cytosol occurs in pancreatic cancer cells
Cyt‑c↑,
ROS↑, induction of ROS production
Ca+2↝, changes in intracellular calcium concentration, leading to increased levels of EndoG, Smac/DIABLO, AIF, cytochrome c, and APAF1 in the cytosol
Endoglin↑,
Diablo↑,
AIF↑,
iNOS↓, decreased expression of Bcl-2, NF-кB, and iNOS were observed after exposure to EA at concentrations of 15 and 30 µg/mL
Casp9↑, increase in caspase 9 activity in EA-treated pancreatic cancer cells PANC-1
Casp3↑, EA-induced caspase 3 activation and PARP cleavage in a dose-dependent manner (10–100 µmol/L)
cl‑PARP↑,
RadioS↑, EA sensitizes and reduces the resistance of breast cancer MCF-7 cells to apoptosis induced by γ-radiation
Hif1a↓, EA reduced the expression of HIF-1α
HO-1↓, EA significantly reduced the levels of two isoforms of this enzyme, HO-1, and HO-2, and increased the levels of sEH (Soluble epoxide hydrolase) in LnCap
HO-2↓,
SIRT1↓, EA-induced apoptosis was associated with reduced expression of HuR and Sirt1
selectivity↑, A significant advantage of EA as a potential chemopreventive, anti-tumor, or adjuvant therapeutic agent in cancer treatment is its relative selectivity
Dose∅, EA significantly reduced the viability of cancer cells at a concentration of 10 µmol/L, while in healthy cells, this effect was observed only at a concentration of 200 µmol/L
NHE1↓, EA had the capacity to regulate cytosolic pH by downregulating the expression of the Na+/H+ exchanger (NHE1)
Glycolysis↓, led to intracellular acidification with subsequent impairment of glycolysis
GlucoseCon↓, associated with a decrease in the cellular uptake of glucose
lactateProd↓, notable reduction in lactate levels in supernatant
PDK1?, inhibit pyruvate dehydrogenase kinase (PDK) -bind and inhibit PDK3
PDK1?,
ECAR↝, EA has been shown to influence extracellular acidosis
COX1↓, downregulation of cancer-related genes, including COX1, COX2, snail, twist1, and c-Myc.
Snail↓,
Twist↓,
cMyc↓,
Telomerase↓, EA, might dose-dependently inhibit telomerase activity
angioG↓, EA may inhibit angiogenesis
MMP2↓, EA demonstrated a notable reduction in the secretion of matrix metalloproteinase (MMP)-2 and MMP-9.
MMP9↓,
VEGF↓, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
Dose↝, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
PD-L1↓, EA downregulated the expression of the immune checkpoint PD-L1 in tumor cells
eff↑, EA might potentially enhance the efficacy of anti-PD-L1 treatment
SIRT6↑, EA exhibited statistically significant upregulation of sirtuin 6 at the protein level in Caco2 cells
DNAdam↓, increase in DNA damage

6410- EGCG,    Evaluation of the neuroprotective effect of EGCG: a potential mechanism of mitochondrial dysfunction and mitochondrial dynamics after subarachnoid hemorrhage
- in-vitro, Nor, NA
*FIS1↓, EGCG ameliorated oxyhemoglobin (OxyHb)-induced impairment of mitochondrial dynamics by regulating the expression of Drp1, Fis1, OPA1, Mfn1, and Mfn2. EGCG dramatically lowered the expression of Drp1 and Fis1
*neuroP↑, EGCG increased the neurological score by decreasing cell death through the cyt c-mediated intrinsic apoptotic pathway.
*Ca+2↓, suggesting that EGCG blocked the Ca 2+ influx via L-type VGCC
*VGCC↝,
*ROS↓, Briefly, ROS increased from 2.15 ± 0.18 in the control group to 3.08 ± 0.31 in the OxyHb group ( p < 0.05 vs. control), and then reduced to 2.34 ± 0.22 in the EGCG group
*DNAdam↓, EGCG downregulated the mitochondrial DNA (mtDNA) copy number after SAH
*Apoptosis↓, EGCG inhibition of apoptosis after SAH

6389- Eug,    Molecular Insights into the Management of Eugenol's Anticancer Action Against Colon Cancer: A Detailed Review
- Review, Colon, NA
Apoptosis↓, Eugenol’s multitargeted action encompasses apoptosis induction, cell cycle arrest, suppression of inflammatory pathways, and inhibition of metastatic progression.
TumCCA↓,
Inflam↓,
TumMeta↓,
BioAv↑, nanotechnological encapsulation strategies have been explored to enhance bioavailability and pharmacokinetic stability.
eff↓, The compound is susceptible to oxidation when exposed to light, atmospheric oxygen, and elevated temperatures[2].
Half-Life↓, eugenol undergoes rapid absorption across the gastrointestinal epithelium, entering the systemic circulation within 30-60 minutes[3]. The swift absorption profile, while ensuring bioavailability, paradoxically limits it therapeutic effectiveness
*ROS↓, eugenol inhibits the endogenous production of reactive oxygen species (ROS) and reactive nitrogen species (RNS)
*RNS↓,
*SOD↓, Eugenol augments the body’s intrinsic antioxidant defense mechanisms, elevating expression of cytoprotective enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferases (GSTs)
*Catalase↑,
*GSTs↑,
*MAOA↓, Through monoamine oxidase (MAO) inhibition, eugenol modulates neurotransmitter homeostasis in the central nervous system, offering neuroprotective benefit
*neuroP↑,
*DNAdam↓, By eliminating reactive molecular species and preventing accumulation of damaged DNA and proteins, eugenol reduces the likelihood of mutations
Apoptosis↑, Multiple investigations have demonstrated eugenol’s capacity to induce apoptosis in diverse colon cancer cell lines, including HT-29, HCT-116, Caco-2, and SW-620
ROS↑, In human promyelocytic leukemia cells (HL-60) and colorectal cancer models, eugenol triggers elevated intracellular ROS accumulation
selectivity↑, This pro-oxidant activity in cancer cells contrasts sharply with eugenol’s cytoprotective antioxidant effects in normal cells, illustrating its selective anticancer action
MMP↓, Loss of mitochondrial membrane integrity triggers cytochrome c release into the cytosol, activating the caspase-9/caspase-3 cascade and culminating in programmed cell death
Cyt‑c↓,
Casp3↑,
Casp9↑,
TumCD↑,
BAX↑, Eugenol enhances expression of the tumor suppressor protein p53, which transactivates pro-apoptotic genes (BAX, BAD, APAF-1) while suppressing anti-apoptotic genes (BCL-2, BCL-XL)
BAD↑,
APAF1↑,
Bcl-2↓,
Bcl-xL↓,
P53↑,
cl‑PARP↑, eugenol activates executioner caspases-3 and -7, facilitating cleavage of critical substrates (PARP, DFF45) and morphological manifestations of apoptosis
TumCCA↑, Eugenol-treated cancer cells exhibit accumulation at the G2/M phase transition, accompanied by downregulation of cell cycle-promoting proteins (cyclin D1, cyclin B1, CDK2, CDK4) and upregulation of CDK inhibitors (p21, p27)
cycD1/CCND1↓,
CycB/CCNB1↓,
CDK2↓,
CDK4↓,
P21↑,
p27/CDKN1B↑,
NF-kB↓, Eugenol inhibits IκB-α phosphorylation, preventing NF-κB nuclear translocation and transcriptional activity[
COX2/PTGS2↓, Eugenol downregulates COX-2 expression, reducing pro-tumorigenic prostaglandin production and associated inflammation[3]
PGE2↓,
MAPK↓, Suppression of MAPK cascade reduces cancer cell proliferation and survival
PI3K↓, PI3K/Akt/mTOR Pathway Blockade
Akt↓,
mTOR↓,
MMPs↓, Eugenol suppresses MMP expression and activity, reducing tumor cell invasive capacity
EMT↓, Eugenol suppresses EMT-promoting transcription factors (Snail, Slug, ZEB1), maintaining E-cadherin expression and cellular adhesion[5].
Snail↓,
Slug↓,
Zeb1↓,
E-cadherin↑,
ChemoSen↑, Emerging evidence suggests eugenol enhances anticancer efficacy of conventional chemotherapeutic agents[5][6].

