MDA Cancer Research Results

MDA, Serum malondialdehyde: Click to Expand ⟱
Source:
Type:
MDA : malondialdehyde. The level of oxidative stress can be measured by assessing the MDA levels.
Since MDA is highly cytotoxic and carcinogenic agent it is frequently used as a biomarker of oxidative stress during major health problems such as cancer, etc.
Malondialdehyde (MDA) is the most widely used agent to estimate the extent of lipid peroxidation. Timely diagnosis of the condition followed by supplementation with antioxidants like beta-carotene, pro-vitamin A, vitamin A, vitamin C, vitamin E, lipoic acid, zinc, selenium, and spirulina can prevent potentially malignant disorders.
MDA is a lipid peroxidation marker
Scientific Papers found: Click to Expand⟱
5263- 3BP,  CET,    3-Bromopyruvate overcomes cetuximab resistance in human colorectal cancer cells by inducing autophagy-dependent ferroptosis
- in-vitro, CRC, DLD1 - NA, NA, HCT116
eff↑, Our results demonstrated that the co-treatment of 3-BP and cetuximab synergistically induced an antiproliferative effect in both CRC cell lines
Ferroptosis↓, co-treatment induced ferroptosis, autophagy, and apoptosis.
TumAuto↑,
Apoptosis↑,
FOXO3↑, co-treatment inhibited FOXO3a phosphorylation and degradation and activated the FOXO3a/AMPKα/pBeclin1 and FOXO3a/PUMA pathways, leading to the promotion of ferroptosis, autophagy, and apoptosis in DLD-1
AMPKα↑,
p‑Beclin-1↑,
HK2↓, 3-Bromopyruvate (3-BP), also known as hexokinase II inhibitor II, has shown promise as an anticancer agent against various types of cancer
ATP↓, 3-BP exerts its anticancer effects by manipulating cell energy metabolism and regulating oxidative stress, as evidenced by the accumulation of reactive oxygen species (ROS) [13,14,15,16].
ROS↑,
Dose↝, Eight days postinoculation, xenografted mice were randomly divided into four groups and intraperitoneally injected with PBS, 3-BP, cetuximab, or a combination of 3-BP and cetuximab every four days for five injections.
TumVol↓, 3-BP alone or co-treatment with 3-BP and cetuximab significantly reduced the tumor volume and tumor weight on Day 28, but co-treatment showed a greater reduction than 3-BP alone
TumW↓,
xCT/SLC7A11↑, The protein level of SLC7A11 was significantly upregulated in all three cell lines following co-treatment (Fig. 2B).
GSH↓, co-treatment with 3-BP and cetuximab led to glutathione (GSH) depletion (Fig. 2D), reactive oxygen species (ROS) production
eff↓, Knockdown of either ATG5 or Beclin1 attenuated the cell death and MDA production induced by co-treatment
MDA↑,

4417- AgNPs,    Caffeine-boosted silver nanoparticles target breast cancer cells by triggering oxidative stress, inflammation, and apoptotic pathways
- in-vitro, BC, MDA-MB-231
ROS↑, Caf-AgNPs significantly increased ROS, malondialdehyde, COX-2, IL-1β, and TNF-α level in BC cells, which was accompanied by a decrease in glutathione levels.
MDA↑,
COX2/PTGS2↑,
IL1β↑,
TNF-α↑,
GSH↓,
Cyt‑c↑, increased levels of cytosolic cytochrome c, caspase-3, and Bax proteins, as well as a significant decrease in Bcl-2 expression and Bcl-2/Bax ratio
Casp3↑,
BAX↑,
Bcl-2↓,
LDH↓, Cancer cells subjected to Caf-AgNPs demonstrated elevated lactate dehydrogenase (LDH) membrane leakage
cycD1/CCND1↓, notable downregulation of cyclin D1 and cyclin-dependent kinase 2 (CDK2) mRNA expression
CDK2↓,
TumCCA↑, several mechanisms for cellular destruction, including cell cycle arrest, oxidative stress induction, modulation of the inflammatory response, and mitochondrial apoptosis
mt-Apoptosis↑,

373- AgNPs,    Cytotoxic Potential and Molecular Pathway Analysis of Silver Nanoparticles in Human Colon Cancer Cells HCT116
- in-vitro, Colon, HCT116
LDH↓, Increased lactate dehydrogenase leakage (LDH),
ROS↑,
MDA↑,
ATP↓,
GSH↓,
MMP↓, loss of

