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↑, Amla is also reported to possess radiomodulatory, chemomodulatory, chemopreventive effects, free radical scavenging, antioxidant, anti-inflammatory, antimutagenic and immunomodulatory activities,
ChemoSen↑, Together these observations suggest that it is quite possible that amla prevents doxorubicin-induced cardiotoxicity to the normal cardiac myoblasts and, concomitantly, sensitizes the antineoplastic effects on cancer cells.
chemoPv↑,
*ROS↓,
antiOx↑,
Inflam↓,
Imm↑, Studies have shown that amla enhances natural killer (NK) cell activity and antibody-dependent cellular cytotoxicity in BALB/c mice bearing Dalton’s lymphoma ascites tumor.
*hepatoP↑, Amla is also reported to possess hepatoprotective, cardioprotective, diuretic, laxative, refrigerant, stomachic, restorative, alterative, antipyretic, anti-inflammatory properties
*cardioP↑,
*lipid-P↓, Amla decreases lipid peroxidation
TumCCA↑, It also induces G2/M phase cell cycle arrest by regulating 14-3-3b release from Cdc25C; activation of chk2; decreasing CDK1, cyclin B1, and Cdc25C;
Chk2↑,
CDK1↓,
CycB/CCNB1↓,
CDC25↓,
TumMeta↓, Amla and some of its constituents prevent metastasis
*eff↑, E.officinalis is one of the major component in various health tonics, also exerts synergistic effects in enhancing the medicinal efficacy.
*antiOx↑, antioxidant, anticancer, immunomodulator, anti-inflammatory, cyto-protective properties
*AntiCan↑,
*Imm↑,
*Inflam↓, In trial phase I, oral doses of 3 capsules per day for two weeks showed significant immuno-stimulatory effects on cytotoxic T cells and natural killer cells.
*AntiArt↑, The present review analysed and summarized the pharmacological actions, experimental studies and clinical trials of E. officinalis with emphasis on its immuno-enhancer, antiinflammatory and anticancer activities
*Dose↝, The fruit of amla consists of many bioactive compounds including ellagic acid, chebulinic acid, apigenin, gallic acid, quercetin, chebulagic acid, isostrictiniin, corilagin, methyl gallate, luteolin etc
*VitC↑, It has been reported that 100 g of edible fruit provides 470–680 mg of Vit. C.
radioP↑, figure 1
*cardioP↑,
*GastroP↑,
*Wound Healing↑,
*Diar↓,
eff↑, They reported that IC50 of Amla alone and PE-AgNP were 30 mg/mL and 20 mg/mL respectively, while these nanoparticles demonstrated potential antiproliferative effect by oxidative stress, mitochondrial depolar
ization, DNA damage and apoptotic functio
NK cell↑, Enhanced natural killer (NK) cell activity and antibody dependent cellular cytotoxicity
BAX↑, Up-regulation of Bax expression and down-regulation of Bcl-2 expression.Cell cycle arres
Bcl-2↓,
TumCCA↑,
Dose↝, Powdered amla fruit at dosage of 1, 2 or 3 g orally given with 30 ml water once daily in the morning after breakfast for 21 days
radioP↑, apigenin's radioprotective and radiosensitive properties
RadioS↑,
*COX2/PTGS2↓, 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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MDA-MB-231 |
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MCF10 |
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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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HL7702 |
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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/KDR/Flk1↓, 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/PTGS2↓,
*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↓,
Casp3↑, Asiaticoside has potential for hydrogen peroxide cytotoxicity, and the caspase-3 activity increased with increasing asiaticoside dose in MCF-7 cells treated for 48 h.
TNF-α↓, TNF-α and IL-1β was significantly decreased and correlated with MIBI uptake ratios in vitro and in vivo after asiaticoside administration.
IL1β↓,
Apoptosis↑, This study demonstrates that asiaticoside is effective in vitro and in vivo in inducing apoptosis and enhancing anti-tumour activity.
TumCCA↑, S phase values were highly significantly higher at all concentrations (0, 20, 40, and 80 μm asiaticoside) compared with other cell cycle phases,
TumVol↓, The results showed that rat tumours from groups III and IV (treated with asiaticoside) showed significant less tumour progression (p < 0.001) as compared to group II (positive control,
radioP↑, our results are in agreement with studies that have investigated the effects of Centella asiatica (aqueous extract) and asiaticoside in protecting against the adverse effects of radiation (gamma-irradiation).
Inflam↓, asiaticoside has anti-inflammatory activities in several inflammatory models
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/PTGS2↓,
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.
Bcl-2↓, Crocin significantly reduced cell viability of BXPC3 and Capan-2 by triggering caspase signaling via the downregulation of Bcl-2.
Apoptosis↑, crocin treatment-induced apoptosis by inducing the release of cytochrome c from mitochondria to cytosol.
Cyt‑c↑,
TumCG↓, In mice bearing pancreatic tumors, crocin significantly reduced tumor burden without a change in body weight.
radioP↑, Additionally, it showed significant protection against radiation-induced hepatic oxidative damage, reduced the levels of hepatic toxicity and preserved liver morphology.
TumCCA↑, Various studies have shown that carotenoids of saffron extract, crocin and crocetin, arrest the cell cycle at S, G0/G1and G2/M stages [26,27,28,29,30,31,32,33,34], inhibiting mitosis, cell proliferation and triggering apoptosis.
