radioP Cancer Research Results
radioP, RadioProtective: Click to Expand ⟱
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Protect against the damaging effects of radiation therapy.
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Scientific Papers found: Click to Expand⟱
*ICAM-1↓, Allicin significantly inhibited gamma IR-induced surface expression of ICAM-1 and ICAM mRNA in a dose-dependent manner.
*AP-1↓, pretreatment with allicin resulted in the decrease of AP-1 activation and phosphorylation of the c-Jun NH2-terminal kinase (JNK) induced by gamma IR.
*p‑cJun↓,
*radioP↑, may be considered in therapeutic strategies for the management of patients treated with radiation therapy
JNK↓, downregulates gamma IR-induced ICAM-1 expression via inhibition of both AP-1 activation and the JNK pathway
*radioP↑, radio-protective role of alpha-lipoic acid.
*antiOx↑, Alpha-lipoic acid has anti-oxidant, anti-apoptosis, anti-inflammatory actions, etc.
*Inflam↓,
radioP↑, apigenin's radioprotective and radiosensitive properties
RadioS↑,
*COX2↓, When exposed to irradiation, apigenin reduces inflammation via cyclooxygenase-2 inhibition and modulates proapoptotic and antiapoptotic biomarkers.
*ROS↓, Apigenin's radical scavenging abilities and antioxidant enhancement mitigate oxidative DNA damage
VEGF↓, It inhibits radiation-induced mammalian target of rapamycin activation, vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP), and STAT3 expression,
MMP2↓,
STAT3↓,
AMPK↑, while promoting AMPK, autophagy, and apoptosis, suggesting potential in cancer prevention.
Apoptosis↑,
MMP9↓, radiosensitizer, apigenin inhibits tumor growth by inducing apoptosis, suppressing VEGF-C, tumor necrosis factor alpha, and STAT3, reducing MMP-2/9 activity, and inhibiting cancer cell glucose uptake.
glucose↓,
ChemoSen↑, Apigenin has also been studied for its potential as a sensitizer in cancer therapy, improving the efficacy of traditional chemotherapeutic drugs and radiotherapy
RadioS↑, Apigenin enhances radiotherapy effects by sensitizing cancer cells to radiation-induced cell death
eff↝, It works by suppressing the expression of involucrin (hINV), a hallmark of keratinocyte development. Apigenin inhibits the rise in hINV expression caused by differentiating agents
DR5↑, Apigenin also greatly upregulates the expression of death receptor 5 (DR5
selectivity↑, Surprisingly, apigenin-mediated increase of DR5 expression is missing in normal mononuclear cells from human peripheral blood and doesn't subject these cells to TRAIL-induced death.
angioG↓, Apigenin has been found to prevent angiogenesis by targeting critical signaling pathways involved in blood vessel creation.
selectivity↑, Importantly, apigenin has been demonstrated to selectively kill cancer cells while sparing normal ones
chemoP↑, This selective cytotoxicity is beneficial in cancer therapy because it reduces the negative effects frequently associated with traditional treatments like chemotherapy
MAPK↓, Apigenin's ability to suppress MAPK signaling adds to its anticancer properties.
PI3K↓, Apigenin suppresses the PI3K/Akt/mTOR pathway, which is typically dysregulated in cancer.
Akt↓,
mTOR↓,
Wnt↓, Apigenin inhibits Wnt signaling by increasing β-catenin degradation
β-catenin/ZEB1↓,
GLUT1↓, fig 3
radioP↑, while reducing radiation-induced damage to healthy tissues
BioAv↓, obstacles associated with apigenin's low bioavailability and stability
chemoPv↑, Especially as a chemopreventive agent for cancer
*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
antiOx↑, confirming antioxidant, anti-inflammatory
Inflam↓,
TumCP↓, Withania somnifera reduces tumor cell proliferation while increasing overall animal survival time.
OS↑,
RadioS↑, enhance the effectiveness of radiation therapy
radioP↑, while potentially mitigating undesirable side effects
chemoP↑, reduces the side effects of chemotherapeutic agents cyclophosphamide and paclitaxel without interfering with the tumor-reducing actions of the drugs.
*DNAdam↓, DNA damage was reduced in the radiation+astaxanthin group compared with the radiation group
*radioP↑,
*radioP↑, First, with a mice model of RILI, the protected effects of astaxanthin were observed
Inflam↓, and reduces the elevation of inflammatory factors.
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TumCP↓, application of ASX significantly reduced proliferation rates and inhibited breast cancer cell migration compared to control normal breast epithelial cells.
TumCMig↓,
selectivity↑,
*BDNF↑, ASX increases brain derived neurotropic factor (BDNF) protein levels, while concurrently decreasing oxidative stress levels [6]
*ROS↓,
*TNF-α↓, ASX decreases the amount of inflammatory markers such as TNF-α, IL-6, and IFN-γ via NFκβ inhibition [7].
*IL6↓,
*IFN-γ↓,
*NF-kB↓,
BAX⇅, In the triple-negative cell line MDA-MB-231 both BAX and BCL-2 mRNA levels were reduced following ASX treatments. while BAX levels were elevated following treatment with 50 μM ASX.
Bcl-2↓,
*antiOx↑, ASX is a marine-based ketocarotenoid that has potent antioxidant characteristics
radioP↑, Incorporation of ASX into anticancer therapy will help control tumor growth and potentially reduce the impact of radiation therapy and chemotherapy associated side effects.
ChemoSen↑,
radioP↑, Treatment with pravastatin for 24 hours after irradiation reduced the loss of endothelium‐dependent vasorelaxation and protected against enhanced vasoconstriction.
radioP↑, Treatment with pravastatin for 1 year after irradiation completely reversed irradiation‐induced changes.
radioP↑, conclude that the prophylactic use of Aloe vera reduces the intensity of radiationinduced dermatitis.
Dose↝, about two thirds of patients diagnosed with cancer are treated with radiotherapy. Acute dermatitis is a common side effect of radiation therapy, occurring in about 95% of patients treated with this modality
eff↑, The effect was more evident in patients undergoing radiotherapy with larger treatment fields and higher doses of radiation.
*toxicity↓, It was observed that the administration of β-glucan is safe and well-tolerated.
Imm↑, concomitant administration of β-glucan with chemo or radiotherapy reduced the immune depression caused by such treatments and/or accelerated the recovery of white blood cells counts.
radioP↑,
chemoP↑,
*radioP↑, Baicalein rebalances gut microbial composition pattern destroyed by irradiation. upport the potential of baicalein as a radioprotective medicine
GutMicro↑,
*P53↓, baicalein inhibited the activation of p53 and p53 mediated mitochondrial apoptosis and death receptor apoptosis in the intestine.
*Apoptosis↑,
*DR4↓,
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*toxicity↓, Berberine (Ber), an isoquinolin alkaloid with low toxicity and protective effects against radiotherapy
radioP↑,
BioAv↑, We preloaded Ber into folic acid targeting Janus gold mesoporous silica nanocarriers (FA-JGMSNs) for overcoming the poor bioavailability of Ber.