377- AgNPs,    Anticancer Action of Silver Nanoparticles in SKBR3 Breast Cancer Cells through Promotion of Oxidative Stress and Apoptosis
- in-vitro, BC, SkBr3
ROS↑,
Apoptosis↑,
Bax:Bcl2↑,
VEGF↑, VEGF-A
Akt↓,
PI3K↓,
TAC↓,
TOS↑,
OSI↑,
MDA↑,
Casp3↑,
Casp7↑,

400- AgNPs,  MF,    Polyvinyl Alcohol Capped Silver Nanostructures for Fortified Apoptotic Potential Against Human Laryngeal Carcinoma Cells Hep-2 Using Extremely-Low Frequency Electromagnetic Field
- in-vitro, Laryn, HEp2
TumCP↓, especially in the G0/G1 and S phases.
Casp3↑,
P53↑,
Beclin-1↑,
TumAuto↑,
GSR↑, oxidative stress biomarker
ROS↑, oxidative stress biomarker
MDA↑, oxidative stress biomarker
ROS↑,
SIRT1↑,
Ca+2↑, induce apoptosis in osteoclasts by increasing intracellular and nucleus Ca2+ concentration
Endon↑, increases endonuclease activity
DNAdam↑,
Apoptosis↑,
NF-kB↓,

398- AgNPs,    Silver nanoparticles induced testicular damage targeting NQO1 and APE1 dysregulation, apoptosis via Bax/Bcl-2 pathway, fibrosis via TGF-β/α-SMA upregulation in rats
- in-vivo, Testi, NA
Bcl-2↓,
Casp3↑,
GSH↓,
MDA↑,
NO↑,
H2O2↑,
SOD↓,

2287- AgNPs,    Silver nanoparticles induce endothelial cytotoxicity through ROS-mediated mitochondria-lysosome damage and autophagy perturbation: The protective role of N-acetylcysteine
- in-vitro, Nor, HUVECs
*TumCP↓, AgNPs affects the morphology and function of endothelial cells which manifests as decreased cell proliferation, migration, and angiogenesis ability
*ROS↑, AgNPs can induce excessive cellular production of reactive oxygen species (ROS), leading to damage to cellular sub-organs such as mitochondria and lysosomes
*eff↓, treatment with ROS scavenger-NAC can effectively suppress AgNP-induced endothelial damage.
*MDA↑, exposure to AgNPs increased MDA levels and decreased GSH levels.
*GSH↓,
*MMP↓, significantly reduced both MMP and ATP levels (Fig. 7) in HUVECs,
*ATP↓,
*LC3II↑, expression levels of LC3-II and p62 were significantly increase
*p62↑,
*Bcl-2↓, the anti-apoptotic protein expression level of Bcl-2 in HUVECs decreased, while the pro-apoptotic protein expression levels of Bax and Caspase-3 increased significantly.
*BAX↑,
*Casp3↑,

1069- AL,    Allicin promotes autophagy and ferroptosis in esophageal squamous cell carcinoma by activating AMPK/mTOR signaling
- vitro+vivo, ESCC, TE1 - vitro+vivo, ESCC, KYSE-510 - in-vitro, Nor, Het-1A
TumCP↓,
LC3‑Ⅱ/LC3‑Ⅰ↑,
p62↓,
p‑AMPK↑,
mTOR↓,
TumAuto↑,
NCOA4↑,
MDA↑,
Iron↑, elevated malondialdehyde and Fe2+ production levels
TumW↓,
TumVol↓,
ATG5↑,
ATG7↑,
TfR1/CD71↓,
FTH1↓, suppressed the expression of ferritin heavy chain 1 (the major intracellular iron-storage protein)
ROS↑,
Iron↑,
Ferroptosis↑,
*toxicity↓, 80 μg/mL allicin for 24 h did not change the viability of Het-1A cells. A slight reduction in cell viability was observed when Het-1A cells were treated with 160 μg/mL allicin for 24 h