6871- FA,  Sesame,    Nano-encapsulated ferulic acid in sesame protein isolate alleviates acrylamide-induced liver toxicity and genotoxicity in rats via oxidative stress and DNA damage modulation
- in-vivo, Nor, NA
*GSH↑, Both encapsulated forms significantly improved liver function, elevated levels of GSH, GPx, SOD, and CAT were observed, along with decreased concentrations of MDA, interleukin-6, and tumor necrosis factor-α.
*GPx↑,
*SOD↓,
*Catalase↑,
*MDA↓,
*IL6↓,
*TNF-α↑,
*DNAdam↓, The treatments also provided protection against DNA damage and genotoxicity, alleviated histological damage, and reduced liver toxicity and genotoxicity.
*hepatoP↑,
*BioAv↓, FA ‘s bioavailability and stability are limited.
*BioAv↑, Therefore, encapsulating FA within nanocarriers can enhance its delivery and efficacy.

6877- FA,    The protective role of ferulic acid on sepsis-induced oxidative damage in Wistar albino rats
- in-vivo, Nor, NA
*antiOx↑, Ferulic acid (FA), a well-established natural antioxidant, has several pharmacological activities including anti-inflammatory, anticancer and hepatoprotective.
*Inflam↓,
*AntiCan↑,
*hepatoP↑,
*DNAdam↓, DNA damage in sepsis+FA-treated group was significantly lower than the sepsis group.
*Sepsis↓,
*MDA↓, FA treatment also decreased the MDA levels and increased the GSH levels and SOD and GSH-Px activities in the sepsis-induced rats. I
*GSH↑,
*GPx↑,
*ROS↓, It seems that FA might have ameliorative effects against sepsis-induced oxidative damage.

2846- FIS,    Fisetin protects against cardiac cell death through reduction of ROS production and caspases activity
- in-vitro, Nor, NA
*cardioP↑, Fisetin enhances viability of rat cardiomyocytes following hypoxia/starvation – reoxygenation.
*ROS↓, It inhibits apoptosis, decreases ROS generation and caspase activation and protects from DNA damage
*Casp↓,
*DNAdam↓,

7012- Fuc,    Fucoidan: A promising natural therapeutic agent for protecting human kidney health
- Review, EC, NA
*RenoP↑, Fucoidan exhibits significant anti-inflammatory effects in kidney protection.
*Inflam↓,
*antiOx↑, Antioxidant properties effectively reduce oxidative stress in renal tissues.
*ROS↓,
*BloodF↑, Enhances renal function by improving blood flow and diuresis.
*diuretic↑,
*BioAv↓, High-MW fucoidans often display stronger anticoagulant and viscosity-modulating effects. However, they may have limited oral bioavailability,
*BioAv↑, whereas low- to medium-MW fractions show improved tissue penetration, more favorable absorption, and can retain potent anti-inflammatory and anti-fibrotic activities, making them attractive for chronic kidney disease applications
*MAPK↓, (LMWF) has been reported in models of renal ischemia-reperfusion injury, where it inhibits the MAPK signaling pathway and subsequently reduces inflammation and fibrosis
*ERK↑, fucoidan can activate the ERK/MAPK signaling pathway, which plays a crucial role in preserving the endothelial glycocalyx in CKD
*NLRP3↓, fucoidan attenuates NLRP3 inflammasome activation and subsequent podocyte pyroptosis, ultimately leading to improved renal function and reduced inflammation in diabetic kidney disease (DKD)
*NRF2↑, By inhibiting ROS-generating systems (e.g., NADPH oxidase) and activating Nrf2-dependent transcription of antioxidant genes, fucoidan limits mitochondrial dysfunction and prevents oxidative injury to podocytes and tubular epithelial cells
*MDA↓, fucoidan nanoparticles significantly reduced levels of malondialdehyde (MDA), a marker of lipid peroxidation and oxidative stress, while simultaneously upregulating the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx)
*SOD↑,
*GPx↑,
*Catalase↑, Altogether, fucoidan directly reduces renal oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defenses (e.g., SOD, CAT, GPx) in tubular and glomerular cells, by suppressing upstream ROS generation
*lipid-P↓, fucoidan limits lipid peroxidation and DNA damage, thereby preserving podocyte integrity and tubular epithelial viability
*DNAdam↓,
*Fibrosis↓, Inhibition of fibrosis
*JAK2↓, fucoidan combats renal fibrosis is via the restriction of the JAK2/STAT3 signaling pathway.
*STAT3↓,
*uricA↓, By reducing serum uric acid levels, fucoidan significantly inhibits the activation of JAK2/STAT3, consequently decreasing the expression of key fibrotic markers such as collagen I and α-smooth muscle actin (α-SMA)
*COL1↓,
*α-SMA↓,
*SIRT1↑, fucoidan’s anti-fibrotic effects are further attributed to its activation of protective pathways such as Sirt-1, GLP-1R, and Nrf2/HO-1(
*HO-1↑,
*GLP-1R↑,
*HMGB1↓, Stimulating these protective pathways results in the inhibition of pro-fibrotic signaling cascades, including the HMGB1/RAGE/NF-κB/TGF-β1 pathway
*RAGE↓,
*NF-kB↓,
*TGF-β1↓,
*PI3K↓, Fucoidan also exhibits potential in curtailing the inflammatory processes associated with renal fibrosis through its inhibitory effects on the PI3K/Akt/NF-κB signaling cascade.
*Akt↓,
*GutMicro↑, research has elucidated the important role of gut microbiota in mediating the protective effects of fucoidan, suggesting that modulation of microbial communities may underlie its benefits in renal health
*SCFAs↑, Fucoidan’s positive impact on gut microbiota includes enhancing the production of short-chain fatty acids (SCFAs), especially butyrate, which are known to support gut integrity and overall health (
*Buty↑,
*IBI↑, Fucoidan's ability to enhance SCFA production has been linked to improved intestinal barrier integrity, a crucial factor in preventing the translocation of harmful substances into the bloodstream, which can exacerbate kidney injury
*TJ↑, Studies indicate that fucoidan can upregulate the expression of tight junction proteins, crucial for maintaining the integrity of the intestinal epithelium
*Dose↝, national approval in China for renal indications, indicate that fucoidan is generally safe at oral doses of 50–300 mg/day and up to 1–3 g/day in short‑ to mid‑term studies, with no major hematologic, hepatic, or renal toxicity reported.

7119- GEO2,    Germanium oxide enhances the radiosensitivity of cells
- in-vitro, Nor, CHO K1
RadioS↑, Complete survival curves showed a 2.3- and 2.75-fold increase in radiosensitivity for 50% cell death in the presence of 5 and 15 mM GeO(2), respectively.
ROS↑, combined treatment dramatically increased the synthesis of ROS.
eff↓, Addition of N-acetyl cysteine (NAC, 20 mM) decreased the production of ROS in cells.
DNAdam↓, The combination of GeO(2) and X radiation, however, significantly increased the frequency of DNA double-strand breaks (DSBs).
Catalase∅, Neither catalase nor GST activity was affected by GeO2 treatment
GSTs∅,

7253- Gink,    Ginkgetin Alleviates Inflammation and Senescence by Targeting STING
*cGAS–STING↓, thereby inhibiting STING activation and signal transduction.
*Inflam↓, Accumulating evidence has revealed that Ginkgo extract possesses anti‐inflammatory[ 12 ] and anti‐oxidant[ 13 ] properties and is effective in treating aging‐related diseases.[ 14 , 15 , 16 , 17 , 18 , 19 ]
*antiOx↑,
*AntiAge↑,
*DNAdam↓, otably, Ginkgetin exhibits inhibitory activity against oxidation, inflammation, and DNA damage, all of which are major factors inducing senescence
*cellSen↓, Ginkgetin Alleviates Cellular Senescence and Improves Pathologies in Multiple Tissues of Aging Mice