AntiTum↑, highly efficient anti-tumor effect, good biosafety
selectivity↑, as well as the effective protection of normal tissue of this nanoplatform.
eff↑, These selective distributions of Ber in cancer cells and normal cells originated from selective endocytosis as well as pH-responsive drug release, which were conducive to achieving an improved therapeutic effect of Ber.
chemoP↑, Notably, chemo/radio/photothermal therapeutics didn’t cause the amounts of deaths of HL-7702 cells, indicating an excellent biosafety of the triple-model therapy.
radioP↑, These properties enable alpha particles tagged with B-10 to selectively kill various types of cancer cells without damaging the normal cells, that helps to prevent the side effects for patients.
selectivity↑,
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ROS↑, modulation of reactive oxygen species (ROS) formation and the resulting endoplasmic reticulum stress is central to BA’s molecular and cellular anticancer activities
ER Stress↑,
TumCG↓, Cell cycle arrest, growth inhibition, apoptosis induction, and control of inflammation are all the effects of BA’s altered gene expression
Apoptosis↑,
Inflam↓,
ChemoSen↑, BA has additional synergistic effects, increasing both the sensitivity and cytotoxicity of doxorubicin and cisplatin
Casp↑, BA decreases viability and induces apoptosis by activat-
ing the caspase-dependent pathway in human pancreatic
cancer (PC) cell lines
ERK↓, BA might inhibit the activation of Ak strain transforming (Akt) and extracellular signal–regulated kinase (ERK)1/2,
cl‑PARP↑, initiation of cleavage of PARP were prompted by the treatment with AKBA
AR↓, AKBA affects the androgen receptor by reducing its expression,
cycD1/CCND1↓, decrease in cyclin D1, which inhibits cellular proliferation
VEGFR2↓, In prostate cancer, the downregulation of vascular endothelial growth factor receptor 2–mediated angiogenesis caused by BA
CXCR4↓, Figure 6
radioP↑,
NF-kB↓,
VEGF↓,
P21↑,
Wnt↓,
β-catenin/ZEB1↓,
Cyt‑c↑,
MMP2↓,
MMP1↓,
MMP9↓,
PI3K↓,
MAPK↓,
JNK↑,
*5LO↓, Table 1 (non cancer)
*NRF2↑,
*HO-1↑,
*MDA↓,
*SOD↑,
*hepatoP↑, Preclinical studies demonstrated hepatoprotective impact for BA against different models of hepatotoxicity via tackling oxidative stress, and inflammatory and apoptotic indices
*ALAT↓,
*AST↓,
*LDH↑,
*CRP↓,
*COX2↓,
*GSH↑,
*ROS↓,
*Imm↑, oral administration of biopolymeric fraction (BOS 200) from B. serrata in mice led to immunostimulatory effects
*Dose↝, BA at low concentration tend to stimulate an immune response, as those utilized in the study of Beghelli et al. (2017) however, utilizing higher concentration suppressed the immune response
*eff↑, Useful actions on skin and psoriasis
*neuroP↑, AKBA has substantially diminished the levels of inflammatory markers such as 5-LOX, TNF-, IL-6, and meliorated cognition in lipopolysaccharide-induced neuroinflammation rodent models
*cognitive↑,
*IL6↓,
*TNF-α↓,
Dose↝, treatment with micro-encapsulated sodium butyrate (MESB) (3 tablets/day). (600 mg of butyrate), a dosage recommended by the manufacturer (Butyrose® Lsc Microcaps-EP2352386B1, BLM, Sila Srl, Noale (VE), Italy).
radioP↑, MESB appears effective in reducing radiation-induced bowel toxicity during RT, minimizing stool changes, incontinence, and abdominal pain.
Pain↓,
AntiCan↑, Chlorogenic acid (5-caffeoylquinic acid, CGA), found in plants and vegetables, is promising in anticancer mechanisms.
*chemoP↑, CGA can overcome resistance to conventional chemotherapeutics and alleviate chemotherapy-induced toxicity by scavenging free radicals effectively.
TNF-α↓, CGA reduces inflammation levels in renal tissues by down-regulating tumor necrosis factor-alpha (TNF-α) and cyclooxygenase-2 (COX-2),
COX2↓,
IL6↓, Moreover, CGA exhibits a protective effect against 5-FU-induced ovarian tissue damage, reducing Interleukin 6 (IL-6) levels;
eff↑, CGA suppresses the expression of Programmed Cell Death Ligand 1 (PD-L1) on cancer cells, boosting the antitumor effect of the anti-PD-1 antibody and enhancing anticancer immunotherapy
PD-L1↓,
*cognitive↓, CGA, have shown promise in preventing cognitive dysfunction and suppressing amyloid β plaques
*Aβ↓,
*TAC↑, hyperlipidemic patients who ingested 200 mL of Mate tea (12.5 mg/mL) daily experienced a significant increase in serum total antioxidant status and the enzymatic activity of superoxide dismutase (SOD),
*SOD↑,
*eff↑, In blueberry jam production, the high-temperature processing of blueberries with sucrose promoted the formation of 11 CGA derivatives
*eff↑, roasting process (170 to 200 °C/10 to 30 min) of coffee beans promotes CGA transformation to four chlorogenic acid lactones
ChemoSen↑, CGA was found to increase the sensitivity of hepatocellular carcinoma cells to 5-FU treatment
tumCV↓, CGA was shown to collaborate by significantly reducing cell viability and growth through induction of apoptosis, attributed to inhibition of extracellular signal-regulated kinases (ERKs)
Apoptosis↑,
ERK↓,
chemoP↑, Protective Role of Chlorogenic Acid against Toxicity Induced by Chemotherapy
*GPx↑, figure4
*GSTs↑,
*GSH↑,
*SOD↑,
*Catalase↑,
*ROS↓,
*lipid-P↓,
*MDA↓,
*Casp3↓,
*HO-1↓,
cardioP↑, reported the cardioprotective effect of CGA against doxorubicin-induced cardiotoxicity in female Swiss albino mice.
radioP↑, The radioprotective potential of CGA against γ-radiation-induced chromosomal damage in male albino Swiss mice was initially demonstrated in 1993.
ChemoSen↑, Such effects of curcumin were due to its ability to sensitize cancer cells for increased production of ROS
NF-kB↓, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-κB, STAT3, COX2, Akt
*STAT3↓, curcumin acts as a chemosensitizer and radiosensitizer has also been studied extensively. For example, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-kB, STAT3, COX2, Akt,
*COX2↓,
*Akt↓,
*NRF2↑, The protective effects of curcumin appear to be mediated through its ability to induce the activation of NRF2 and induce the expression of antioxidant enzymes (e.g., hemeoxygenase-1, glutathione peroxidase
*HO-1↑,
*GPx↑,
*NADPH↑,
*GSH↑, increase glutathione (a product of the modulatory subunit of gamma-glutamyl-cysteine ligase)
*ROS↓, dietary curcumin can inhibit chemotherapy-induced apoptosis via inhibition of ROS generation and blocking JNK signaling
*p300↓, inhibit p300 HAT activity
radioP↑, radioprotector for normal organs
chemoP↑, curcumin has also been shown to protect normal organs such as liver, kidney, oral mucosa, and heart from chemotherapy and radiotherapy-induced toxicity.
RadioS↑,
*antiOx↑, Curcumin is an antioxidant agent with both radiosensitizing and radioprotective properties
radioP↑,
RadioS∅, In the present study we have failed to observe any radiosensitizing or prooxidant feature for curcumin in the prescribed dose;
*TAC↑, The present study showed that curcumin can increase TAC and decrease SOD activity in the plasma of patients with prostate cancer receiving radiotherapy; these observations are thought to be possibly brought about by the antioxidant effect of curcumin
*SOD↓, 3 mo after completion of radiotherapy, TAC increased significantly (P < 0.001) and the activity of
SOD decreased significantly
chemoP↑, In head and neck cancer patients, the VFJ was significantly associated with a lower risk of chemoradiotherapy-induced ulcerative oral mucositis.
radioP↑,
eff↑, incidence of ulcerative OM was significantly lower in VFJ (64.0%) than in control (95.8%) subjects at week 6 of CCRT.