1349- And,    Andrographolide promoted ferroptosis to repress the development of non-small cell lung cancer through activation of the mitochondrial dysfunction
- in-vitro, Lung, H460 - in-vitro, Lung, H1650
TumCG↓,
TumMeta↓,
Ferroptosis↑,
ROS↑,
MDA↑,
Iron↑,
GSH↓, lipid ROS reduced glutathione (GSH) accumulation
GPx4↓,
xCT/SLC7A11↓, SLC7A11
MMP↓,
ATP↓,

1565- Api,    Apigenin-7-glucoside induces apoptosis and ROS accumulation in lung cancer cells, and inhibits PI3K/Akt/mTOR pathway
- in-vitro, Lung, A549 - in-vitro, Nor, BEAS-2B - in-vitro, Lung, H1975
TumCP↓, AGL significantly reduced proliferation, promoted cell apoptosis, and attenuated the migration and invasion of A549 or H1975 cell
Apoptosis↑,
TumCMig↓,
TumCI↓,
Cyt‑c↑, elevated the levels of cytochrome C and MDA
MDA↑,
GSH↓, but reduced the production of GSH in A549 and H1975 cells.
ROS↑, AGL enhanced the accumulation of ROS
PI3K↓, induces ROS accumulation in lung cancer cells by repressing PI3K/Akt/mTOR pathway
Akt↓,
mTOR↓,

3386- ART/DHA,    Effects of Caffeine-Artemisinin Combination on Liver Function and Oxidative Stress in Selected Organs in 7,12-Dimethylbenzanthracene-Treated Rats
- in-vivo, Nor, NA
*MDA↑, Table 1 normal vs art
*SOD↓, Table 2 normal vs art
*GSH∅, Table 3 normal vs art (slight increase)
*Catalase↓, table 4 normal vs art

3345- ART/DHA,    Dihydroartemisinin-induced unfolded protein response feedback attenuates ferroptosis via PERK/ATF4/HSPA5 pathway in glioma cells
- in-vitro, GBM, NA
ROS↑, Dihydroartemisinin (DHA) has been shown to exert anticancer activity through iron-dependent reactive oxygen species (ROS) generation, which is similar to ferroptosis, a novel form of cell death
Ferroptosis↑, DHA induced ferroptosis in glioma cells, as characterized by iron-dependent cell death accompanied with ROS generation and lipid peroxidation.
lipid-P↑,
HSP70/HSPA5↑, DHA treatment simultaneously activated a feedback pathway of ferroptosis by increasing the expression of heat shock protein family A (Hsp70) member 5 (HSPA5)
ER Stress↑, DHA caused endoplasmic reticulum (ER) stress in glioma cells, which resulted in the induction of HSPA5 expression by protein kinase R-like ER kinase (PERK)-upregulated activating transcription factor 4 (ATF4)
ATF4↑,
GRP78/BiP↑, HSPA5
MDA↑, DHA significantly increased lipid ROS and MDA levels in glioma cells in a dose- and time-dependent manner.
GSH↓, As an important antioxidant, reduced form GSH was exhausted by DHA
eff↑, Inhibitor of HSPA5 synergistically enhanced anti-tumor effects of DHA
GPx4↑, DHA induced-ER stress in turn activated cell protection against ferroptosis through PERK-ATF4- HSPA5 activation, which promoted the expression of GPX4 to detoxify peroxidized membrane lipids

3172- Ash,    Implications of Withaferin A for the metastatic potential and drug resistance in hepatocellular carcinoma cells via Nrf2-mediated EMT and ferroptosis
- in-vitro, HCC, HepG2 - in-vitro, Nor, HL7702
Keap1↑, Notably, Withaferin A elevated Keap1 expression to mitigate Nrf2 signaling activation-mediated epithelial to mesenchymal transition (EMT) and ferroptosis-related protein xCT expression
NRF2↓,
EMT↓, Withaferin A suppresses epithelial-to-mesenchymal transition (EMT) in non-small cell lung cancer
TumCP↓, Withaferin A restrains proliferation, invasion, and VM of hepatoma cells while preserving normal hepatocytes
TumCI↓,
selectivity↑, , treatment with Withaferin A ranging from 1 to 100 μM had little effect on cell viability of human normal liver cells (HL-7702 cells), indicating the little cytotoxicity on normal hepatocytes.
*toxicity↓,
ROS↑, Withaferin A strikingly enhanced ROS () and MDA levels (), but reduced the GSH levels (), indicating the induction of ferroptosis by Withaferin A
MDA↑,
GSH↓,
Ferroptosis↑,