TumCP↓,
DNAdam↑, crocin induces DNA fragmentation, apoptosis and cell cycle arrest at the G1 phase in Bx-PC-3 pancreatic cancer cells
TBARS↓, Crocin showed dose-dependent inhibition of TBARS
P53↑, Crocin upregulated P53, P38, cytochrome c, P21cip1 and P27kip1, whereas CDK2 and c-Myc were downregulated dose-dependently in BXPC3 and Capan-2 cells
p38↑,
CDK2↓,
cMyc↓,
*MDA↓, IR (4Gy) increased the MDA levels in mice and crocin treatment restores the MDA level
GSH↑, In this study, increased GSH level (Table 1) suggests that protection by the crocin mediated through the restoration of IR altered hepatic antioxidant status (Table 1 and Table 2).
*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
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/PTGS2↓,
*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↑,
RadioS↑, overall level of evidence for curcumin as a radiosensitizer and radioprotector is low, it must be recognized that risks of adverse effects are exceedingly low, and clinicians may need to judge the yet-unproven rewards with low toxicity risks.
ChemoSen↑,
NF-kB↓, suppressing NF-κB
radioP↑, substantial volume of evidence exists that curcumin is a radiosensitizer of multiple cancers as well as a radioprotector of several normal tissues.
BioAv↓, Further research is greatly needed to strengthen curcumin’s major weakness - poor gastrointestinal absorption leading to low oral bioavailability.
*toxicity↓, curcumin is extremely safe and not harmful to the cancer patient undergoing radio(chemo)therapy.
TumCD↓, Curcumin plays the antitumor effect by directly promoting tumor cell death and reducing tumor cells' invasive ability.
TumCI↓,
*Inflam↓, curcumin has many pharmacological effects, such as anti-inflammation, antioxidation, antitumor, etc.
*antiOx↓,
*AntiTum↓,
NF-kB↓, Curcumin exerts the therapeutic effect mainly by inhibiting the nuclear factor-κB (NF-κB) signal pathway, inhibiting the production of cyclooxygenase-2 (COX-2),
COX2/PTGS2↓,
Casp9↓, promoting the expression of caspase-9, and directly inducing reactive oxygen species (ROS) production in tumor cells.
ROS↑, Curcumin can induce lethal levels of reactive oxygen species (ROS) in tumors
BioAv↑, Curcumin nanoparticles can solve curcumin's shortcomings, such as poor water solubility and high metabolic rate, and can be effectively used in antitumor therapy.
RadioS↑, Figure 1, Curcumin Increases Radiosensitivity of Tumor
ChemoSen↑,
Imm↑,
PhotoS↑, Curcumin Mediates the Antitumor Effect of PDT
sonoS↑, Curcumin Mediates the Antitumor Effect of SDT
5LO↓, down-regulating the activities of cyclooxygenase-2 (COX-2), lipoxygenase (LOX), inducible nitric oxide synthase (iNOS) and so on, reducing the production of proinflammatory cytokines such as IL-2, tumor necrotic factor-α (TNF-α),
iNOS↓,
IL2↓,
TNF-α↓,
Casp9↑, activating intracellular caspase-9 and caspase-3, reducing the expression of p53, inhibiting Bcl2, and promoting the expression of Bax and down-regulating the proportion of Bcl2/Bax
Casp3↑,
Bcl-2↓,
BAX↑,
Apoptosis↑, promote apoptosis by activating caspase-4 and stimulating the Endoplasmic reticulum (ER) stress pathway and mitochondria stress pathway in tumor cells [
ER Stress↑,
cycD1/CCND1↓, It reduces the expression of cyclin D1, cyclin kinase-dependent kinase 2 (CDK2), cdc2/cyclin B complex, and other cell cycle-related proteins,
CDK2↓,
CycB/CCNB1↓,
TumCCA↑, blocks tumor cells from G1 / S phase and G2 / M phase, thus exerting an antitumor effect
MMPs↓, curcumin inhibits tumor invasion and metastasis by inhibiting NF-κB and other signaling pathways, such as chemokine and matrix metalloproteinases (MMPs)
*radioP↑, Curcumin can effectively treat and prevent radiation adverse reactions such as radiation dermatitis and radiation pneumonia by reducing the expression of inflammatory factors such as fibrotic cytokines, TNF-α, and IL-1, inhibiting NF-κB signal pathwa
chemoP↑, Protective Effect of Curcumin on Side Effects of Chemotherapy
hepatoP↑, urcumin alleviates the hepatotoxicity caused by chemotherapy through anti-inflammation and antioxidation, reducing the level of liver fibrosis and blood lipids [
cardioP↑, Using curcumin to reduce the cardiotoxicity of chemotherapy can improve the therapeutic effect of tumors and patients' prognosis and quality of life.
eff↑, Curcumin Enhances the Therapeutic Effect of Immunotherapy
PhotoS↑, it has the potential to be a new photosensitizer
eff↑, Curcumin nanoparticles with functions of relieving hypoxia and consuming GSH could improve the ability of curcumin to induce ROS and promote ROS- mediated tumor cell death
ROS↑,
GSH↓,
*antiOx↑, Curcumin exerts potent antioxidant, anti-inflammatory, and anticancer effects by modulating multiple signaling pathways, including NF-κB, PI3K/Akt, and Wnt/β-catenin.
*Inflam↓,
*BioAv↓, curcumin’s clinical application is limited by poor solubility, rapid metabolism, and low systemic bioavailability.
NF-kB↓, graphical abstract
PI3K↓,
Akt↓,
Wnt↓,
β-catenin/ZEB1↓,
DNMTs↓,
TumCI↓,
TumMeta↓,
*BioAv↑, Advanced drug delivery systems such as nanoparticles, liposomes, and micelles have been developed to address these challenges. These systems enhance curcumin’s solubility, stability, and targeted delivery, improving therapeutic efficacy while minimiz
*BioAv↑, coadministration with piperine, lipid-based formulations, and nanoparticle microencapsulation have been developed. Piperine has been shown to increase curcumin absorption by up to 2000 percent
angioG↓, Curcumin is also known for its antiangiogenic action through its inhibitory activity against vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs)
VEGF↓,
MMPs↓,
*ROS↓, suppresses oxidative stress by scavenging free radicals and enhancing the activity of endogenous antioxidant enzymes such as superoxide dismutase (SOD) and catalase
*SOD↑,
*Catalase↑,
*GSTs↑, timulating phase II detoxifying enzymes such as glutathione S-transferase (GST), UDP-glucuronosyltransferase, and heme oxygenase-1 (HO-1).