*DNMTs↓, EGCG (epigallocatechin gallate), a tea polyphenol with known DNMT inhibitory property, in C57 Bl/6 mice model.
*radioP↑, EGCG reduced cytogenetic damage to bone marrow cells in radiation exposed mice significantly
*HDAC↑, ELISA assay with bone marrow cell lysates showed EGCG as an inhibitor of HDAC activity
*antiOx↑, antioxidant, anti-inflammatory and antidiabetic, thus suggesting it could be exploited as a possible novel neuroprotective strategy.
*Inflam↓,
*neuroP↑, neuroprotective strategy against AD due to its promising antioxidant and anti-inflammatory properties.
*NF-kB↓, inhibition of the nuclear factor kappa-B (NF-κ B), a key mediator of proinflammatory cytokine signaling pathway, which promotes the synthesis of interleukin (IL)-1β, IL-6, and tumor necrosis factor alpha (TNF-α), leading to neuroinflammation
*NLRP3↓, also inhibited the NLR pyrin domain-containing protein 3 (NLRP3) inflammasome
*iNOS↓, A down-regulation by ferulic acid of proinflammatory molecules, such as nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, IL-1β, vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1),
*COX2↓,
*TNF-α↓,
*IL1β↓,
*VCAM-1↓,
*ICAM-1↓,
*p‑MAPK↓, Ferulic acid was also able to affect the mitogen activated protein kinases (MAPKs) pathway, by inhibiting the phosphorylation of MAPKs, including p38 and c-Jun N-terminal kinase (JNK)
*p38↓,
*JNK↓,
*IL6↓, reduction of proinflammatory cytokines (IL-1β, IL-6, TNF-α and IL-8) mRNA expression
*IL8↓,
*hepatoP↑, ferulic acid reduces the liver damage induced by acetaminophen
*RenoP↑, renal protective effects by enhancing the CAT activity and PPAR γ gene expression
*Catalase↑,
*PPARγ↑,
*ROS↓, it was able to scavenge free radicals, inhibit the generation of reactive oxygen species (ROS)
*Fenton↓, inhibit the generation of reactive oxygen species (ROS) through the Fenton reaction, acting as a chelator of metals (i.e., Fe and Cu)
*IronCh↑,
*SOD↑, increasing the activity of the antioxidant superoxide dismutase (SOD) and catalase (CAT) enzymes
*MDA↓, lowering in the levels of malondialdehyde (MDA), a lipid peroxidation marker,
*lipid-P↓,
*NRF2↑, ferulic acid has been found associated to the modulation of several signaling pathways, and to an increased expression of the nuclear translocation of the transcription factor NF-E2-related factor (Nrf2)
*HO-1↑, Particularly, Nrf2 binds the antioxidant responsive element (ARE) in the promoter region of the heme oxygenase-1 (HO-1) gene,
*ARE↑,
*Bil↑, production of bilirubin, which acts as an efficient ROS scavenger, in human umbilical vein endothelial cells (HUVEC) under radiation-induced oxidative stress
*radioP↑,
*GCLC↑, HO-1 upregulation, an increased expression of other antioxidant genes, such as glutamate-cysteine ligase catalytic subunit (GCLC), glutamate-cysteine ligase regulatory subunit (GCLM), and NADPH quinone oxidoreductase-1 (NQO1) were induced by ferulic
*GCLM↑,
*NQO1↑,
*Half-Life↝, highest plasma concentration varies greatly depending on the investigated species: it is reached at 24 min and 2 min after ingestion in humans and rats, respectively
*GutMicro↑, ferulic acid esterified forms have been shown to act as a prebiotic, since they stimulate the growth of eubacteria, such as Lactobacilli and Bifidobacteria, in the human gastrointestinal tract, so preserving the homeostasis of gut microbiota,
*Aβ↓, ferulic acid was able to inhibit the aggregation of Aβ25–35, Aβ1–40, and Aβ1–42 and to destabilize pre-aggregated Aβ.
*BDNF↑, up-regulation of brain-derived neurotrophic factor (BDNF) gene were observed after treatment with ferulic acid
*Ca+2↓, prevented membrane damage, scavenged free radicals, increased SOD activity, and decreased the intracellular free Ca2+ levels, lipid peroxidation, and the release of prostaglandin E2 (PGE2);
*lipid-P↓,
*PGE2↓,
*cognitive↑, highlighted that ferulic administration (0.002–0.005% in drinking water) for 28 days improved the trimethyltin-induced cognitive deficit: an increase in the choline acetyltransferase activity was hypothesized as a possible mechanism of action.
*ChAT↑,
*memory↑, Another study showed that ferulic acid, administered intragastrically (30 mg/kg) for 3 months, improved memory in the transgenic APP/PS1 mice, and reduced Aβ deposits,
*Dose↝, 4-week prospective, open-label trial, in which patients (n = 20) assumed daily Feru-guard® (3.0 g/day), was designed.
*toxicity↓, Salau et al. [130] did not find signs of toxicity of ferulic acid in hippocampal neuronal cell lines HT22 cells, thus concluding that the substance seems to be safe in healthy brain cells
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*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↑,
Apoptosis↑, (GLA) induced apoptosis of tumor cells without harming normal cells.
selectivity↑,
eff↓, anti-oxidants such as vitamin E blocked the tumoricidal action of GLA.
ROS↑, GLA-treated tumor but not normal cells produced a 2-3-fold increase in free radicals and lipid peroxides.
lipid-P↑,
P53↑, enhanced the activity of p53
radioP↑, protected normal cells and tissues from the toxic actions of radiation and anti-cancer drugs, enhanced the cytotoxic action of anti-cancer drugs and reversed tumor cell drug resistance.
chemoP↑,
ROS↓, previous studies have shown that H2 can selectively scavenge highly toxic reactive oxygen species (ROS) and inhibit various ROS-dependent signaling pathways in cancer cells, thus inhibiting cancer cell proliferation and metastasis.
TumCP↓,
TumMeta↓,
AntiTum↑, Anti-tumor barrier: H2 produced by intestinal flora
GutMicro↑, hydrogen-rich water (HRW) supplementation significantly inhibited the expansion of opportunistic pathogenic E. coli and increased intestinal integrity in mice with colitis
Inflam↓, H2 maintains the integrity of the intestinal barrier, reduces intestinal inflammation and damage in rat
OS↑, inhalation of H2 for 3 h daily significantly prolonged progression-free survival and overall survival in stage IV colon and rectal patients
radioP↑, administration of inhaled H2 during radiotherapy treatment reduced the damage to the hematological and immune systems
selectivity↑, Through these studies, we believe that the ability of H2 to selectively scavenge highly toxic ROS may be the core and fundamental mechanism of its anti-tumor effects, so this paper mainly focuses on this point of discussion.
SOD↑, H2 inhibited ROS expression and increased SOD, IL-1β, IL-8, IL-13, and tumor necrosis factor-α (TNF-α) expression in lung tissue of cancer
IL1β↑,
IL8↑,
TNF-α↑,
neuroP↑, Ono et al. found that 3% H2 inhaled twice daily for 1 h significantly improved vital signs, stroke scale scores, physiotherapy index, and 2-week brain MRI in stroke patients compared with conventional treatment.