1392- BBR,    Based on network pharmacology and experimental validation, berberine can inhibit the progression of gastric cancer by modulating oxidative stress
- in-vitro, GC, AGS - in-vitro, GC, MKN45
TumCG↓,
TumCMig↓,
ROS↑, intracellular
MDA↑, intracellular
SOD↓, intracellular
NRF2↓,
HO-1↓,
Hif1a↓,
EMT↓,
Snail↓,
Vim↓,

2717- BetA,    Betulinic Acid Induces ROS-Dependent Apoptosis and S-Phase Arrest by Inhibiting the NF-κB Pathway in Human Multiple Myeloma
- in-vitro, Melanoma, U266 - in-vivo, Melanoma, NA - in-vitro, Melanoma, RPMI-8226
Apoptosis↑, BA mediated cytotoxicity in MM cells through apoptosis, S-phase arrest, mitochondrial membrane potential (MMP) collapse, and overwhelming reactive oxygen species (ROS) accumulation.
TumCCA↑, S-Phase Arrest in U266 Cells
MMP↓,
ROS↑, exhibited concentration-dependent increases in intracellular ROS
eff↓, ROS scavenger N-acetyl cysteine (NAC) effectively abated elevated ROS, the BA-induced apoptosis was partially reversed
NF-kB↓, BA resulted in marked inhibition of the aberrantly activated NF-κB pathway in MM
Cyt‑c↑, BA mediated the release of cyt c and activated cleaved caspase-3, caspase-8, and caspase-9 and cleaved PARP1
Casp3↑,
Casp8↑,
Casp9↑,
cl‑PARP1↑,
MDA↑, here is a concentration-dependent increase in MDA contents and reduction in SOD activities, especially for the high concentration group.
SOD↓,
SOD2↓, expression of genes SOD2, FHC, GCLM, and GSTM was all decreased following treatment with BA (40 μM)
GCLM↓,
GSTA1↓,
FTH1↓, FHC
GSTs↓, GSTM
TumVol↓, BA Inhibits the Growth of MM Xenograft Tumors In Vivo. BA-treated group were significantly reduced (inhibition ratio of approximately 72.1%).

739- Bor,    Borax regulates iron chaperone- and autophagy-mediated ferroptosis pathway in glioblastoma cells
- in-vitro, GBM, U87MG - in-vitro, Nor, HMC3
TumCG↓,
TumCP↓,
TumCCA↑, remarkably reduced S phase in the U87-MG cells (opposite on normal cells)
PCBP1↓,
GSH↓,
GPx4↓,
Beclin-1↑,
MDA↑,
ACSL4↑,
Casp3↑,
Casp7↑,
Ferroptosis↑,
*toxicity↓, exhibited selectivity by having an opposite effect on normal cells (HMC3).

738- Bor,    Borax induces ferroptosis of glioblastoma by targeting HSPA5/NRF2/GPx4/GSH pathways
- in-vitro, GBM, U251 - in-vitro, GBM, A172 - in-vitro, Nor, SVGp12
TumCP↓,
GPx4↓, borax treatment decreased GPx4, GSH, HSPA5 and NRF2 levels in U251 and A172 cells while increasing MDA levels and caspase‐3/7 activity.
GSH↓,
HSP70/HSPA5↓,
NRF2↓,
MDA↑,
Casp3↑,
Casp7↑,
Ferroptosis↑, Consequently, borax may induce ferroptosis in GBM cells
selectivity↑, Treating SVG cells with borax concentrations ranging from 0 to 800 μM for 24 h did not result in a significant reduction in viability compared to the control group

729- Bor,    Promising potential of boron compounds against Glioblastoma: In Vitro antioxidant, anti-inflammatory and anticancer studies
- in-vitro, GBM, U87MG - in-vivo, Nor, HaCaT
TOS↑,
TumCG↓,
MDA↑,
SOD↑,
Catalase↑,
TAC↓,
GSH↓,
BRAF↑,
MAPK↓,
PTEN↓, BA application was found more favorable because of its inhibitory effect on PIK3CA, PIK3R1, PTEN and RAF1 genes
Raf↓, RAF1
*toxicity↓, We verified the selectivity of the compounds using a normal cell line, HaCaT and found an exact opposite condition after treating HaCaT cells with BA and BX