*HO-1↑,
*NRF2↑, It also enhances the activity of the transcription factor Nrf2, which regulates genes crucial for cellular redox homeostasis and safeguarding cells against oxidative damage
mTOR↓, 0 to 50 μM, treatment was associated with decreased phosphorylation of Akt kinase (Akt), mammalian target of rapamycin (mTOR), glycogen synthase kinase (GSK3β), Forkhead box protein O1 (FOXO1), and other proteins
GSK‐3β↓,
FOXO1↓,
*radioP↑, Reduced radiation-induced dermatitis and inflammatory cytokine expression (IL-1, IL-6, TNF-α)
*IL1↓,
*IL6↓,
*TNF-α↓,
HATs↓, curcumin has been described as an agent that reduces histone acetylation by inhibiting HAT (histone acetyltransferases), such as the p300/CBP family of proteins
HDAC↓, curcumin has been detected to be an HDI and has the ability to inhibit the expressions of HDACs, like HDAC1, HDAC3, and HDAC8,
ROS↑, Elevating the levels of reactive oxygen species (ROS) in colon adenocarcinoma cells is one of the outcomes of treatment with curcumin, which results in a decline in cell proliferation and viability
ROS↑, at higher concentrations or in the presence of transition metal ions (e.g. Cu2+, Fe2+/Fe3+), curcumin can paradoxically act as a pro-oxidant.
MMP↓, Excess ROS damages mitochondrial membranes, oxidizes nucleic acids, lipids, and proteins, and activates apoptotic cascades via cytochrome c release and caspase activation
Casp↑,
Cyt‑c↑,
COX1↓, curcumin acts as a partial and condition-dependent inhibitor of both COX-1 and COX-2.
COX2/PTGS2↓,
PGE2↓, At lower or therapeutic concentrations, curcumin predominantly downregulates COX-2 and reduces prostaglandin E2 (PGE2) synthesis.
*cytoP450↓, curcumin’s capacity to inhibit cytochrome P450 enzymes may influence the metabolism of numerous medicines over extended durations.
ChemoSen↑, curcumin has been integrated with standard chemotherapy agents, including doxorubicin, cisplatin, and paclitaxel, to enhance cancer treatment efficacy
cardioP↑, co-delivery of curcumin and doxorubicin via nanoparticles improved anticancer effectiveness and decreased cardiotoxicity.
eff↑, concurrent treatment of curcumin and resveratrol has demonstrated increased anti-inflammatory and anticancer properties
RadioS↑, Although curcumin can sensitize cancer cells to irradiation, healthy cells are much less sensitive to this effect, and thus, curcumin is thought to be a potent, yet safe anti-cancer agent
*radioP↑, curcumin has been found to possess radioprotective properties, since it can lessen inflammatory toxicities associated with radiotherapy, like dermatitis, mucositis, and myelosuppression
EGFR↓, Curcumin can suppress the gene expression of EGFR, and downregulate the TGF-β pathway, thus leading to inhibition of cancer-associated fibroblasts (CAF)
TGF-β↓,
ROS↑, Curcumin can induce ROS generation and suppress DNA repair machinery, thus leading to increased radiation-induced cell death
P53↑, upregulation of both the expression and activity of p53, regulation of the anti-apoptotic PI3K signaling, and suppression of the activity of NF-κB and COX-2
PI3K↓,
NF-kB↓, curcumin increased radiation-induced apoptotic death primarily through inhibition of the NF-κB signaling pathway
COX2/PTGS2↓,
EMT↓, Curcumin was found to suppress radiation-induced EMT resulting in the inhibition of NSCLC migration and invasion
Hif1a↓, inhibition of the expression of both hypoxia-inducible factor 1-alpha (HIF-1a) and heat shock protein 90 (HSP90) proteins and increase in the levels of ROS
HSP90↓,
mTOR↓, In cervical cancer, curcumin has been studied as a potent mTOR inhibitor when given together with irradiation.
*Catalase↑, 40 rats were exposed to curcumin 1 day before irradiation to 3 consecutive days after irradiation, the levels of antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA), were found to be considerably eleva
*SOD↑,
*MDA↑,
*Wound Healing↑, treatment with curcumin stimulated wound healing,
*hepatoP↑, curcumin treatment prior to radiation can prevent liver damages, mainly through the modulation of the NF-κB pathway and reduction of oxidative stress (upregulation of SOD, CAD and GSH levels in the curcumin-treated group)
*NF-kB↓,
*ROS↓,
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.
*radioP↑, DRE administration attenuated oxidative stress in the liver and testis denoted by a significant reduction in the level of MDA and PCO with a marked elevation in GSH and the activity of SOD, CAT and Gpx.
*ROS↓,
*MDA↓,
*GSH↑,
*SOD↑,
*IL1β↓, DRE reduced the level of IL-1β, TNF-α, and caspase-3.
*TNF-α↓,
*Casp3↓,
*eff↑, In conclusion, treatment with DRE pre-irradiation is effective on both liver and testicular tissues of rats. better to use the dandelion before exposure to radiation rather than after it.