4511- GLA,    Gamma-Linolenic Acid (GLA) Protects against Ionizing Radiation-Induced Damage: An In Vitro and In Vivo Study
- vitro+vivo, Nor, RAW264.7
*radioP↑, mice exposed to lethal radiation (survival~20%) is significantly enhanced (to ~80%) by GLA treatment
*ROS↓, GLA reduced DNA damage (as evidenced by micronuclei formation) and enhanced metabolic viability, which led to an increase in the number of surviving RAW 264.7 cells in vitro by reducing ROS generation
*DNAdam↓, GLA reduced DNA damage
*IL6↓, by restoring altered levels of duodenal HMGB1, IL-6, TNF-α, and IL-10 concentrations, as well as the expression of NF-kB, IkB, Bcl-2, Bax, delta-6-desaturase, COX-2, and 5-LOX genes, and pro- and anti-oxidant enzymes (SOD, catalase, glutathione), to
*TNF-α↓,
*IL10↓,
*NF-kB↓,
*SOD↑, GLA pre-treated RAW cells (GLA + irradiation) showed improved antioxidant status and a significant (p < 0.01) increase in SOD, catalase, and GPx
*Catalase↑,
*GSH↑,

7332- GSE,    The impact of grape seed extract treatment on blood pressure changes: A meta-analysis of 16 randomized controlled trials
- Review, Nor, NA
*BP↓, Overall analyses found significant reductions for SBP (WMD = −6.077; 95% CI: −10.736 to −1.419; P = 0.011) and DBP (WMD = −2.803; 95% CI: −4.417 to −1.189; P = 0.001) after grape seed extract treatment
*eff↑, impact was more obvious in younger or obese subjects, as well as in patients with metabolic disorders.
*ROS↓, Overwhelming evidence from in vitro experiments suggests that grape seed extract has an antioxidant property that can protect cells from ROS-mediated DNA damage
*DNAdam↓,
*cardioP↑, French paradox that refers to the low rate of coronary heart disease mortality in France people despite the diets being rich in saturated fat.
*eff↝, With aging, it has been postulated that the effectiveness of grape seed extract on blood pressure regulation may be less obvious in the presence of these triggers. This proposition was substantiated in our age-stratified analysis.

7330- GSE,    Free radicals and grape seed proanthocyanidin extract: importance in human health and disease prevention
- Review, Var, NA
*BioAv↑, GSPE is highly bioavailable and provides significantly greater protection against free radicals and free radical-induced lipid peroxidation and DNA damage than vitamins C, E and beta-carotene.
*ROS↓,
AntiCan↑, GSPE was also shown to demonstrate cytotoxicity towards human breast, lung and gastric adenocarcinoma cells, while enhancing the growth and viability of normal human gastric mucosal cells.
selectivity↑,
RenoP↑, GSPE also demonstrated excellent protection against acetaminophen overdose-induced liver and kidney damage by regulating bcl-X(L) gene, DNA damage and presumably by reducing oxidative stress.
*hepatoP↑,
*DNAdam↓,
*Stroke↓, GSPE demonstrated excellent protection against myocardial ischemia-reperfusion injury and myocardial infarction in rats.
*Bcl-2↑, GSPE was also shown to upregulate bcl(2) gene and downregulate the oncogene c-myc.
cMyc↓,

7487- H2,    A comprehensive review of molecular hydrogen as a novel nutrition therapy in relieving oxidative stress and diseases: Mechanisms and perspectives
- Review, Nor, NA
*Inflam↓, H2 demonstrates numerous biologically therapeutic properties, including anti-inflammatory, antioxidant, anti-cancer, anti-stress, anti-apoptotic, anti-allergic effects, signaling molecule functions, regulation of redox balance
*antiOx↓,
*Stress↓,
*Dose↝, The administration methods of hydrogen include inhalation, hydrogen-rich water, hydrogen-rich saline, hydrogen-rich eye drops, and hydrogen-rich bathing.
*cardioP↑, graphical abstract and figure 4
*GastroP↑,
*BBB↑, H2 is its ability to easily cross the blood-brain barrier and penetrate biomembranes, diffusing throughout the different tissues and organs.
*eff↑, The above-cited properties led some researchers to refer to it as a "miracle" molecule
*toxicity↓, Regarding the biosafety of hydrogen, numerous reports, including those from the US government and the EU, have indicated that hydrogen is safe for biological systems, showing no acute or chronic toxicity under normal pressure
*Dose↝, human large intestine often produces approximately 70–140 mL of hydrogen daily through the action of coliform bacteria such as Escherichia coli under typical environmental conditions.
*hepatoP↑, including cardioprotective properties, improved liver function, reduced oxidative stress, and prevention of Parkinson's disease
*ROS↓,
*SOD↑, 1.5–2.0 L/day drinking HRW orally 0.55–0.65 mM 1.65–2.6 mg H2/day 8 weeks SOD: ↑ TRABS: ↓ HDL: ↑
*TBARS↓,
*HDL↑,
*LDL↓, figure 4
*Obesity↓, figure 5 obesity
*GSH↑, HRW treatment partially alleviated colitis symptoms, improved histopathological changes, significantly increased glutathione (GSH) concentration, and reduced the level of TNF-α.
*TNF-α↓,
*GutMicro↑, HRW was found to exhibit partial relief of inflammation, oxidative stress, and dysbiosis in the intestinal flora of mice with chronic ulcerative colitis (UC) induced by dextran sulfate sodium (DSS)
*DNAdam↓, HRW-treated mice exhibited decreased levels of markers associated with oxidative DNA damage, such as phosphorylated histone H2AX and 8-hydroxy-2′-deoxyguanosine, as well as markers indicative of aging
*γH2AX↓,
*p‑p38↓, Treatment with HRS also inhibited the activation of p-p38 and NF-κB while suppressing the production of several pro-inflammatory mediators,
*NF-kB↓,