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Inflam↑, Oxyhydrogen gas, a mixture of 66% molecular hydrogen (H2) and 33% molecular oxygen (O2) has shown exceptional promise as a novel therapeutic agent due to its ability to modulate oxidative stress, inflammation, and apoptosis.
ROS↓, neutralises reactive oxygen and nitrogen species
ChemoSen↑, enhancing existing treatments and reducing harmful oxidative states in cancer cells. boosting the effectiveness of conventional therapies
p‑PI3K↓, inhibiting the PI3K/Akt phosphorylation cascade.
p‑Akt↓,
QoL↑, Similar results have been observed in breast cancer, where patients reported improved quality of life.
GutMicro↑, improves intestinal microflora dysbiosis.
chemoP↑, reduced oxidative stress and mitigated tissue damage, suggesting its potential as a cytoprotective agent in cancer patients undergoing radiation therapy or chemotherapy
radioP↑,
*NRF2↑, documented role in activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway.
*Catalase↑, consequently, hydrogen can enhance the expression of endogenous antioxidant enzymes, including catalase (CAT), glutathione peroxidase (GPx), haem oxygenase (e.g., HO-1), and superoxide dismutase (SOD) [45]
*GPx↑,
*HO-1↑,
*SOD↑,
*TNF-α↓, reducing the expression of proinflammatory mediators such as chemokines (e.g., CXCL15), cytokines (e.g., TNF-α), interleukins (e.g., IL-4, IL-6)
*IL4↓,
*IL6↓,
ChemoSen↑, further research demonstrates that oxyhydrogen gas enhanced the sensitivity of lung cancer cells to chemotherapy drugs, suggesting its potential as an adjuvant therapy
Appetite↑, inhaled oxyhydrogen gas over a minimum of 3 months. The results indicated substantial improvements in appetite, cognition, fatigue, pain, and sleeplessness
cognitive↑,
Pain↓,
Sleep↑,
other?, It is recommended that hydrogen should not exceed 4.6% in air or 4.1% by volume in pure oxygen gas (explosion risk)
*Half-Life↓, Except the thigh muscle required a longer time to saturate, the other organs need 5–10 min to reach Cmax (maximum hydrogen concentration).
*ROS↓, regulate several key players in cancer, including ROS, and certain antioxidant enzymes
*selectivity↑, hydrogen gas could selectively scavenge the most cytotoxic ROS, •OH, as tested in an acute rat model of cerebral ischemia and reperfusion
*SOD↑, the expression of superoxide dismutase (SOD) (48), heme oxyganase-1 (HO-1) (49), as well as nuclear factor erythroid 2-related factor 2 (Nrf2) (50), increased significantly, strengthening its potential in eliminating ROS.
*HO-1↑,
*NRF2↑,
*chemoP↑, reduce the adverse effects in cancer treatment while at the same time doesn't abrogate the cytotoxicity of other therapy, such as radiotherapy and chemotherapy
*radioP↑,
ROS↑, Interestingly, due the over-produced ROS in cancer cells (38), the administration of hydrogen gas may lower the ROS level at the beginning, but it provokes much more ROS production as a result of compensation effect, leading to the killing of cancer
*Inflam↓, By regulating inflammation, hydrogen gas can prevent tumor formation, progression, as well as reduce the side effects caused by chemotherapy/radiotherapy
eff↑, More importantly, hydrogen-rich water didn't impair the overall anti-tumor effects of gefitinib both in vitro and in vivo, while in contrast, it antagonized the weight loss induced by gefitinib and naphthalene, and enhanced the overall survival rate
*TNF-α↓, hydrogen-rich saline treatment exerted its protective effects via inhibiting the inflammatory TNF-α/IL-6 pathway, increasing the cleaved C8 expression and Bcl-2/Bax ratio, and attenuating cell apoptosis in both heart and liver tissue
*IL6↓,
*cl‑Casp8↑,
*Bax:Bcl2↓,
*Apoptosis↓,
*cardioP↑,
*hepatoP↑,
*RenoP↑, Hydrogen-rich water also showed renal protective effect against cisplatin-induced nephrotoxicity in rats.
*chemoP↑, nother study showed that both inhaling hydrogen gas (1% hydrogen in air) and drinking hydrogen-rich water (0.8 mM hydrogen in water) could reverse the mortality, and body-weight loss caused by cisplatin via its anti-oxidant property
eff↝, More importantly, hydrogen didn't impair the anti-tumor activity of cisplatin against cancer cell lines in vitro and in tumor-bearing mice
chemoP↑, hydrogen-rich water combinational treatment group exhibited no differences in liver function during the treatment, probably due to its antioxidant activity, indicating it a promising protective agent to alleviate the mFOLFOX6-related liver injury
radioP↑, consumption of hydrogen-rich water reduced the radiation-induced oxidative stress while at the same time didn't compromise anti-tumor effect of radiotherapy
eff↑, Hydrogen Gas Acts Synergistically With Thermal Therapy
TumCG↓, in vivo study showed that under hydrogen gas treatment, tumor growth was significantly inhibited, as well as the expression of Ki-67, VEGF and SMC3
Ki-67↓,
VEGF↓,
selectivity↑, H2-silica could concentration-dependently inhibit the cell viability of human esophageal squamous cell carcinoma (KYSE-70) cells, while it need higher dose to suppress normal human esophageal epithelial cells (HEEpiCs), indicating its selective profi
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AntiTum↑, Hydrogen also has direct and indirect antitumor effects, which could be useful for the treatment of cancer patients. Hydrogen therapy improves overall survival, quality of life, blood parameters, and tumor reduction.
OS↑,
QoL↑,
TumVol↓,
radioP↑, In addition, hydrogen attenuates the risk of carcinogenesis induced by radiation.
Dose↑, Patients begin hydrogen inhalation 10 minutes prior to vitamin C injection. Patients are treated with high-dose vitamin C injection while inhaling simultaneous hydrogen
Dose↝, patients also performed the hydrogen and vitamin C combination therapy at home on their own as much as possible
eff↑, These results suggest that in normal cells, the combination of 1 mM vitamin C and hydrogen is the most effective radioprotective agent.
*TrxR1↑, HKL pre-exposure significantly increased the expressions of TrxR1 and Trx proteins in general, in particular at doses ranging between 0.05 and 5 µM HKL
*Trx↑,
*radioP↑, Overall, the findings presented here demonstrate that HKL has the potential to be a novel radioprotector capable of cellular protection against radiation-induced injuries
*ROS↓, Compared to the IR group, there was a significant decrease in the ROS levels of the HKL+IR treated group
*radioP↑, Studies have designated lycopene to be an effective radio-protector with negligible side effects.
*antiOx↑, Antioxidant and radioprotective effects of lycopene
*lipid-P↓, Pretreatment of lycopene to ã-irradiated lymphocytes resulted in decreased lipid peroxidation and improved antioxidant status which prevented damage to the lymphocytes
AntiCan↑, From an anti-cancer perspective, lycopene is often associated with reduced risk of prostate cancer and people often look for it as a dietary supplement which may help to prevent cancer.
TumCP↓, Lycopene was known to be able to suppress cancerous cell proliferation, migration, invasion and adhesion activity in cell culture studies.