TumCCA↑, Ellagic acid effectively induced G1-phase cell cycle arrest and suppressed CDK4, thereby reducing S-phase entry and enhancing radiation-induced apoptosis in TNBC cells.
CDK4↓,
RadioS↑,
TumCG↓, In vivo, ellagic acid significantly enhanced tumor growth inhibition when combined with radiotherapy.
*radioP↑, Importantly, ellagic acid also mitigated RIMI by reducing cardiomyocyte apoptosis, preserving myocardial structure, and maintaining left ventricular systolic function.
*cardioP↑, it sensitizes tumors by targeting the CARM1-CDK4 axis while protecting the heart through potent antioxidant activity.
*antiOx↑,
*ROS↓, The results showed that EA treatment significantly reduced the ROS fluorescence signal in H9C2 cardiomyocytes
Dose↑, ellagic acid was administered daily via intraperitoneal injection. (mice)
selectivity↑, In stark contrast, EA operates with tissue selectivity. It does not act as a blanket protector; instead, it exploits the fundamental biological difference between proliferating cancer cells and cardiomyocytes.
BioAv↓, its notoriously poor aqueous solubility and moderate oral bioavailability present significant translational hurdles.
*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/PTGS2↓,
*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
*Bacteria↓, Fucoidans have bacteria-inhibiting qualities against the ulcer-causing Helicobacter pylori
*BioAv↓, The oral bioavailability of fucoidan preparations is generally low, although recent studies have elegantly demonstrated the uptake and tissue distribution of Fucus vesiculosus fucoidan in a rat model
*Dose↝, permit daily consumption of high-concentration fucoidan extracts from Undaria pinnatifida or Fucus vesiculosus at rates of up to 250 mg/day.
*GutMicro↑, ucoidans have been noted to create favourable changes in the microbiome [66] and additionally, to independently modulate checkpoint PD-L1 in cancer cells [
PD-1↝,
ROS⇅, They include induction [79], or even inhibition [76], of reactive oxygen species, destabilization of mitochondria, and the cleavage of caspases and PARP.
cl‑Casp↑,
cl‑PARP↑,
RadioS↑, In a Russian study, fucoidan from Fucus evanescens was found to increase cancer susceptibility towards radiation
*radioP↑, Conversely, fucoidans may confer radiation protection effects that help to prevent lung damage and subsequent fibrosis of healthy tissues
*neuroP↑, research into fucoidans as neuroprotective agents are promising.
*Aβ↓, In Alzheimer’s related research, a fucoidan extract inhibited the formation of amyloid fibrils in vitro, and their toxic effect on neuronal cells
*cognitive↑, X-ray-treated mice exhibited cognitive impairment and depression-like behavior, which was ameliorated by GB treatment.
*radioP↑,
*ROS↓, GB also reduced the ROS production and the number of TUNEL-positive cells in the hippocampus
*p‑Akt↑, GB increased the protein levels of p-AKT and Bcl2, while decreased the protein levels of MST1, p-p38, p-JNK, cleaved-caspase-3 and Bax both in vivo and in vitro.
*Bcl-2↑,
*Mst1↓,
*p‑p38↓,
*JNK↓,
*cl‑Casp3↓,
*BAX↓,
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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↑,
Dose↝, The experimental group received inhalation therapy with a hydrogen-oxygen gas mixture (66.6% hydrogen, 33.3% oxygen; 3 L/min, 2 h/d) on each radiation therapy day.
CRP↓, experimental group showed significantly lower levels of C-reactive protein, neutrophil-to-lymphocyte ratio, interleukin 6, and fecal occult blood positivity rates
NLR↓,
IL6↓,
AntiTum∅, Importantly, no significant difference in tumor response was observed between groups based on the Response Evaluation Criteria in Solid Tumors
*toxicity↓, Hydrogen inhalation is a safe and effective adjunctive therapy that significantly alleviates inflammation and mitigates clinical symptoms of ARE in patients with cervical cancer who are undergoing CCRT, without compromising antitumor treatment outcom
Inflam↓,
radioP↑,
*IBI↑, significant reduction in fecal occult blood positivity in the hydrogen group (χ² = 16.278, P < .001), reinforcing its protective effect on intestinal mucosa integrity.
*ROS↓, Molecular hydrogen has demonstrated a unique capacity to selectively scavenge cytotoxic ROS
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Var, |
NA |
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IBD, |
NA |
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Review, |
Stroke, |
NA |
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Review, |
Sepsis, |
NA |
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AD, |
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Dose↝, H2 can be administered exogenously and is also produced endogenously within the intestinal tract.
*Inflam↓, Anti‐Inflammatory Effect
*IL1β↓, diabetes combined with stroke, H₂ intervention downregulates the expression levels of proinflammatory factors (IL‐1β, IL‐6, TNF‐α), while activating the TLR4/NF‐κB signaling pathway to achieve neuroprotective effects
*IL6↓,
*TNF-α↓,
*neuroP↑,
*mTOR↓, sepsis model, H₂ regulates macrophage polarization (inhibiting the M1 phenotype/promoting the M2 phenotype) and inhibits (mTOR) phosphorylation, reducing the release of inflammatory mediators such as IL‐6, TNF‐α, and HMG
*IL10↑, while increasing the levels of anti‐inflammatory factors IL‐10 and Transforming Growth Factor‐beta (TGF‐β)
*TGF-β↑,
*Sepsis↓,
*NRF2↑, whereas Nrf2 induction suppresses these pathways via redox homeostasis modulation
*antiOx↑, figure 1
*Catalase↑,
*SOD↑,
*GPx↑,
*ROS↓, H₂ mediates ROS regulation through Nrf2, inhibiting NF‐κB/NLRP3 inflammasome activation and achieving an antioxidant–anti‐inflammatory synergistic effect
*HO-1↑, H2 can increase the expression of heme oxygenase‐1 (HO‐1) or activate the phosphatidylinositol‐3‐kinase (PI3K)–Akt signaling pathway to improve liver I/R injury
*PI3K↑,
*Akt↑,
*hepatoP↑,
*MPO↓, reduce myeloperoxidase (MPO) activity and IL‐1β/TNF‐α levels to alleviate myocardial injury
*cardioP↑,
CDK4↓, Studies have demonstrated that H2 inhibits CDK4 and CDK6 to restrict lung cancer progression
CDK6↑,
CD47↓, H₂ can reverse immune escape in lung cancer cells by inhibiting the expression of CD47 and activating the apoptosis program
PI3K↓, H2 promotes apoptosis by downregulating Akt phosphorylation and inhibiting the PI3K signaling pathway in non‐small cell lung cancer.