7489- H2,    Molecular Hydrogen in the Treatment of Respiratory Diseases
- Review, Asthma, NA
*antiOx↑, Molecular hydrogen is gaining increasing attention as an antioxidant, anti-inflammatory, and antiapoptotic agent.
*Inflam↓,
*Apoptosis↓,
*Dose↓, It reaches a maximum level of about 0.78 mM (≈1.6 mg/L) at room temperature with a loss of about 2–5% per 3 min
*Dose↝, It is produced (and consumed) by bacteria of the gut microbiota .The most prominent bacterial phyla involved in this process are the Firmicutes and Bacteroidetes phyla, which include the anaerobic Clostridium species
*eff↑, hydrogen mixed with oxygen at a ratio of 96%-to-4%, known as the Hydrox gas mixture, was used by deep-sea divers to prevent decompression sickness and allow diving to depths of up to 500 m
*ROS↓, The antioxidant activity of H2 is based on two processes: a direct scavenging of the most toxic reactive oxygen and nitrogen species (ROS/RNS),
*RNS↓,
*NRF2↑, H2 activates the Nrf2 (nuclear factor erythroid 2-related factor 2) pathway, a key transcription factor involved in oxidative stress-related responses, including cytoprotective, antioxidant, and detoxifying enzymes such as HO-1
*HO-1↑,
*Fenton↓, removal of free heme and inhibition of the Fenton reaction
*NLRP3↓, the activation of the Nrf2 pathway has been shown to inhibit the NLRP3 (NLR family pyrin domain containing 3) inflammasome,
*NADPH↓, H2 suppresses the activation of the NADPH oxidase pathway and downregulates the expression of NOX2 and NOX4
*NOX4↓,
*NOX↓,
*MPO↓, H2 has been shown to reduce the overactivation of myeloperoxidase (MPO)
*NF-kB↓, would further suppress the NFκB
*TNF-α↓, figure 3
*IL6↓,
*IL1β↓,
*HMGB1↓,
*IL4↑,
*IL10↑,
*M2 MC↑, Additionally, H2 promotes the polarization of macrophages from the proinflammatory M1 type to the anti-inflammatory M2 type
*Treg lymp↝, It also inhibits Th2 responses, restores regulatory T cells (Treg), and, thus, normalizes an overactivated immune system
*Bcl-2↑, upregulate the antiapoptotic factors, including Bcl-2 and Bcl-xl.
*Bcl-xL↑,
*PI3K↑, phenomenon is likely facilitated by the activation of the PI3K/Akt and JAK2/STAT3 signaling pathways
*Akt↑,
*JAK2↑,
*STAT3↑,
*Dose↑, The consumption of certain prebiotics, especially those rich in dietary fiber, indigestible starches, and sugars (lactulose), has been demonstrated to enhance intestinal H2 production through the activity of intestinal flora
*CD4+↑, H2 increased the population of CD4+CD25+Foxp3+ Treg cells, which are often decreased in allergic rhinitis (AR)
*CD25+↑,
*FOXP3↑,
*MDA↓, H2 administration attenuated oxidative stress expressed as lower MDA and other lipid peroxidation markers along with an enhancement in the expression and activity of endogenous antioxidant enzymes such as SOD or CAT
*SOD↑,
*Catalase↑,
*Casp3↓, inhibition of proapoptotic processes like the caspase 3 and 9 pathways
*Casp9↓,
*TBARS↓, drinking of HRW by patients with asthma and COPD leads to an increase in blood oxygen saturation, vitamin E levels, along with lower oxidative stress markers such as thiobarbituric acid reactive substances (TBARS), MDA,
*SpO2↑,
*VitE↓,
*OS↑, COPD:In general, H2 administration has been found to lead to enhanced survival and reduced weight loss [110], improved lung function and static lung compliance, and decreased arterial blood pressure
*Weight↑,
*DNAdam↓, reduction in levels of oxidative DNA damage markers
*PGE2↓, H2 reduced elevated inflammatory markers, including IL-1β, IL-6, TNF-α, prostaglandin E2 (PGE2) [29,65,71,128,130], macrophage protein 1α 2 (MP1α), and monocyte chemoattractant protein-1 (MCP-1)
*MCP1/CCL2↓,
*lipid-P↓, Further, a reduction in oxidative stress markers such as lipid peroxidation and proapoptotic markers, including Bax and caspase-3, was observed.
*TumCP↓, H2-rich medium reduced the colony size and formation of tongue cancer cells and decreased proliferation in human fibrosarcoma and esophageal cancer cells, as well as A549 cells
*tumCV↓, decrease in cell viability, migration, and invasion
*TumCMig↓,
*TumCI↓,
TumW↓, A reduction in tumor weight and size, as well as a lower number of cells of squamous cell carcinoma, was revealed by animal studies.
TumVol↓,
selectivity↑, Notably, as previously reported, H2 administration exhibited no effect on healthy animals or non-cancerous cell lines
QoL↑, Patients reported improved quality of life with better physical status and fewer pulmonary symptoms
ChemoSen↑, In combination with conventional (such as cis-platin) and modern (including antibodies like nivolumab) therapeutics, H2 enhanced drug activity, resulting in enhanced outcomes and improved disease control
chemoP↑, and reduced side effects of the treatment, such as nephrotoxicity, weight loss, insomnia, pain, or hearing loss in the case of radiotherapy
radioP↑, radioprotective effects of H2 are primarily attributed to its hydroxyl radical scavenging activity
ROS↑, As indicated by Yang et al., the latter include the activation of the ROS/NLRP3/caspase-3/gasdermin D-mediated pyroptotic pathways
NLRP3↑,
Casp3↑,
VEGF↓, suppression of vascular endothelial growth factor (VEGF) expression
Wnt↓, H2 result in the suppression of the overactivated Wnt/beta-catenin signaling pathways, which further leads to suppression of tumor progression
β-catenin/ZEB1↓,

7339- Hne,    Apoptosis-inducing activity of Helleborus niger in ALL and AML
- in-vitro, AML, NA
TumCP↓, HNPT Inhibits Proliferation and Specifically Induces Apoptotic DNA Fragmentation in Lymphoma and Leukemia Cell Lines
DNAdam↓,
Casp3↑, HNPT-Induced Apoptosis in BJAB Cells Is Mediated by Caspase-3 Activation, Loss of Mitochondrial Membrane Potential and Partly Dependent on Bcl-2 Expression
MMP↓,
eff↑, In combination with vincristine, a strong increase in apoptosis induction was observed in BJAB cells, which was up to 208% higher than with additive alone
Apoptosis↑, These studies demonstrate that an aqueous extract of H. niger specifically induces apoptosis in different types of cancer cell lines and primary tumor cells from patients with childhood ALL and AML.

1787- LE,    Licorice and cancer
- Review, Var, NA
Inflam↓, known or suspected (anti-inflammatory, antivirus, antiulcer, anticarcinogenesis, and others
AntiCan↓,
DNAdam↓, Licorice and its derivatives may protect against carcinogen-induced DNA damage
LOX1↓, Glycyrrhizic acid is an inhibitor of lipoxygenase and cyclooxygenase, inhibits protein kinase C, and downregulates the epidermal growth factor receptor
COX2/PTGS2↓,
PKCδ↓,
EGFR↓,

3268- Lyco,    Lycopene as a Natural Antioxidant Used to Prevent Human Health Disorders
- Review, AD, NA
*BioAv↓, Lycopene bioavailability can be decreased by ageing, and some of the pathological states, such as cardiovascular diseases (CVDs)
*AntiCan↑, For instance, it has been shown that a higher dietary intake and circulating concentration of lycopene have protective effects against prostate cancer (PCa), in a dose-dependent way
*ROCK1↓, It remarkably lessened the expression of ROCK1, Ki-67, ICAM-1 and ROCK2,
*Ki-67↓,
*ICAM-1↓,
*cardioP↑, Lycopene is a cardioprotective nutraceutical.
*antiOx↑, Lycopene is a well-known antioxidant.
*NQO1↑, Furthermore, lycopene supplementation improves mRNA expressions of the NQO-1 and HO-1 as antioxidant enzymes.
*HO-1↑,
*TNF-α↓, downregulate inflammatory cytokines (i.e., TNF-α, and IL-1β) in the hippocampus of the mice.
*IL22↓,
*NRF2↑, Lycopene decreased neuronal oxidative damage by activating Nrf2, as well as by inactivating NF-κB translocation in H2O2-related SH-SY5Y cell model
*NF-kB↓,
*MDA↓, significantly reduced the malondialdehyde (MDA)
*Catalase↑, Furthermore, it improved the catalase (CAT), superoxide dismutase (SOD), and GSH levels, and antioxidant capacity [109].
*SOD↑,
*GSH↑,
*cognitive↑, Lycopene administration considerably improved cognitive defects, noticeably reduced MDA levels and elevated GSH-Px activity, and remarkably reduced tau
*tau↓,
*hepatoP↑, Lycopene was also found to be effective against hepatotoxicity by acting as an antioxidant, regulating total glutathione (tGSH) and CAT concentrations
*MMP2↑, It also elevated MMP-2 down-regulation
*AST↓, lowering the liver enzymes levels, like aspartate transaminase (AST), alanine transaminase (ALT), LDL, free fatty acid, and MDA.
*ALAT↓,
*P450↑, Moreover, tomato powder has been shown to have a protective agent against alcohol-induced hepatic injury by inducing cytochrome p450 2E1
*DNAdam↓, lycopene decreased DNA damage
*ROS↓, It has been revealed that they inhibited ROS production, protected antioxidant enzymes, and reversed hepatotoxicity in rats’ liver
*neuroP↑, lycopene consumption relieved cognitive defects, age-related memory loss, neuronal damage, and synaptic dysfunction of the brain.
*memory↑,
*Ca+2↓, Lycopene suppressed the 4-AP-invoked release of glutamate and elevated intra-synaptosomal Ca2+ level.
*Dose↝, an in vivo study revealed that lycopene (6.5 mg/day) was effective against cancer in men [147]. However, lycopene dose should be increased up to 10 mg/day, in the case of advanced PCa.
*Dose↑, lycopene supplementation (15 mg/day, for 12 weeks) in an old aged population improved immune function through increasing natural killer cell activity by 28%
*Dose↝, Finally, according to different epidemiological studies, daily lycopene intake can be suggested to be 2 to 20 mg per day
*toxicity∅, A toxicological study on rats showed the no-observed-adverse-effect level at the highest examined dose (i.e., 1.0% in the diet)
PGE2↓, Lycopene doses of 0, 10, 20, and 30 µM were used to treat human colorectal cancer cell. Prostaglandin E2 (PGE2), and NO levels declined after lycopene administration,
CDK2↓, Treatment with lycopene reduced cell hyperproliferation induced by UVB and ultimately promoted apoptosis and reduced CDK2 and CDK4 complex in SKH-1 hairless mice
CDK4↓,
STAT3↓, lycopene reduced the STAT3 expression in ovarian tissues
NOX↓, (SK-Hep-1) cells and indicated a substantial reduction in NOX activity. Moreover, it inhibits the protein expression of NOX4, NOX4 mRNA and ROS intracellular amounts
NOX4↓,
ROS↓,
*SREBP1/SREBF1↓, Lycopene decreases the fatty acid synthase (FAS), sterol regulatory element-binding protein 1c (SREBP-1c), and Acetyl-CoA carboxylase (ACC1) expression in HFD mice.
*FASN↓,
*ACC↓,