TumCMig↓,
TumCI↓,
TumCA↓,
ROS↓, Such suppression was often observed with changes of cancer-related gene expression and relief of oxidative stress
MMP2↓, In general, lycopene could suppress the expression of MMP-2, MMP-7, MMP-9, Sp1, IGF-1R, VEGF while increasing E-cadherin stabilization, connexin 43, nm23-H1, TIMP-1 and TIMP-2 levels
MMP7↓,
MMP9↓,
VEGF↓,
E-cadherin↑,
TIMP1↑,
TIMP2↑,
BioAv↝, it is recommended to avoid consumption of lycopene concurrently with high dietary fiber intake as several types of dietary fiber were found to be able to reduce the bioavailability of lycopene
*IL12↓, lycopene could suppress proinflammatory cytokines such as IL-12, TNF-α, IL-1, IL-1β, IL-6
*TNF-α↓,
*IL1↓,
*IL1β↓,
*IL6↓,
COX2↓, Sprague Dawley rat model, lycopene treatment after induction by azoxymethane caused suppression of aberrant crypt foci, preneoplastic lesion and biomarkers such as COX-2 and iNOS expression
iNOS↓,
*radioP↑, lycopene before induction of DNA damage via X-irradiation as lycopene treatment after irradiation failed to show such DNA protective effect
NF-kB↓, anti-cancer effect of lycopene was also observed in pancreatic cancer cells (PANC-1 cell line) whereby significant reduction of ROS, NF-κB and anti-apoptotic biomarkers (cIAP1, cIAP2 and survivin) was detected while an increment of caspase-3 and Bax:
survivin↓,
Casp3↑,
Bax:Bcl2↑,
chemoP↑, According to the findings, it was shown that melatonin co-treatment alleviates the ototoxic damage induced by chemotherapy and radiotherapy
radioP↑,
antiOx↑, melatonin may exert its otoprotective effects via its anti-oxidant, anti-apoptotic, and anti-inflammatory activities and other mechanisms.
Inflam↑,
Remission↑, tumor remission rate in the MLT group was significantly higher than that in the control group
OS↑, MLT group had an overall survival rate of 28.24% (n=294/1,041), which was greatly increased compared with the control group (RR =2.07; 95% CI, 1.55–2.76; P<0.00001; I2=55%)
neuroP↑, MLT could effectively reduce the incidence of neurotoxicity
VEGF↓, by the downregulation of vascular endothelial growth factor (VEGF)
KISS1↑, MLT could suppress the metastasis of triple-negative breast cancer by inducing KISS1 expression
TumCP↓, MLT can significantly inhibit the proliferation of cancer cells
ChemoSideEff↓, while reducing the incidence of side effects in chemotherapy or radiotherapy
radioP↑, In the 20 randomized trials included, MLT was beneficial to reduce multiple side effects of radiotherapy and chemotherapy
Dose∅, mostly 20 mg/day and taken orally and taken at night, respectively
*ROS↓, Preclinical experimental research has confirmed that MLT was capable of scavenging ROS and repairing damaged DNA to exert antitumor effects
DNArepair↑,
ROS↑, The mechanisms of MLT exerting antitumor effect might involve with other pathways, such as antiangiogenesis and pro-oxidant
Dose∅, dosage of melatonin used in the 8 included RCTs was 20 mg orally, once a day.
Remission↑, Melatonin significantly improved the complete and partial remission (16.5 vs. 32.6%; RR = 1.95, 95% CI, 1.49-2.54; P < 0.00001)
OS↑, as well as 1-year survival rate (28.4 vs. 52.2%; RR = 1.90; 95% CI, 1.28-2.83; P = 0.001)
radioP↑, dramatically decreased radiochemotherapy-related side effects
AntiCan↑, involvement of melatonin in different anticancer mechanisms
Apoptosis↑, apoptosis induction, cell proliferation inhibition, reduction in tumor growth and metastases
TumCP↓,
TumCG↑,
TumMeta↑,
ChemoSideEff↓, reduction in the side effects associated with chemotherapy and radiotherapy, decreasing drug resistance in cancer therapy,
radioP↑,
ChemoSen↑, augmentation of the therapeutic effects of conventional anticancer therapies
*ROS↓, directly scavenge ROS and reactive nitrogen species (RNS)
*SOD↑, melatonin can regulate the activities of several antioxidant enzymes like superoxide dismutase, glutathione reductase, glutathione peroxidase, and catalase
*GSH↑,
*GPx↑,
*Catalase↑,
Dose∅, demonstrated that 1 mM melatonin concentration is the pharmacological concentration that is able to produce anticancer effects
VEGF↓, downregulatory action on VEGF expression in human breast cancer cells
eff↑, tumor-bearing mice were treated with (10 mg/kg) of melatonin and (5 mg/kg) of cisplatin. The results have shown that melatonin was able to reduce DNA damage
Hif1a↓, MDA-MB-231-downregulation of the HIF-1α gene and protein expression coupled with the production of GLUT1, GLUT3, CA-IX, and CA-XII
GLUT1↑,
GLUT3↑,
CAIX↑,
P21↑, upregulation of p21, p27, and PTEN protein is another way of melatonin to promote cell programmed death in uterine leiomyoma
p27↑,
PTEN↑,
Warburg↓, FIGURE 3
PI3K↓, in colon cancer cells by downregulation of PI3K/AKT and NF-κB/iNOS
Akt↓,
NF-kB↓,
cycD1/CCND1↓,
CDK4↓,
CycB/CCNB1↓,
CDK4↓,
MAPK↑,
IGF-1R↓,
STAT3↓,
MMP9↓,
MMP2↓,
MMP13↓,
E-cadherin↑,
Vim↓,
RANKL↓,
JNK↑,
Bcl-2↓,
P53↑,
Casp3↑,
Casp9↑,
BAX↑,
DNArepair↑,
COX2↓,
IL6↓,
IL8↓,
NO↓,
T-Cell↑,
NK cell↑,
Treg lymp↓,
FOXP3↓,
CD4+↑,
TNF-α↑,
Th1 response↑, FIGURE 3
BioAv↝, varies 1% to 50%?
RadioS↑, melatonin’s radio-sensitizing properties
OS↑, In those individuals taking melatonin, the overall tumor regression rate and the 5-year survival were elevated
QoL↑, melatonin combined with standard chemotherapy lines would derive, at least, a better quality of life for breast cancer patients
OS↑, Moreover, regular doses of 20 mg/day seemed to increase partial response and 1-year survival rates.
Dose∅, regular doses of 20 mg/day
antiOx↑, melatonin possesses antioxidant properties, which may help to protect cells from damage caused by free radicals
ROS↑, elimination of free radicals non-enzymatically transforms melatonin into metabolites with greater antioxidant capacity, which enabling the removal of 10 reactive species per molecule
SOD↑, melatonin upregulates various antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase
Catalase↑,
GPx↑,
Risk↓, individuals with higher melatonin levels show a lower risk of developing breast cancer, and melatonin supplementation may help inhibit the growth and spread of breast cancer cells
NK cell↑, enhance natural killer cell activity
IL1β↓, inhibit the production of pro-inflammatory cytokines such as interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α)
IL6↓,
TNF-α↓,
radioP↑, protect hematopoietic progenitor cells from radiation therapy and chemotherapy
chemoP↑,
TumVol↓, most frequent observations was the ability of melatonin to reduce tumor size
TumMeta↓, decrease the risk of metastasis
angioG↓,
ChemoSen↑, melatonin can synergistically potentiate drug cytotoxicity.
eff↑, it has been suggested that administering melatonin at the appropriate phase of the circadian cycle may enhance its anti-tumor activity and reduce the side effects of chemotherapy and radiation therapy
radioP↑, A unique pulsed-burst EMF (PEMF) at 15 Hz and 2 mT induces notable Ca2+ oscillations with robust Ca2+ spikes in osteoblasts in contrast to other waveforms. This waveform parameter substantially inhibits radiotherapy-induced bone loss
*Ca+2↑,
RAS↑, PEMF-induced activation of Ras/MAPK signaling.