Akt↓,
Hif1a↓, inhalation of H2 suppresses Hypoxia‐Inducible Factor 1 Alpha Subunit (HIF‐1α)/NF‐κB signaling pathway activation and promotes apoptosis in HeLa cells
selectivity↑, This bidirectional regulatory capability allows H₂ to protect normal tissues from excessive apoptosis (such as inflammation‐induced cell death) while selectively inducing apoptosis in tumor cells.
*MMP↑, howed that after treating septic rats with HRS, the decline in mitochondrial membrane potential (MMP) and ATP content was improved.
*ATP↑,
*ER Stress↓, H₂ alleviated inflammation and organ damage by inhibiting ER stress and activating the autophagy pathway in septic mice
*CHOP/DDIT3↓, H2 could downregulate the expression of CHOP, caspase‐12, and GRP78, while inhibiting p38 and c‐Jun N‐terminal kinase (JNK) phosphorylation, and upregulating the LC3‐II/I ratio
*Casp12↓,
*GRP78/BiP↓,
*p38↓,
*p‑JNK↓,
*LC3‑Ⅱ/LC3‑Ⅰ↑,
*p‑eIF2α↓, HRW prevents IBD in mice by reducing levels of p‐eIF2α, ATF4, XBP1, and CHOP, key proteins in ER stress.
*ATF4↓,
*XBP-1↓,
*Imm↑, H₂ exhibit multidimensional characteristics, primarily enhancing immunity by protecting immune organs,
*IFN-γ↓, H2 treatment inhibited several T‐cell effector molecules, such as IFN‐γ, IL‐4, and GZMB
*IL4↓,
*GranB/GZMB↓,
NK cell↑, After inhaling H₂ for 2 weeks, patients with advanced non‐small cell lung cancer showed significant improvement in T‐cell exhaustion. (NK) subgroups was higher than the pretreatment percentag
radioP↑, HRS can protect against radiation‐induced immune dysfunction by restoring the number of CD4+ T and CD8+ T cells in the spleen.
*CD4+↑,
CD8+↑,
*Dose↝, Common delivery methods include inhalation, oral administration of HRW, injection of HRS, promotion of endogenous H2 production
*other↑, H2, which fall within the explosive range at concentrations ranging from 4 to 74%, it is essential to specify the concentration of H2 for inhalation therapy.
*Dose↝, China National Health Commission recommends the administration of oxygen–H2 mixture (33.3% O2 and 66.6% H2)
*antiPs↑, HRW baths exhibit inhibitory effects on inflammation and oxidative stress while demonstrating therapeutic benefits for conditions such as psoriasis
*BioAv↝, the solubility of H2 in water at room temperature and pressure is limited to a maximum of 0.8mM109, resulting in limited efficacy when orally administered.
*GutMicro↑, inhalation of H2 modulates the gut flora to ameliorate acute alcoholic liver injury. H2 altered the composition of the GM, leading to an increase in the relative abundance of Mycobacterium anisopliae and Mycobacterium thickum
Dose↝, CRC cell lines (ROK/SW480/HCT116) and xenograft mouse models,Inhalation of 66% H2 (66% H2 and 33% O2);Duration: 2 h a day for 21 days
*IBI↑, orally administered silicon H2 nanoparticles (SiH NPs) for targeted scavenging of ROS at inflammatory sites, thereby alleviating symptoms of IBD and restoring GM diversity by enhancing the abundance of beneficial bacteria.
TumCP↓, H2 inhibits tumor cell activity, proliferation, invasion, and migration through various molecular mechanisms, in a manner that depends on both dose and time.
TumCI↓,
TumCMig↓,
CD8+↑, H2 Improves Prognosis by Restoring Depleted CD8+ T Cells in Patients with CRC Cancer
PGC-1α↑, It has been shown that H2 can activate PGC‐1α to restore mitochondrial function and rescue depleted CD8+T cells
Akt↓, H2 Inhibits CRC Cell Proliferation by Suppressing the AKT/SCD1 Pathway
SCD1↓,
*MDA↓, The results showed that H2 water alone significantly improved detected antioxidant markers (SOD and CAT) and reduced MDA levels.
eff↑, combination of H2 water and 5‐fluorouracil significantly attenuated MDA levels more effectively than 5‐fluorouracil alone
*APP↓, H2 gas significantly inhibited the overexpression of APP, BACE1, and sAP, thereby reducing Aβ production.
*BACE/β-secretase↓,
*Aβ↓,
*cognitive↑, This intervention effectively halted the progression of AD, alleviating cognitive impairment, synaptic deficits, and neuronal death
*neuroP↑, regulation of GM(gutmicrobiome) by HRW considered a key mechanism underlying its neuroprotective effects.
NP/CIPN↓, mice with chemotherapy‐induced neuropathic pain caused by oxaliplatin, drinking HRW significantly reduced inflammation by inhibiting the LPS–TLR4 pathway and decreasing the expression of TNF‐α and IL‐6.