3277- Lyco,    Recent trends and advances in the epidemiology, synergism, and delivery system of lycopene as an anti-cancer agent
- Review, Var, NA
antiOx↑, lycopene provides a strong antioxidant activity that is 100 times more effective than α-tocopherol and more than double effective that of β-carotene
TumCP↓, In vivo and in vitro experiments have demonstrated that lycopene at near physiological levels (0.5−2 μM) could inhibit cancer cell proliferation [[22], [23], [24]], induce apoptosis [[25], [26], [27]], and suppress metastasis [
Apoptosis↑,
TumMeta↑,
ChemoSen↑, lycopene can increase the effect of anti-cancer drugs (including adriamycin, cisplatin, docetaxel and paclitaxel) on cancer cell growth and reduce tumour size
BioAv↓, low water solubility and bioavailability of lycopene
Dose↝, The concentration of lycopene in plasma (daily intake of 10 mg lycopene) is approximately 0.52−0.6 μM
BioAv↓, significant decrease in lycopene bioavailability in the elderly
BioAv↑, oils and fats favours the bioavailability of lycopene [80], while large molecules such as pectin can hinder the absorption of lycopene in the small intestine due to their action on lipids and bile salt molecules
SOD↑, GC: 50−150 mg/kg BW/day ↑SOD, CAT, GPx ↑IL-2, IL-4, IL-10, TNF-α ↑IgA, IgG, IgM ↓IL-6
Catalase↑,
GPx↑,
IL2↑, lycopene treatment significantly enhanced blood IL-2, IL-4, IL-10, TNF-α levels and reduced IL-6 level in a dose-dependent manner.
IL4↑,
IL1↑,
TNF-α↑,
GSH↑, GC: ↑GSH, GPx, GST, GR
GPx↑,
GSTA1↑,
GSR↑,
PPARγ↑, ↑GPx, SOD, MDA ↑PPARγ, caspase-3 ↓NF-κB, COX-2
Casp3↑,
NF-kB↓,
COX2/PTGS2↓,
Bcl-2↑, AGS cells Lycopene 5 μM ↑Bcl-2 ↓Bax, Bax/Bcl-2, p53 ↓Chk1, Chk2, γ-H2AX, DNA damage ↓ROS Phase arrest
BAX↓,
P53↓,
CHK1↓,
Chk2↓,
γH2AX↓,
DNAdam↓,
ROS↓,
P21↑, CRC: ↑p21 ↓PCNA, β-catenin ↓COX-2, PGE2, ERK1/2 phosphorylated
PCNA↓,
β-catenin/ZEB1↓,
PGE2↓,
ERK↓,
cMyc↓, AGS cells: ↓Wnt-1, c-Myc, cyclin E ↓Jak1/Stat3, Wnt/β-catenin alteration ↓ROS
cycE/CCNE↓,
JAK1↓,
STAT3↓,
SIRT1↑, Huh7: ↑SIRT1 ↓Cells growth ↑PARP cleavage ↓Cyclin D1, TNFα, IL-6, NF-κB, p65, STAT3, Akt activation ↓Tumour multiplicity, volume
cl‑PARP↑,
cycD1/CCND1↓,
TNF-α↓,
IL6↓,
p65↓,
MMP2↓, SK-Hep1 human hepatoma cells Lycopene 5, 10 μM ↓MMP-2, MMP-9 ↓
MMP9↓,
Wnt↓, AGS cells Lycopene 0.5 μM, 1 μM ↓Wnt-1, c-Myc, cyclin E ↓Jak1/Stat3, Wnt/β-catenin alteration ↓ROS

4780- Lyco,    Potential inhibitory effect of lycopene on prostate cancer
- Review, Pca, NA
TumCP↓, Lycopene suppress the progression and proliferation
TumCCA↑, Lycopene has been found to effectively suppress the progression and proliferation, arrest in-cell cycle, and induce apoptosis of prostate cancer cells in both in-vivo and in-vitro conditions.
Apoptosis↑,
*neuroP↑, the neuro-protective effect of lycopene, mediates the signaling pathways, by inhibiting NF-κB (nuclear factor-κB) and JNK protein (c-Jun N-terminal kinase), and activating Nrf2 (Nuclear factor erythroid 2-related factor 2) and BDNF (
*NF-kB↓,
*JNK↓,
*NRF2↑,
*BDNF↑,
*Ca+2↝, as well as keeping homeostasis by restoring intracellular Ca2+
*antiOx↑, most powerful and natural antioxidants, and its role in preventing prostate cancer.
*AntiCan↑,
*Inflam↓, Anti-inflammatory properties of lycopene depends on time, and it has been found to be through the decrease of inflammatory cytokines (i.e. IL1, IL6, IL8 and tumor necrosis factor-α (TNF-α)
*IL1↓,
*IL6↓,
*IL8↓,
*TNF-α↓,
NF-kB↓, lycopene increased the expression of BCO2 enzyme in an androgen-sensitive cell line that prevented cancer cell proliferation and reduced the NF-κB activity
DNAdam↓, 20 and 50 μM doses of lycopene had an effect on PC3 and DU145 cell lines in inducing apoptosis with DNA damages, and preventing cell growth and colony formation
PSA↓, lycopene twice a day for 3 weeks, showed that lycopene decreases the risk and growth of prostate cancer cells, and also a decrease in the level of PSA,
P53↓, down-regulation of p53, Cyclin-D1, and Nrf-2 have occurred after the incubation of prostate cancer cells with the lycopene received patient’s sera in comparison with placebo
cycD1/CCND1↓,
NRF2↓,
Akt2↓, treatment with lycopene in PC3 cancer cell lines was associated with down-regulation of AKT2 [
PPARγ↓, Another anti-proliferative effect of lycopene was done by increasing PPARγ-LXRα-ABCA1signaling molecules in protein and mRNA level

4794- Lyco,    Anticancer Effect of Lycopene in Gastric Carcinogenesis
- Review, GC, NA
*AntiCan↑, Lycopene from red fruits and vegetables has strong anticancer activity in gastric carcinogenesis.
*ROS↓, As one of the most potent antioxidants, lycopene is effective in decreasing oxidative damage by activating antioxidant enzymes such as GSH, GPx and GST.
*GSH↑,
*GPx↑,
*GSTs↑,
TumCG↓, Lycopene treatment inhibits cancer cell growth and induces apoptosis by suppressing ERK signaling pathway.
Apoptosis↑,
ERK↓,
Bcl-2↓, Lycopene decreases Bcl-2 and increases Bax expression, which induce release of cytochrome C from mitochondria, leading to apoptosis.
BAX↑,
Cyt‑c↑,
TumCCA↑, Lycopene treatment inhibits gastric cancer cell proliferation by increasing cell cycle arrest in G0–G1 phase
*DNAdam↓, Lycopene inhibits H. pylori-induced increases in ROS levels and DNA damage in gastric epithelial cells