MAPK↓,
*OS↑, The RMF treatment increased the survival rate and survival days among the irradiated mice
*radioP↑, RMF treatment had an obvious protective effect against the effects of irradiation and it accelerated the recovery of hematopeiesis and the hematopoietic microenvironment in mouse bone marrow
AntiCan↑, RMF can inhibit the growth of various types of cancer cells in vitro and in vivo and improve clinical symptoms of patients with advanced cancer.
breath↑, 0.4T, 7Hz RMF was applied to treat 13 advanced non-small cell lung cancer patients (2 h/day, 5 days per week, for 6–10 weeks)
Pain↓, Decreased pleural effusion (2 patients, 15.4%), remission of shortness of breath (5 patients, 38.5%), relief of cancer pain (5 patients, 38.5%), increased appetite (6 patients, 46.2%), improved physical strength (9 patients, 69.2%), regular bowel mov
Appetite↑,
Strength↑,
BowelM↑,
TumMeta↓, The same RMF (2 h/day, for 43 days) can also suppress the growth and metastasis of B16-F10 cells in vivo
TumCCA↑, The up-regulated transcription of miR-34a induced cell proliferation inhibition, cell cycle arrest, and cell senescence by targeting E2F1/E2F3, two members of E2F family which are major regulators of the cell cycle,
ETC↓, 2h exposure) effectively inhibited the growth of two types of cultured brain cancer cells, glioblastoma cells and diffuse intrinsic pontine glioma cells. They found that the mitochondrial electron transport chain was significantly disturbed by RMF,
MMP↓, which caused loss of mitochondrial integrity, decreased mitochondrial carbon flux in cancer cells, and eventual cancer cell death (Sharpe et al., 2021).
TumCD↑,
selectivity↑, same group further reported that the
same RMF can also selectively kill cultured human glioblastoma and
non-small cell lung cancer cells, and leave normal cells unharmed
ROS↑, Mechanistic studies revealed that RMF can increase the mitochondrial ROS level, which further activated the caspase-3 and disturbed the electron fflow in the respiratory chain pathway in cancer cells. (Helekar et al., 2021).
Casp3↑,
TumCG↓, 0.4T, 7.5Hz RMF (2 h/day, for 5 days) inhibited the growth of mouse melanoma cell line B16–F10 in vitro,
TumCCA↑, and its mechanism involved cell cycle arrest and decomposition of chromatins.
ChrMod↑,
TumMeta↓, (2 h/day, for 43 days) can also suppress the
growth and metastasis of B16–F10 cells in vivo,
Imm↑, benefiting from improved immune function, including decreased regulatory T cells, increased T cells, and dendritic cells
DCells↑,
Akt↓, inhibiting the activation of the AKT pathway (Tang et al., 2016). T
OS⇅, 51 women with advanced breast cancer underwent RMF treatment. The results showed that 27 patients among them achieved signicant therapeutic effects, and there were no side-effects
toxicity↓,
QoL↑, 13 advanced non-small cell lung cancer patients the quality of life was improved in different degrees. Median survival and 1-year survival rate was 50% and 100% longer
hepatoP↑, In addition, it seems that the RMF can also attenuate liver damage in mice bearing MCF7 and GIST-T1 cells (Zha et al., 2018)
Pain↓, The results showed that the RMF treatment reduced abdominal pain by 42.9% (9/21), nausea/vomiting by 19.0% (4/21), weight loss by 52.4% (11/21), ongoing blood loss by 9.5% (2/21), improved physical strength by 23.8% (5/21) and sleep quality by 19.0%
Weight↑,
Strength↑,
Sleep↑,
IL6↓, Furthermore, decreased levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and keratinocyte-derived chemokine (KC) were observed
CD4+↑, it was discovered that macrophages and dendritic cells were
activated, CD4+ T and CD8+ T lymphocytes increased, and the ratio of
Th17/Treg was balanced.
CD8+↑,
Ca+2↑, effects of RMF were strongly
associated with increased calcium tunnel activity and intracellular Ca2+
level in CNS
radioP↑, These results suggest that RMF may be helpful to alleviate the
damage of hematopoietic function caused by radiotherapy and chemotherapy
chemoP↑,
*BMD↑, 0.4T, 8Hz RMF treatment (30min/day, for 30 days) along with calcium supplement, synergistically improved bone density
*AntiAge↑, In 2019, Xu et al. reported that a 4h exposure to a 0.2T, 4Hz RMF
delayed the aging of human umbilical vein endothelial cells (HUVEC)
*AMPK↑, Mechanistic research revealed that RMF treatment increased the expression of AMPK while reducing the expression of p21, p53 and mTOR.
*P21↓,
*P53↓,
*mTOR↓,
*OS↑, They also discovered that the RMF (2 h/day, for 6, 10 or 14days) can prolong the
health status lifespan of Caenorhabditis elegans.
*β-Endo↑, 0.1–0.8T, 0.33Hz RMF treatment signicantly increased the β-endorphin level in the blood of rabbits and humans (23 times higher than before). Moreover, it decreased serotonin (5-HT) in brains, small intestine tissue and serum of mice.
*5HT↓,
*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
*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
Hif1a↓, Flavonoid components from propolis, as inhibitors of HIF-1, have the ability to regulate critical glycolytic components in cancer cells, including (PKM2), (LDHA), (GLUTs), (HKII), (PFK-1), and (PDK)
Glycolysis↓,
PKM2↓,
LDHA↓,
GLUT2↓,
HK2↓,
PFK1↓,
PDK1↓,
chemoP↓, The positive effects of combining propolis with chemotherapeutics include reduced cytotoxicity to peripheral blood leukocytes, liver, and kidney cells.
radioP↑, Their selective nature makes them suitable for protecting normal cells while inducing cell death in cancer cells during chemotherapy or radiotherapy.
| - |
in-vitro, |
Pca, |
LNCaP |
|
|
|
- |
in-vitro, |
Pca, |
DU145 |
|
|
|
- |
in-vitro, |
Nor, |
PrEC |
|
|
|
- |
in-vivo, |
NA, |
NA |
|
|
|
ROS↑, parthenolide enhances ROS production in prostate cancer cells through activation of NADPH oxidase
NADPH↑,
RadioS↑, In vivo, parthenolide increases radiosensitivity of mouse xenograft tumors but protects normal prostate and bladder tissues against radiation-induced injury
radioP↑, DMAPT, the water soluble prodrug of parthenolide, is a promising agent for selectively enhancing the sensitivity of prostate cancer cells to radiation while protecting normal tissues from damage caused by radiation.
Trx↓, causes oxidation of thioredoxin (TrX) in prostate cancer cells
*ox-Keap1↑, three normal cell lines, parthenolide increased the oxidized form of Keap1 but decreased the reduced form of Keap1
ox-Keap1↓, results from the three cancer cell lines appeared to be completely opposite to results observed in normal cells treated with parthenolide
rd-Keap1↑, in vivo results show that parthenolide decreased the oxidized form of Keap1 but increased the reduced form of Keap1 in the tumors
*NRF2↑, Oxidization of Keap1 leads to activation of the Nrf2 pro-survival pathway in normal cells. Nrf2 pathway is a major mechanism by which parthenolide protects normal cells against radiation injury
NRF2∅, but no changes were observed in the three cancer cell lines.