*Stroke↓, inhalation of 2% H2 gas significantly reduced levels of myocardial injury markers, such as creatine kinase‐MB and cardiac troponin‐T, while protecting myocardial tissue from further damage by inhibiting autophagy.
*NLRP3↓, daily inhalation of 2% H2 gas for 3 h over 28 days effectively suppressed the activation of the NLRP3 inflammasome, reduced cardiac fibrosis, and improved cardiac function
*ALAT↓, 4% H2 outperforming 67% H2 in reducing liver enzyme levels Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) and lipid accumulation.
*AST↓,
*LPS↓, inhalation of 4% H2 in an NAFLD rat model significantly lowered plasma LPS levels, inhibited the LPS/TLR4/NF‐κB signaling pathway to reduce liver inflammation
*hepatoP↑, drinking HRW, indicating its hepatoprotective effects
chemoP↑, injecting HRS in rats effectively reduced ALT and AST levels caused by doxorubicin, decreased ROS and MDA production, and regulated the Bax/Bcl‐2 ratio to alleviate inflammation and apoptosis.
*creat↓, mouse model of kidney injury induced by a high‐oxalate diet, HRW consumption markedly improved serum creatinine, blood urea nitrogen, and kidney injury markers such as kidney injury molecule‐1 (KIM‐1)
*Urea↓,
*RenoP↑,
*eff↑, higher concentrations of H2 gas (67%) produced more pronounced improvements in kidney histology and morphology compared with lower concentrations (4%)
Apoptosis↑, H2 gas increased apoptosis in A549 cells while reducing the expression of XIAP and BIRC3 proteins in studies on A549 cells and their nude mouse models.
XIAP↓,
IAP2/BIRC3↓,
TumVol↓, inhalation of 60% H2 gas significantly reduced tumor volume in experimental mice
MALAT1↓, In gastric cancer research, Zhu et al. [10] found that H2 gas downregulated the expression of lncRNA MALAT1 and EZH2 while upregulating miR‐124‐3p
EZH2↓,
miR-124-3p↓,
eff↑, combining platinum nanocolloid (Pt‐nc) with H2 gas effectively inhibited the growth of human promyelocytic leukemia HL60 cells
ChemoSen↑, combining H2 therapy with conventional treatments such as chemotherapy and radiotherapy, demonstrating improved efficacy and reduced side effects
*compII↑, allergic airway inflammation, showing that H2 increased ATP production as well as the activity of mitochondrial respiratory chain complexes I and III
*compIII↑,
*LDL↓, H2‐enriched water in humans, showing that supplementation with H2‐enriched water appeared to reduce serum low‐density lipoprotein cholesterol (LDL‐C) and apolipoprotein B (apoB) levels,
*Obesity↓, H2 may play a beneficial role in the prevention of potential metabolic syndrome
QoL↑, 82 patients with stage III and IV cancers receiving H2 inhalation therapy. They found that H2 inhalation improved the quality of life
PFS↑, Sixteen months of follow‐up found that progression‐free survival in the control group was lower than that in the H2 inhalation group alone, and significantly lower than that in the other three combination therapy groups.
*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↓,
*ROS↓, reduces reactive oxygen species, which have very strong oxidative capacity, and indirectly exerts antioxidant, anti-inflammatory
*antiOx↑,
*Inflam↓,
*chemoP↑, Our comprehensive literature review revealed that H2 protects against tissue injuries induced by cisplatin, oxaliplatin, doxorubicin, bleomycin, and gefitinib.
AntiCan↑, Animal and clinical studies showed that H2 itself exhibits anticancer activity, and its combination with anticancer drugs achieved excellent anticancer activity
ChemoSen↑,
chemoP↑, Our literature review revealed that H2 reduced the side effects of CIS-induced nephrotoxicity, ototoxicity, and ovarian injury, CIS- or OXA-induced peripheral neuropathy, DXR-induced cardiotoxicity and hepatotoxicity, and BLM- or GEF-induced lung inj
*BUN↓, CIS Nephrotoxicity BUN ↓, Creatinine ↓, TUNEL ↓
*creat↓,
*TUNEL↓,
*MDA↓, CIS Ototoxicity MDA ↓, 8-iso-PGF2α ↓
*SOD↑, CIS Ovarian injury SOD ↑, CAT ↑, MDA ↓, Nrf2 ↑
*Catalase↑,
*NRF2↑,
*BNP↓, DXR Cardiotoxicity and hepatotoxicity BNP ↓, AST ↓, ALT ↓, ROS ↓, MDA ↓, TNF-α ↓, IL-1β ↓, IL-6 ↓, TUNEL ↓, Bax/Bcl-2 ↓, Caspase-3 ↓, Caspase-8 ↓
*AST↓,
*ALAT↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*Casp3↓,
*Casp9↓,
*GPx↑, BLM Lung injury ROS ↓, MDA ↓ TGF-β1 ↓,TNF-α ↓, GSH-PX ↑, E-cadherin ↑, Vimentin ↓, α-SMA ↓, Collagen I ↓
*E-cadherin↑,
*Vim↓,
*α-SMA↓,
*COL1↓,
*cardioP↑, H2 ameliorated DXR-induced cardiotoxicity and hepatotoxicity by attenuating inflammation and apoptosis.