3844- Moringa,    Review of the Safety and Efficacy of Moringa oleifera
- Review, NA, NA
*antiOx↑, biological activities including antioxidant, tissue protective (liver, kidneys, heart, testes, and lungs), analgesic, antiulcer, antihypertensive, radioprotective, and immunomodulatory actions.
*RenoP↑,
*hepatoP↑,
*radioP↑, Two studies have shown that extracts of M. oleifera can provide radioprotection in mice.
*eff↑, leaves are widely used as a basic food because of their high nutrition content
*toxicity↓, authors concluded that consumption of M. oleifera leaves at doses of up to 2000 mg/kg were safe.
*ROS↓, Chumark et al. (2008) demonstrated the free radical scavenging ability of an aqueous extract of M. oleifera leaves in several in vitro systems, and also showed that the extract inhibited lipid peroxidation in both in vitro and ex vivo systems.
*lipid-P↓,
*DNAdam↓, inhibit oxidative damage to DNA
*Catalase↑, increased the antioxidant enzymes catalase and superoxide dismutase while decreasing lipid peroxidases
*SOD↑,
*GPx↑, increases in the antioxidant enzymes glutathione peroxidase, glutathione reductase, catalase, superoxide dismutase, and glutathione S‐transferase (Sreelatha and Padma, 2010).
*GSR↑,
*GSTs↑,
*AST↓, M. oleifera leaves protects against liver damage as demonstrated by reductions in tissue histopathology and serum activities of marker enzymes aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP)
*ALAT↓,
*ALP↓,
*Bil↓, extract decreased drug‐induced levels of AST, ALT, ALP, and bilirubin

4035- NAD,  VitB3,    NAD+ supplementation reduces neuroinflammation and cell senescence in a transgenic mouse model of Alzheimer's disease via cGAS-STING
- in-vitro, AD, NA
*Inflam↓, Treatment of AD mice with NR reduced neuroinflammation, attenuated DNA damage, and prevented cellular senescence.
*DNAdam↓,
*NLRP3↓, NR treatment also reduced NLRP3 inflammasome expression, DNA damage, apoptosis, and cellular senescence in the AD mouse brains.
*cGAS–STING↓, cGAS–STING elevation was observed in the AD mice and normalized by NR treatment

4036- NAD,  VitB3,    NAD+ supplementation normalizes key Alzheimer’s features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency
- in-vivo, AD, NA
*Inflam↓, NAD+ supplementation with nicotinamide riboside significantly normalized neuroinflammation, synaptic transmission, phosphorylated Tau, and DNA damage as well as improved learning and memory and motor function.
*p‑tau↓, NR Decreases Tau Phosphorylation but Not Aβ Accumulation in AD and AD/Polβ Mice.
*DNAdam↓,
*memory↑,
*motorD↑,
*cognitive↑, NR improved cognitive function in multiple behavioral tests and restored hippocampal synaptic plasticity in 3xTgAD mice and 3xTgAD/Polβ+/− mice.
*BBB↑, NR enters the brain and boosts cellular NAD+ levels when administered orally.
IL1β↓, AD/Polβ mice had elevated levels of proinflammatory cytokines and chemokines, including IL-1α, TNFα, MCP-1, IL-1β, MIP-1α, and RANTES, and decreased levels of antiinflammatory cytokines such as IL-10 (Fig. 3G and Fig. S4A). NR treatment normalized
*TNF-α↓,
*MCP1/CCL2↓,
*RANTES↓,
*ROS↓, NR treatment of AD fibroblasts resulted in decreased levels of mitochondrial ROS compared with vehicle-treated cells
*SIRT3↑, NR Treatment Decreases DNA Damage and Apoptosis Through SIRT3 and SIRT6.
*SIRT6↑,

2933- NAD,    Nicotinamide mononucleotide (NMN) as an anti-aging health product – Promises and safety concerns
- Review, Nor, NA - NA, AD, NA - NA, Diabetic, NA - NA, Stroke, NA - NA, LiverDam, NA - NA, Park, NA
*mtDam↓, The mitochondrial decay, which is responsible for aging, can be reversed by the increased levels of nicotinamide adenine dinucleotide (NAD+) in the body.
*BioAv↝, NMN is a precursor of NAD+ that acts as an intermediate in NAD+ biosynthesis, while dietary supplements of NMN are found to increase the NAD+ levels in the body
*BioAv↑, molecular weight is 334.22 g/mol. It is fairly acidic and water-soluble compound. The solubility has been reported to be 1.8 mg/mL
*OS↑, plays a vital role in a variety of biological processes of the body including cell death, aging, gene expression, neuroinflammation and DNA repair, which indicating a significance role of NAD+ in longevity and health of human life
*eff↑, NMN has therapeutic effects towards a range of diseases, including age-induced type 2 diabetes, obesity, cerebral and cardiac ischemia, heart failure and cardiomyopathies
*eff↑, Alzheimer’s disease and other neurodegenerative disorders, corneal injury, macular degeneration and retinal degeneration, acute kidney injury and alcoholic liver disease
*cognitive↑, cognitive impairments, DNA damage and sirtulin gene inactivation, are brought about by aging which can be evaded by enhancing NAD+ count in the body
*DNAdam↓,
*SIRT1↑, NMN, the NAMPT reaction product, is able to be utilised to trigger the SIRT1 activity
*cardioP↑, NMN also can restore gene expression linked to circadian rhythm, inflammatory response and oxidative stress, and improve hepatic insulin sensitivity, partially by SIRT1 activation.
*ROS↓, NMN has been proven to reduce DNA damage and accumulation of ROS
*Dose↝, NMN in available commercial products vary from 50 to 150 mg/capsule, whereas some consumers take two 150 mg capsules per day
*BioAv↑, NMN was speedily absorbed in the small intestine by a specific transporter, which was encoded by the Slc12a8 gene as demonstrated in in vitro and in vivo studies
*hepatoP↑, NMN supplementation has been found to have significant recovering effects on hepatocyte functions and liver pathologies in early-stage of ethanol toxicity, instead of causing adverse effects to the liver
*eff↑, supplementation of NMN has been found to be a promising therapeutic remedy for PD
*BG↓, Oral administration of NMN increased serum bilirubin contents and decreased blood glucose, chloride and serum creatinine levels, but within the normal range.
*creat↓,

2936- NAD,    The Safety and Antiaging Effects of Nicotinamide Mononucleotide in Human Clinical Trials: an Update
*ROS↓, vitro/in vivo studies have demonstrated that NMN supplementation increases NAD+ concentration and could mitigate aging-related disorders such as oxidative stress, DNA damage, neurodegeneration, and inflammatory responses.
*DNAdam↓,
*neuroP↑, NAD+ concentrations in the human brain declined 10% to 25% from young adulthood to old age
*Inflam↓,
*BioAv↑, In fact, it has been shown that caloric restriction increases NAD+ bioavailability by activating
*SIRT1↑, whereas it lowers NADH levels and activates sirtuins to extend the life span of yeast
BioAv↝, NR holds an edge over NMN because cells cannot directly absorb NMN, and NMN must be converted to NR before entering cells.

2939- NAD,  Rad,    NMN ameliorated radiation induced damage in NRF2-deficient cell and mice via regulating SIRT6 and SIRT7
- in-vitro, Nor, NA
*SIRT6↑, NMN, the agonist of SIRT6/7, alleviated DNA damage in NRF2 KO cells.
*DNAdam↓,
*radioP↑, Administration of NMN could reverse IR induced intestinal injury in NRF2−/− mice.
*ROS↓, concomitant with reduced cellular ROS level and ameliorated DNA damage