NF-kB↓, It has been reported that parthenolide is a potent inhibitor of NF-κB
| - |
in-vitro, |
Pca, |
PC3 |
|
|
|
- |
in-vitro, |
Nor, |
PrEC |
|
|
|
selectivity↑, parthenolide (PN), a sesquiterpene lactone, selectively exhibits a radiosensitization effect on prostate cancer PC3 cells but not on normal prostate epithelial PrEC cells.
RadioS↑,
ROS↑, oxidative stress in PC3 cells but not in PrEC cells
*ROS∅, oxidative stress in PC3 cells but not in PrEC cells
NADPH↑, In PC3 but not PrEC cells, PN activates NADPH oxidase leading to a decrease in the level of reduced thioredoxin, activation of PI3K/Akt and consequent FOXO3a phosphorylation, which results in the downregulation of FOXO3a targets, MnSOD, CAT
Trx↓,
PI3K↑,
Akt↑,
p‑FOXO3↓, downregulation of FOXO3a targets, antioxidant enzyme manganese superoxide dismutase (MnSOD) and catalase
SOD2↓, MnSOD
Catalase↓,
radioP↑, when combined with radiation, PN further increases ROS levels in PC3 cells, while it decreases radiation-induced oxidative stress in PrEC cells
*NADPH∅, Parthenolide activates NADPH oxidase in PC3 cells but not in PrEC cells
*GSH↑, increases glutathione (GSH) in PrEC cells(normal cells)
*GSH/GSSG↑, GSH/GSSG ratio is not significantly changed by parthenolide in PC3 cells but is increased 2.4 fold in PrEC cells (normal cells)
*NRF2↑, The induction of GSH may be due to the activation of the Nrf2/ARE (antioxidant/electrophile response element) pathway
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
Stroke, |
NA |
|
|
|
*antiOx↑, The antioxidant mechanism of quercetin in vivo is mainly reflected in its effects on glutathione (GSH), signal transduction pathways, reactive oxygen species (ROS), and enzyme activities.
*GSH↑,
*ROS↓,
*Dose↑, antioxidant properties of quercetin show a concentration dependence in the low dose range but too much of the antioxidant brings about the opposite result
*NADPH↓, quercetin counteracts atherosclerosis by reversing the increased expression of NADPH oxidase i
*AMP↓, decreases in activation of AMP-activated protein kinase, thereby inhibiting NF-κB signaling
*NF-kB↓,
*p38↑, quercetin improves the antioxidant capacity of cells by activating the intracellular p38 MAPK pathway, increasing intracellular GSH levels and providing a source of hydrogen donors in the scavenging of free radical reactions.
*MAPK↑,
*SOD↑, quercetin achieves protection against acute spinal cord injury by up-regulating the activity of SOD, down-regulating the level of malondialdehyde (MDA), and inhibiting the p38MAPK/iNOS signaling pathway
*MDA↓,
*iNOS↓,
*Catalase↑, quercetin reduces imiquimod (IMQ)-induced MDA levels in skin tissues and enhances catalase, SOD, and GSH activities, which together improve the antioxidant properties of the body
*PI3K↑, It also controls the development of atherosclerosis induced by high fructose diet by enhancing PI3K/AKT and inhibiting ROS
*Akt↑,
*lipid-P↓, Quercetin enhances antioxidant activity and inhibits lipid cultivation, and it is effective in the treatment of oxidative liver damag
*memory↑, reversed hypoxia-induced memory impairment
*radioP↑, Quercetin protects cells from radiation and genotoxicity-induced damage by increasing endogenous antioxidant and scavenging free radical levels
*neuroP↑, This suggests that quercetin may be a potential neuroprotective agent against ischemia, which protects CA1 vertebral neurons from I/R injury in the hippocampal region of animals
*MDA↓, quercetin significantly reduced MDA levels and increased SOD and catalase levels.
Dose↝, weekly doses of cetuximab: 400 mg/m(2) initial dose, followed by seven weekly doses at 250 mg/m(2).
radioP↑, Updated median overall survival for patients treated with cetuximab and radiotherapy was 49.0 months (95% CI 32.8-69.5) versus 29.3 months (20.6-41.4) in the radiotherapy-alone group
OS↑, For patients with LASCCHN, cetuximab plus radiotherapy significantly improves overall survival at 5 years compared with radiotherapy alone, confirming cetuximab plus radiotherapy as an important treatment option in this group of patients.
*SIRT1↑, Here we show that resveratrol, the activator of Sirt1, could alleviate the bowel inflammation induced by irradiation and the expression of Sirt1 is consistent with the inflammation level.
*radioP↑,
*NLRP3↓, against radiation-induced inflammatory bowel disease via NLRP-3 inflammasome repression in mice and supports Sirt1 as a potential biomarker
*Weight↑, The weight of C57BL / 6 mice in each group treated with resveratrol gradually increased from the 6th day after irradiation, while the weight of C57BL/6 mice in the irradiation group still showed a downward trend.
*IL1β↓, Resveratrol Inhibited the Expression of IL-1β and NLRP-3 in Spleen and Thymus
*radioP↑, RA reduced X-ray-induced the expression of inflammatory related factors, and the level of reactive oxygen species.
*Inflam↓,
*ROS↓,
*NF-kB↓, RA down-regulated the phosphorylation of nuclear factor kappa-B (NF-κB)
*Rho↓, RA attenuated RhoA/Rock signaling through upregulating miR-19b-3p, leading to the inhibition of fibrosis.
*ROCK1↓,
*other↓, Rosmarinic Acid Inhibits MYPT1 Expression by Up-Regulating miR-19b-3p
*Inflam↓, RA reduced X-ray-induced the expression of inflammatory related factors, and the level of reactive oxygen species.
*ROS↓,
*p‑NF-kB↓, RA down-regulated the phosphorylation of nuclear factor kappa-B (NF-κB).
*Rho↓, RA attenuated RhoA/Rock signaling through upregulating miR-19b-3p, leading to the inhibition of fibrosis
*ROCK1↓,
*radioP↑, RA attenuated radiation-
induced damage by its capacity to relieve inflammation and
regulate inflammatory factors.
*MCP1↓, RA treatment reduced RNA levels of NF-kB target gene, including MCP-1, RANTES, and ICAM-1
*RANTES↓,
*ICAM-1↓,
*PGC1A↑, Western blot analysis showed that RA promoted the expression of PGC-1a and reduced the expression of NOX-4, this evidence further suggested that RA inhibits the generation of ROS
*NOX4↓,
*Dose↝, RA exerted strongly protective effects in the X-ray-induced inflammation at doses of 60 mg/kg, and treat-
ment with a higher dose (120 mg/kg) do not enhance its anti-
inflammatory effect.