*hepatoP↑,
*p‑mTOR↓, decreased the phosphorylated mammalian target of rapamycin (p-mTOR) to mTOR
*EMT↓, H2 gas also inhibited BLM-mediated epithelial-to-mesenchymal transition by increasing the expression level of the epithelial cell marker E-cadherin and decreasing that of the mesenchymal cell marker vimentin [
eff∅, On the other hand, H2 did not impair the anticancer effects of GEF in in vitro experiments on lung cancer cell lines or in in vivo experiments on carcinoma-bearing mice
*LPS↓, figure 2
*TLR4↓,
radioP↑, radioprotective effects of H2 have also been reported in many in vitro and in vivo studies, and clinical trials recently showed that the inhalation of H2 gas mitigated decreases in quality of life and bone marrow damage associated with radiation [
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.
| - |
Review, |
CRC, |
NA |
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- |
Review, |
Lung, |
NA |
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- |
Review, |
BC, |
NA |
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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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in-vitro, |
Nor, |
HUVECs |
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in-vivo, |
NA, |
NA |
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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↑, In vitro, ISL restored the viability of X-ray-irradiated PC12 cells; reduced LDH release and intracellular ROS accumulation; and enhanced SOD1 activity, GSH content, and T-AOC levels.
*LDH↓,
*ROS↓,
*SOD1↑,
*GSH↑,
*TAC↑,
*NRF2↓, Moreover, ISL upregulated the expression of antioxidant-related genes and induced Nrf2 nuclear translocation.
*cognitive↑, In vivo, oral ISL administration ameliorated radiation-induced cognitive impairment, improved spatial learning and memory, alleviated hippocampal neuronal loss, and increased cerebral cortical Nrf2 expression in C57BL/6J mice
*Learn↑,
*memory↑,
Risk↓, Soy consumption in human diet has been linked to decreased incidence of a variety of cancers, suggesting a potential role of soy products in cancer prevention and control.
ChemoSen↑, substantial body of evidence in the literature suggests that soy supplementation may improve the efficacy and prevent the adverse effects of cancer chemotherapy and radiation therapy.
chemoP↑,
RadioS↑, sensitization of cancer cells to chemotherapy and radiation while at the same time protecting normal cells from the harmful effects of these treatments
radioP↑,
NF-kB↓, inhibition of NF-κB activation and DNA methylation, enhancement of histone acetylation, inhibition of cell growth and metastasis, and antiangiogenic, anti-inflammatory, and anti-oxidant effects.
DNMTs↓,
TumMeta↓,
angioG↓,
antiOx↑,
BioAv↑, Isoflavones are orally bioavailable, easily metabolized, and usually considered safe.
toxicity↓,
*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/PTGS2↓, 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↑,
Showing Research Papers: 1 to 50 of 102
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 102
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
CD47↓, 1, miR-124-3p↓, 1, NLR↓, 1, PFS↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 3, GSH↓, 1, GSH↑, 1, lipid-P↑, 1, ROS↓, 3, ROS↑, 9, ROS⇅, 1, SOD↑, 1, TBARS↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
CDC25↓, 1, MMP↓, 1, PGC-1α↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, cMyc↓, 1, glucose↓, 1, SCD1↓, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 4, p‑Akt↓, 1, Apoptosis↑, 8, BAX↑, 2, BAX⇅, 1, Bax:Bcl2↑, 1, Bcl-2↓, 4, Casp↑, 2, cl‑Casp↑, 1, Casp3↑, 4, Casp9↓, 1, Casp9↑, 1, Chk2↑, 1, Cyt‑c↑, 3, DR5↑, 1, IAP2/BIRC3↓, 1, iNOS↓, 2, JNK↓, 1, JNK↑, 1, MAPK↓, 2, p38↑, 1, survivin↓, 1, TumCD↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
EZH2↓, 1, HATs↓, 1, other?, 1, PhotoS↑, 2, sonoS↑, 1, tumCV↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 2, HSP90↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 1, DNMTs↓, 2, P53↑, 3, cl‑PARP↑, 2,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK1↓, 1, CDK2↓, 2, CDK4↓, 2, CycB/CCNB1↓, 2, cycD1/CCND1↓, 2, P21↑, 1, TumCCA↑, 6,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↓, 1, ERK↓, 2, FOXO1↓, 1, GSK‐3β↓, 1, HDAC↓, 1, mTOR↓, 3, PI3K↓, 5, p‑PI3K↓, 1, STAT3↓, 1, TumCG↓, 4, Wnt↓, 4,
Migration(tgid=13) ⓘ