6486- Nimb,    Nimbolide: promising agent for prevention and treatment of chronic diseases
- Review, Var, NA - Review, AD, NA
*other↝, Nimbolide is one of the most potent limonoids derived from the flowers and leaves of neem (Azadirachta indica), which is widely used to treat a variety of human diseases.
*Inflam↓, Nimbolide has anti-inflammatory, anti-microbial, and anti-cancer properties, which make it an intriguing compound for research.
AntiCan↑,
*Bacteria↓, pharmacological properties including antimalaria, antibacterial, antiviral, antioxidative, anti-inflammatory, antiinvasive, neuroprotective, hepatoprotective, and pro-apoptotic properties
*AntiViral↑,
*neuroP↑,
*hepatoP↑,
*ROS?, Inhibit oxidative stress, Activate Nrf2/HO-1 signaling
*NRF2↑,
*HO-1↑,
*TLR4↓, Inhibit oxidative stress Anti-inflammatory and antioxidant TLR4/NF-κB signaling pathway
*NF-kB↓,
*AChE↓, down regulation of AChE and Aβ GSK-3β interaction
*Aβ↓,
*GSK‐3β↓,
*LDL↓, Nimbolide reduced intracellular cholesterol, free fatty acids, and triglycerides and enhanced hepatocyte function by inhibiting oxidative DNA damage and lipid peroxidation through its antioxidant effects
*DNAdam↓,
*lipid-P↓,
*antiOx↑, Nimbolide showed immense antioxidant properties.
*SOD1↑, nimbolide treatment increased superoxide dismutase (SOD-1), Nrf-2, GSH, and HO-1 protein expression
*GSH↑,
*IL6↓, Nimbolide treatment resulted in a reduction of the inflammatory cytokines IL-6, IL-1β, and TNF-α, as well as inflammatory cellular signaling molecules IkB-α, STAT3, and NF-kB.
*IL1β↓,
*STAT3↓,
*GPx↑, Glutathione peroxidase, catalase (CAT), concentration were all found to be up, while malondialdehyde and nitric oxide levels were shown to be significantly reduced by nimbolide.
*Catalase↑,
*MDA↓,
*AntiDiabetic↑, Anti-diabetic effect of nimbolide in diabetes
*HDL↓, suppression of the levels of pro-inflammatory mediators, (cholesterol, TG, LDL, and HDL, MCP-1, VEGF, and MMP-9)
*MCP1/CCL2↓,
*VEGF↓,
*MMP9↓,
*GutMicro↑, nimbolide showed to reduce inflammation, oxidative stress, and to reverse gut microbiota, which protects them from gestational diabetes.
TumCP↓, Nimbolide reported to decrease cell proliferation, EMT, cell cycle progression, and migration, in breast cancer cells via downregulating the NF-κB pathway
TumCCA↑,
TumCMig↓,
NF-kB↓,
ROS↑, nimbolide stimulates the overproduction of ROS, consequently modulating both autophagy and apoptosis in pancreatic cancer cells.
PI3K↓, nimbolide-induced ROS generation hindered cell proliferation by suppressing PI3K/AKT/mTOR and ERK signaling pathways.
Akt↓,
mTOR↓,
ERK↓,
EMT↓, nimbolide-mediated ROS generation reduced EMT, migration, colony forming abilities and invasion, thereby inhibiting metastasis.
TumMeta↓,
ChemoSen↑, use of nimbolide in combination with 5-FU showed a higher inhibitory rate in breast cancer than 5-FU alone
eff↑, nimbolide synergized the effect of TRAIL to induce apoptosis in tumor cell lines, but not normal breast cells
selectivity↑,
CDK4↓, slows tumor growth by inhibiting CDK4/6 activity
CDK6↓,
Wnt↓, nimbolide suppressed the Wnt/β-catenin signaling pathway mediated by NF-κB in HCC and pancreatic cancer cells
β-catenin/ZEB1↓,
STAT3↓, nimbolide can significantly suppress the activation of oncogenic transcription factor STAT3.
MMP2↓, inhibits tumor cell growth and migration by downregulating VEGF-A and MMP-2/9 expression,
Sp1/3/4↓, nimbolide inhibited MMP-9 activity by inhibiting the binding activity of Sp-1, AP-1 and NFk-B motifs, all of which are important transcription factors.
AP-1↓,
P21↑, Nimbolide exhibited dose-dependent inhibitory effects on HeLa cell viability by causing cell cycle arrest at G0/G1 phase with p53-dependent accumulation of p21.
*AntiArt↑, The findings of the study suggest that nimbolide has the ability to reduce the severity of rheumatoid arthritis by suppressing the expression levels of toll-like receptors, IL-23, IL-17, IFN-γ and HSP70.
*IL23↓,
*IL17↓,
*IFN-γ↓,
*HSP70/HSPA5↓,

1680- PBG,    Protection against Ultraviolet A-Induced Skin Apoptosis and Carcinogenesis through the Oxidative Stress Reduction Effects of N-(4-bromophenethyl) Caffeamide, a Propolis Derivative
- in-vitro, Nor, HS68
*ROS↓, K36H reduced UVA-induced intracellular reactive oxygen species generation
*NRF2↑, increased nuclear factor erythroid 2–related factor 2 translocation into the nucleus to upregulate the expression of heme oxygenase-1, an intrinsic antioxidant enzyme.
*HO-1↑,
*cJun↓, K36H inhibited UVA-induced activation of extracellular-signal-regulated kinases and c-Jun N-terminal kinases,
*MMP1↓, reduced the overexpression of matrix metalloproteinase (MMP)-1 and MMP-2
*MMP2↓,
*p‑cJun↓, K36H inhibited the phosphorylation of c-Jun and downregulated c-Fos expression
*cFos↓,
*BAX↓, K36H attenuated UVA-induced Bax and caspase-3 expression and upregulated antiapoptotic protein B-cell lymphoma 2 expression.
*Casp3↓,
*DNAdam↓, K36H reduced UVA-induced DNA damage.
*iNOS↓, K36H also downregulated inducible nitric oxide synthase, cyclooxygenase-2 and interleukin-6 expression as well as the subsequent generation of prostaglandin E2 and nitric oxide.
*COX2/PTGS2↓,
*IL6↓,
*PGE2↓,
*NO↓,


Showing Research Papers: 1 to 50 of 70
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 70

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

CBR1↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   antiOx↑, 1,   Catalase↓, 1,   Catalase↑, 1,   Catalase∅, 1,   GPx↑, 2,   GSH↓, 1,   GSH↑, 1,   GSR↑, 1,   GSTA1↑, 1,   GSTs∅, 1,   HO-1↓, 1,   HO-2↓, 1,   MDA↑, 1,   NOX4↓, 1,   NRF2↓, 1,   ROS↓, 2,   ROS↑, 8,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 1,   MMP↓, 4,   mtDam↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   cMyc↓, 4,   ECAR↝, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   lactateProd↓, 1,   PDK1?, 2,   PPARγ↓, 1,   PPARγ↑, 1,   SIRT1↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   Akt↑, 1,   p‑Akt↓, 1,   APAF1↑, 1,   Apoptosis↓, 1,   Apoptosis↑, 7,   BAD↑, 1,   BAX↓, 1,   BAX↑, 3,   Bax:Bcl2↑, 2,   Bcl-2↓, 3,   Bcl-2↑, 1,   Bcl-xL↓, 2,   Casp↑, 1,   Casp3↑, 7,   Casp9↑, 4,   Chk2↓, 1,   Cyt‑c↓, 1,   Cyt‑c↑, 2,   Diablo↑, 1,   iNOS↓, 1,   MAPK↓, 1,   Mcl-1↓, 1,   MDM2↓, 1,   Myc↓, 1,   NOXA↑, 1,   p27/CDKN1B↑, 1,   PUMA↑, 2,   survivin↓, 1,   Telomerase↓, 1,   TumCD↑, 2,  

Kinase & Signal Transduction(tgid=6) ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,   PhotoS↑, 1,   tumCV↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

CHK1↓, 1,   DNAdam↓, 6,   DNAdam↑, 1,   P53↓, 2,   P53↑, 2,   cl‑PARP↑, 3,   PCNA↓, 1,   SIRT6↑, 1,   γH2AX↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 3,   CDK4↓, 3,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 4,   cycE/CCNE↓, 2,   P21↑, 4,   p‑RB1↓, 1,   TumCCA↓, 1,   TumCCA↑, 7,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CDK8↓, 1,   EMT↓, 2,   ERK↓, 3,   p‑ERK↓, 1,   mTOR↓, 3,   NOTCH↓, 1,   NOTCH1↑, 1,   PI3K↓, 3,   PTEN↓, 1,   PTEN↑, 1,   STAT3↓, 4,   p‑STAT3↓, 1,   TumCG↓, 2,   Wnt↓, 3,   Wnt/(β-catenin)↓, 1,  

Migration(tgid=13) ⓘ

Akt2↓, 1,   AP-1↓, 1,   Ca+2↓, 1,   Ca+2↝, 1,   E-cadherin↑, 1,   p‑FAK↓, 1,   Ki-67↓, 1,   MMP2↓, 3,   MMP9↓, 3,   MMPs↓, 2,   PKCδ↓, 2,   Slug↓, 1,   SMAD3↓, 1,   Snail↓, 2,   TET1↑, 1,   TGF-β↓, 1,   TumCMig↓, 1,   TumCP↓, 7,   TumMeta↓, 3,   TumMeta↑, 1,   Twist↓, 1,   VCAM-1↓, 1,   Zeb1↓, 1,   β-catenin/ZEB1↓, 3,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 5,   EGFR↓, 2,   Endoglin↑, 1,   Hif1a↓, 1,   LOX1↓, 1,   VEGF↓, 3,  