Showing Research Papers: 1 to 50 of 83
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 83
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 3, Catalase↓, 1, Catalase↑, 1, GPx↑, 1, ox-Keap1↓, 1, rd-Keap1↑, 1, lipid-P↑, 1, NRF2∅, 1, ROS↓, 3, ROS↑, 8, SOD↑, 2, SOD2↓, 1, Trx↓, 2,
Mitochondria & Bioenergetics ⓘ
ETC↓, 1, MMP↓, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, CAIX↑, 1, glucose↓, 1, GLUT2↓, 1, Glycolysis↓, 1, HK2↓, 1, LDHA↓, 1, NADPH↑, 2, PDK1↓, 1, PFK1↓, 1, PKM2↓, 1, Warburg↓, 1,
Cell Death ⓘ
Akt↓, 3, Akt↑, 1, p‑Akt↓, 1, Apoptosis↑, 5, BAX↑, 1, BAX⇅, 1, Bax:Bcl2↑, 1, Bcl-2↓, 2, Casp↑, 1, Casp3↑, 3, Casp9↑, 1, Cyt‑c↑, 1, DR5↑, 1, iNOS↓, 1, JNK↓, 1, JNK↑, 2, MAPK↓, 3, MAPK↑, 1, p27↑, 1, survivin↓, 1, TumCD↑, 1,
Transcription & Epigenetics ⓘ
BowelM↑, 1, ChrMod↑, 1, KISS1↑, 1, other?, 1, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1,
DNA Damage & Repair ⓘ
DNArepair↑, 2, P53↑, 2, cl‑PARP↑, 1,
Cell Cycle & Senescence ⓘ
CDK4↓, 2, CycB/CCNB1↓, 1, cycD1/CCND1↓, 2, P21↑, 2, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
ERK↓, 2, p‑FOXO3↓, 1, IGF-1R↓, 1, mTOR↓, 1, PI3K↓, 3, PI3K↑, 1, p‑PI3K↓, 1, PTEN↑, 1, RAS↑, 1, STAT3↓, 2, TumCG↓, 3, TumCG↑, 1, Wnt↓, 2,
Migration ⓘ
Ca+2↑, 1, E-cadherin↑, 2, Ki-67↓, 1, MMP1↓, 1, MMP13↓, 1, MMP2↓, 4, MMP7↓, 1, MMP9↓, 4, TIMP1↑, 1, TIMP2↑, 1, Treg lymp↓, 1, TumCA↓, 1, TumCI↓, 1, TumCMig↓, 2, TumCP↓, 6, TumMeta↓, 4, TumMeta↑, 1, Vim↓, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, Hif1a↓, 2, NO↓, 1, VEGF↓, 6, VEGFR2↓, 1,
Barriers & Transport ⓘ
GLUT1↓, 1, GLUT1↑, 1, GLUT3↑, 1,
Immune & Inflammatory Signaling ⓘ
CD4+↑, 2, COX2↓, 3, CXCR4↓, 1, DCells↑, 1, FOXP3↓, 1, IL1β↓, 1, IL1β↑, 1, IL6↓, 4, IL8↓, 1, IL8↑, 1, Imm↑, 2, Inflam↓, 4, Inflam↑, 2, NF-kB↓, 5, NK cell↑, 2, PD-L1↓, 1, T-Cell↑, 1, Th1 response↑, 1, TNF-α↓, 2, TNF-α↑, 2,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1, RANKL↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 1, BioAv↝, 2, ChemoSen↑, 9, Dose↑, 1, Dose↝, 4, Dose∅, 4, eff↓, 1, eff↑, 9, eff↝, 2, RadioS↑, 7, RadioS∅, 1, selectivity↑, 11,
Clinical Biomarkers ⓘ
AR↓, 1, GutMicro↑, 3, IL6↓, 4, Ki-67↓, 1, PD-L1↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 4, AntiTum↑, 3, Appetite↑, 2, breath↑, 1, cardioP↑, 1, chemoP↓, 1, chemoP↑, 13, chemoPv↑, 1, ChemoSideEff↓, 2, cognitive↑, 1, hepatoP↑, 1, neuroP↑, 2, OS↑, 8, OS⇅, 1, Pain↓, 4, QoL↑, 4, radioP↑, 32, Remission↑, 2, Risk↓, 1, Sleep↑, 2, Strength↑, 2, toxicity↓, 1, TumVol↓, 2, Weight↑, 1,
Infection & Microbiome ⓘ
CD8+↑, 1,
Total Targets: 167
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 7, ARE↑, 1, Bil↓, 1, Bil↑, 1, Catalase↑, 8, Fenton↓, 1, GCLC↑, 1, GCLM↑, 1, GPx↑, 5, GSH↓, 1, GSH↑, 7, GSH/GSSG↑, 1, GSR↑, 1, GSTs↑, 2, HO-1↓, 1, HO-1↑, 6, ox-Keap1↑, 1, lipid-P↓, 6, MDA↓, 5, NOX4↓, 1, NQO1↑, 1, NRF2↑, 8, Prx↑, 1, ROS↓, 17, ROS∅, 1, SOD↓, 1, SOD↑, 11, TAC↑, 2, Trx↑, 1, TrxR1↑, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 2, AMP↓, 1, AMPK↑, 1, LDH↑, 1, NADPH↓, 1, NADPH↑, 1, NADPH∅, 1, PGC1A↑, 1, PPARγ↑, 1, SIRT1↑, 1,
Cell Death ⓘ
Akt↓, 1, Akt↑, 1, Apoptosis↓, 1, Apoptosis↑, 1, Bax:Bcl2↓, 1, Casp3↓, 2, cl‑Casp8↑, 1, DR4↓, 1, iNOS↓, 2, JNK↓, 1, MAPK↑, 1, p‑MAPK↓, 1, p38↓, 1, p38↑, 1,
Transcription & Epigenetics ⓘ
p‑cJun↓, 1, other↓, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 5, DNMTs↓, 1, P53↓, 2, SIRT6↑, 1,
Cell Cycle & Senescence ⓘ
P21↓, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↑, 1, HDAC↑, 1, mTOR↓, 1, p300↓, 1, PI3K↑, 1, STAT3↓, 1,
Migration ⓘ
5LO↓, 1, AP-1↓, 1, Ca+2↓, 1, Ca+2↑, 1, Rho↓, 2, ROCK1↓, 2, VCAM-1↓, 1, β-Endo↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 4, CRP↓, 1, ICAM-1↓, 3, IFN-γ↓, 1, IL1↓, 1, IL10↓, 1, IL12↓, 1, IL1β↓, 3, IL4↓, 1, IL6↓, 7, IL8↓, 1, Imm↑, 1, Inflam↓, 5, MCP1↓, 1, NF-kB↓, 5, p‑NF-kB↓, 1, PGE2↓, 1, RANTES↓, 1, TNF-α↓, 7,
Synaptic & Neurotransmission ⓘ
5HT↓, 1, BDNF↑, 2, ChAT↑, 1,
Protein Aggregation ⓘ
Aβ↓, 2, NLRP3↓, 2,
Drug Metabolism & Resistance ⓘ
Dose↑, 1, Dose↝, 3, eff↑, 4, Half-Life↓, 1, Half-Life↝, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
ALAT↓, 2, ALP↓, 1, AST↓, 2, Bil↓, 1, Bil↑, 1, BMD↑, 1, CRP↓, 1, GutMicro↑, 1, IL6↓, 7, LDH↑, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, cardioP↑, 1, chemoP↑, 3, cognitive↓, 1, cognitive↑, 2, hepatoP↑, 4, memory↑, 2, neuroP↑, 3, OS↑, 2, radioP↑, 20, RenoP↑, 3, toxicity↓, 4, Weight↑, 1,
Total Targets: 129
Scientific Paper Hit Count for: radioP, RadioProtective
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#:1185 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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