5LO↓, 1, E-cadherin↑, 1, Ki-67↓, 1, MALAT1↓, 1, MMP1↓, 1, MMP2↓, 3, MMP7↓, 1, MMP9↓, 3, MMPs↓, 2, TGF-β↓, 1, TIMP1↑, 1, TIMP2↑, 1, TumCA↓, 1, TumCI↓, 4, TumCMig↓, 3, TumCP↓, 6, TumMeta↓, 4, β-catenin/ZEB1↓, 4,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 3, EGFR↓, 1, Hif1a↓, 2, VEGF↓, 6, VEGFR2/KDR/Flk1↓, 1,
Barriers & Transport(tgid=15) ⓘ
GLUT1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX1↓, 1, COX2/PTGS2↓, 5, CRP↓, 1, CXCR4↓, 1, IL1β↓, 1, IL1β↑, 1, IL2↓, 1, IL6↓, 2, IL8↑, 1, Imm↑, 3, Inflam↓, 7, Inflam↑, 1, NF-kB↓, 8, NK cell↑, 2, PD-1↝, 1, PD-L1↓, 1, PGE2↓, 1, TNF-α↓, 3, TNF-α↑, 1,
Protein Aggregation(tgid=19) ⓘ
NLRP3↑, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
AR↓, 1, CDK6↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 3, BioAv↑, 3, BioAv↝, 1, ChemoSen↑, 15, Dose↑, 2, Dose↝, 7, eff↓, 1, eff↑, 13, eff↝, 2, eff∅, 1, RadioS↑, 10, RadioS∅, 1, selectivity↑, 12,
Clinical Biomarkers(tgid=22) ⓘ
AR↓, 1, CRP↓, 1, EGFR↓, 1, EZH2↓, 1, GutMicro↑, 3, IL6↓, 2, Ki-67↓, 1, PD-L1↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 3, AntiTum↑, 3, AntiTum∅, 1, Appetite↑, 1, cardioP↑, 3, chemoP↑, 15, chemoPv↑, 2, cognitive↑, 1, hepatoP↑, 1, neuroP↑, 1, NP/CIPN↓, 1, OS↑, 3, Pain↓, 2, QoL↑, 4, radioP↑, 31, Risk↓, 1, Sleep↑, 1, toxicity↓, 1, TumVol↓, 4, TumW↓, 1,
Infection & Microbiome(tgid=24) ⓘ
CD8+↑, 2,
Total Targets: 162
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiArt↑, 1, compII↑, 1, Learn↑, 1, SpO2↑, 1, Stroke↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↓, 1, antiOx↑, 11, ARE↑, 1, Bil↑, 1, Catalase↑, 10, Fenton↓, 2, GCLC↑, 1, GCLM↑, 1, GPx↑, 5, GSH↓, 1, GSH↑, 6, GSTs↑, 2, HO-1↓, 1, HO-1↑, 9, lipid-P↓, 6, MDA↓, 8, MDA↑, 1, MPO↓, 2, NOX4↓, 1, NQO1↑, 1, NRF2↓, 1, NRF2↑, 10, Prx↑, 1, RNS↓, 1, ROS↓, 21, SOD↓, 1, SOD↑, 14, SOD1↑, 1, TAC↑, 3, TBARS↓, 1, Trx↑, 1, TrxR1↑, 1, VitC↑, 1, VitE↓, 1,
Metal & Cofactor Biology(tgid=2) ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, compIII↑, 1, MMP↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 3, BUN↓, 1, cytoP450↓, 1, LDH↓, 1, LDH↑, 1, LDL↓, 1, NADPH↓, 1, NADPH↑, 1, PPARγ↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Akt↑, 2, p‑Akt↑, 1, Apoptosis↓, 2, Apoptosis↑, 1, BAX↓, 1, Bax:Bcl2↓, 1, Bcl-2↑, 2, Bcl-xL↑, 1, Casp12↓, 1, Casp3↓, 5, cl‑Casp3↓, 1, cl‑Casp8↑, 1, Casp9↓, 2, DR4↓, 1, GranB/GZMB↓, 1, iNOS↓, 1, JNK↓, 2, p‑JNK↓, 1, p‑MAPK↓, 1, p38↓, 2, p‑p38↓, 1, TUNEL↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
p‑cJun↓, 1, other↑, 1, tumCV↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP/DDIT3↓, 1, p‑eIF2α↓, 1, ER Stress↓, 1, GRP78/BiP↓, 1, XBP-1↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
LC3‑Ⅱ/LC3‑Ⅰ↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 4, DNMTs↓, 1, P53↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↓, 1, ERK↑, 1, HDAC↑, 1, Mst1↓, 1, mTOR↓, 1, p‑mTOR↓, 1, p300↓, 1, PI3K↑, 2, STAT3↓, 1, STAT3↑, 1,
Migration(tgid=13) ⓘ
5LO↓, 1, AP-1↓, 1, APP↓, 1, Ca+2↓, 1, COL1↓, 1, E-cadherin↑, 1, TGF-β↑, 1, Treg lymp↝, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1, VCAM-1↓, 1, Vim↓, 1, α-SMA↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
ATF4↓, 1,
Barriers & Transport(tgid=15) ⓘ
GastroP↑, 1, IBI↑, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD25+↑, 1, CD4+↑, 2, COX2/PTGS2↓, 4, CRP↓, 1, FOXP3↑, 1, HMGB1↓, 1, ICAM-1↓, 2, IFN-γ↓, 2, IL1↓, 2, IL10↓, 1, IL10↑, 2, IL12↓, 1, IL1β↓, 6, IL4↓, 2, IL4↑, 1, IL6↓, 11, IL8↓, 1, Imm↑, 3, Inflam↓, 9, JAK2↑, 1, LPS↓, 2, M2 MC↑, 1, MCP1/CCL2↓, 1, NF-kB↓, 5, PGE2↓, 2, TLR4↓, 1, TNF-α↓, 12,
Cellular Microenvironment(tgid=17) ⓘ
NOX↓, 1,
Synaptic & Neurotransmission(tgid=18) ⓘ
BDNF↑, 2, ChAT↑, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 4, BACE/β-secretase↓, 1, NLRP3↓, 3,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
BNP↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 2, BioAv↑, 2, BioAv↝, 1, Dose↓, 1, Dose↑, 1, Dose↝, 7, eff↑, 7, Half-Life↓, 1, Half-Life↝, 1, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 3, AST↓, 3, Bil↑, 1, creat↓, 2, CRP↓, 1, GutMicro↑, 3, IL6↓, 11, LDH↓, 1, LDH↑, 1, Urea↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, antiPs↑, 1, AntiTum↓, 1, cardioP↑, 6, chemoP↑, 4, cognitive↓, 1, cognitive↑, 5, hepatoP↑, 8, memory↑, 2, neuroP↑, 5, Obesity↓, 1, OS↑, 1, radioP↑, 21, RenoP↑, 3, toxicity↓, 5, Weight↑, 1, Wound Healing↑, 2,
Infection & Microbiome(tgid=24) ⓘ
Bacteria↓, 1, Diar↓, 1, Sepsis↓, 1,
Total Targets: 188
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
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