Barriers & Transport(tgid=15) ⓘ

NHE1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2/PTGS2↓, 4,   ICAM-1↓, 1,   IL1↑, 1,   IL1β↓, 1,   IL2↑, 1,   IL4↑, 1,   IL6↓, 1,   Imm↑, 1,   Inflam↓, 4,   JAK↓, 1,   JAK1↓, 1,   Neut↓, 1,   NF-kB↓, 5,   NK cell↑, 1,   p65↓, 1,   PD-L1↓, 1,   PGE2↓, 3,   PSA↓, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Cellular Microenvironment(tgid=17) ⓘ

NOX↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↑, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 3,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4,   BioAv↑, 2,   BioAv↝, 2,   ChemoSen↑, 8,   DDS↑, 1,   Dose↝, 3,   Dose∅, 1,   eff↓, 2,   eff↑, 10,   Half-Life↓, 2,   RadioS↑, 5,   selectivity↑, 8,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   EGFR↓, 2,   IL6↓, 1,   Ki-67↓, 1,   Myc↓, 1,   PD-L1↓, 1,   PSA↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↓, 1,   AntiCan↑, 2,   AntiTum↑, 2,   chemoP↑, 1,   chemoPv↑, 1,   QoL↑, 1,   radioP↑, 1,   RenoP↑, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 188

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiArt↑, 2,   Buty↑, 1,   diuretic↑, 1,   GLP-1R↑, 1,   SCFAs↑, 1,   SpO2↑, 1,   Stress↓, 1,   Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   antiOx↑, 19,   Bil↓, 1,   Catalase↑, 11,   Fenton↓, 1,   GPx↑, 7,   GSH↓, 1,   GSH↑, 12,   GSR↑, 1,   GSTs↑, 3,   HDL↓, 1,   HDL↑, 1,   HO-1↑, 9,   lipid-P↓, 11,   lipid-P↑, 1,   MDA↓, 8,   MPO↓, 1,   NOX4↓, 1,   NQO1↑, 1,   NRF2↑, 10,   p‑NRF2↑, 1,   Prx↑, 1,   RNS↓, 2,   ROS?, 1,   ROS↓, 35,   SIRT3↑, 1,   SOD↓, 2,   SOD↑, 11,   SOD1↑, 1,   TBARS↓, 2,   uricA↓, 1,   VitE↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

FIS1↓, 1,   MMP↑, 2,   mtDam↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACC↓, 1,   ALAT↓, 2,   BUN↓, 1,   FASN↓, 1,   LDL↓, 2,   NADPH↓, 1,   SIRT1↑, 3,   SREBP1/SREBF1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Akt↑, 1,   Apoptosis↓, 4,   BAX↓, 4,   Bax:Bcl2↓, 1,   Bcl-2↑, 3,   Bcl-xL↑, 1,   Casp↓, 1,   Casp3↓, 5,   cl‑Casp3↓, 1,   Casp9↓, 2,   Cyt‑c↓, 1,   iNOS↓, 1,   JNK↓, 1,   MAPK↓, 1,   p‑p38↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

cJun↓, 1,   p‑cJun↓, 1,   other↓, 1,   other↑, 1,   other↝, 2,   tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 2,   HSP70/HSPA5↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 44,   SIRT6↑, 2,   γH2AX↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

cFos↓, 1,   ERK↑, 2,   GSK‐3β↓, 1,   PI3K↓, 1,   PI3K↑, 1,   STAT3↓, 2,   STAT3↑, 1,   VGCC↝, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,   Ca+2↓, 3,   Ca+2↝, 1,   COL1↓, 1,   Fibrosis↓, 1,   Ki-67↓, 1,   MMP1↓, 1,   MMP2↓, 1,   MMP2↑, 1,   MMP9↓, 1,   RAGE↓, 1,   ROCK1↓, 1,   TGF-β1↓, 1,   TJ↑, 1,   Treg lymp↝, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   ZO-1↑, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 2,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 2,   GastroP↑, 1,   IBI↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD25+↑, 1,   CD4+↑, 1,   cellSen↓, 1,   COX2/PTGS2↓, 2,   FOXP3↑, 1,   HMGB1↓, 2,   ICAM-1↓, 1,   IFN-γ↓, 1,   IL1↓, 1,   IL10↓, 1,   IL10↑, 2,   IL17↓, 1,   IL1β↓, 3,   IL22↓, 1,   IL23↓, 1,   IL4↑, 1,   IL6↓, 7,   IL8↓, 1,   Imm↑, 2,   Inflam↓, 22,   JAK2↓, 1,   JAK2↑, 1,   M2 MC↑, 1,   MCP1/CCL2↓, 3,   NF-kB↓, 12,   PGE2↓, 2,   RANTES↓, 1,   TLR1↓, 1,   TLR4↓, 1,   TNF-α↓, 8,   TNF-α↑, 1,  

Cellular Microenvironment(tgid=17) ⓘ

cGAS–STING↓, 2,   NOX↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↑, 1,   AChE↓, 3,   BChE↓, 1,   BDNF↑, 3,   GABA↑, 1,   MAOA↓, 1,   tau↓, 1,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,   Aβ↓, 3,   NLRP3↓, 3,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4,   BioAv↑, 9,   BioAv↝, 1,   ChemoSen↑, 1,   Dose↓, 1,   Dose↑, 2,   Dose↝, 8,   eff↑, 9,   eff↝, 1,   P450↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   Albumin↝, 1,   ALP↓, 1,   AST↓, 2,   BG↓, 1,   Bil↓, 1,   BloodF↑, 1,   BP↓, 1,   creat↓, 2,   GutMicro↑, 4,   IL6↓, 7,   Ki-67↓, 1,   RAGE↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 2,   AntiCan↑, 6,   AntiDiabetic↑, 6,   cardioP↑, 9,   chemoP↑, 2,   cognitive↑, 4,   hepatoP↑, 10,   memory↑, 5,   motorD↑, 1,   neuroP↑, 13,   Obesity↓, 1,   OS↑, 3,   radioP↑, 5,   RenoP↑, 4,   Sleep↑, 1,   toxicity?, 1,   toxicity↓, 3,   toxicity↝, 1,   toxicity∅, 1,   Weight↓, 1,   Weight↑, 1,   Wound Healing↑, 3,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,   Bacteria↓, 2,   Sepsis↓, 1,  
Total Targets: 203

Scientific Paper Hit Count for: DNAdam, DNA damage
9 Radiotherapy/Radiation
5 nicotinamide adenine dinucleotide
4 Lycopene
4 Vitamin B3,Niacin
3 Selenium
3 Selenium NanoParticles
3 Selenite (Sodium)
2 Boron
2 doxorubicin
2 Chemotherapy
2 Chrysin
2 Ferulic acid
2 Grapeseed extract
2 Hydrogen Gas
2 Silymarin (Milk Thistle) silibinin
2 Vitamin C (Ascorbic Acid)
1 5-Hydroxytryptophan
1 Allicin (mainly Garlic)
1 Ashwagandha(Withaferin A)
1 Astaxanthin
1 Aloe anthraquinones
1 Baicalein
1 Berberine
1 Curcumin
1 Boswellia (frankincense)
1 α-Bisabolol / Chamomile oil
1 Cat’s Claw
1 Cichoric acid / Chicoric acid
1 Cinnamon
1 Coenzyme Q10
1 Carica papaya leaf extract
1 Calorie Restriction Mimetics
1 Crocetin
1 D-limonene
1 Dandelion Root
1 Cisplatin
1 Ellagic acid
1 EGCG (Epigallocatechin Gallate)
1 Eugenol
1 Sesame seeds and Oil
1 Fisetin
1 Fucoidan
1 Germanium inorganic
1 Ginkgetin
1 γ-linolenic acid (Borage Oil)
1 Helleborus niger extracts – Christmas Rose
1 Licorice
1 Moringa oleifera
1 Nimbolide
1 Propolis -bee glue
1 Resveratrol
1 Sulforaphane (mainly Broccoli)
1 Thymoquinone
1 Urolithin
1 Vitamin K2
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:82  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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