726- Bor,    Redox Mechanisms Underlying the Cytostatic Effects of Boric Acid on Cancer Cells—An Issue Still Open
- Review, NA, NA
NAD↝, high affinity for the ribose moieties of NAD+
SAM-e↝, high affinity for S-adenosylmethione
PSA↓,
IGF-1↓,
Cyc↓, reduction in cyclins A–E
P21↓,
p‑MEK↓,
p‑ERK↓, ERK (P-ERK1/2)
ROS↑, induce oxidative stress by decreasing superoxide dismutase (SOD) and catalase (CAT)
SOD↓,
Catalase↓,
MDA↑,
GSH↓,
IL1↓, IL-1α
IL6↓,
TNF-α↓,
BRAF↝,
MAPK↝,
PTEN↝,
PI3K/Akt↝,
eIF2α↑,
ATF4↑,
ATF6↑,
NRF2↑,
BAX↑,
BID↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Bcl-xL↓,

5887- CAR,  TV,    Antitumor Effects of Carvacrol and Thymol: A Systematic Review
- Review, Var, NA
Apoptosis↑, It was attested that carvacrol and thymol induced apoptosis, cytotoxicity, cell cycle arrest, antimetastatic activity,
TumCCA↑, accumulation of cells in the G1 phase, together with a reduction of cells in the S phase, slowing cell cycle/mitosis and provoking cell death.
TumMeta↓,
TumCP↓, antiproliferative effects and inhibition of signaling pathways (MAPKs and PI3K/AKT/mTOR).
MAPK↓,
PI3K↓,
Akt↓,
mTOR↓,
eff↑, carvacrol appears to be more potent than thymol
*Inflam↓, these compounds present anti-inflammatory (Li et al., 2018; Chamanara et al., 2019) and antioxidant
*antiOx↑,
AXL↓, These effects occurred mainly through the inhibition of tyrosine kinase receptor (AXL) expression and an increase in malondialdehyde (MDA
MDA↑,
Casp3↑, caspase-3 activation and Bcl-2 inhibition
Bcl-2↓,
MMP2↓, promoted a decrease in Bcl-2, metalloproteinase-2 and -9 (MMP-2 and MMP-9), p-ERK, p-Akt, cyclin B1 levels and an increase in p-JNK, Bax levels, resulting in cell cycle arrest at the G2/M phase
MMP9↓,
p‑JNK↑,
BAX↑,
MDA↓, In respect of breast cancer, treatment with carvacrol decreases MDA-MB231 (Jamali et al., 2018; Li et al., 2021) and MCF-7 cells line viability
TRPM7↓, TRPM7 pathway is one of the suggested pharmacological mechanisms of action
MMP↓, decreased mitochondrial membrane potential, cytochrome C release, caspase activation, PARP cleavage
Cyt‑c↑,
Casp↑,
cl‑PARP↑,
ROS↑, Carvacrol also induced cytotoxicity and apoptosis (via caspase-3 and reactive oxygen species—ROS) of human oral squamous cell carcinoma (OC2 cell line)
CDK4↓, In tongue cancer (Tca-8113, SCC-25 cell lines), Dai et al. (2016) reported that carvacrol effectively inhibited cell proliferation through the negative regulation of CCND1 and CDK4 expression, and the positive regulation of p21 expression,
P21↑,
F-actin↓, A blockade of TRPM7 channels, reduced expression of MMP-2 and F-actin, was also observed, together with the inhibition of PI3K/Akt and MAPK
GSH↓, by increasing ROS, Bax, Caspase-3, -9 levels and reducing Bcl-2 and GSH levels.
*SOD↑, Moreover, carvacrol was able to increase the levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione (GSH), along with a reduction of lipid peroxides and the enzymes AST, ALT, AL
*Catalase↑,
*GPx↑,
*GSR↑,
*GSH↑,
*lipid-P↓,
*AST↓,
*ALAT↓,
*ALP↓,
*LDH↓,
DNAdam↑, hepatocellular carcinoma induced by diethylnitrosamine (DEN), carvacrol treatment promoted DNA fragmentation
AFP↓, carvacrol showed a reduction in serum levels of alpha-fetoprotein (AFP), alpha l-fucosidase (AFU), vascular endothelial growth factor (VEGF
VEGF↓,
Weight↑, Carvacrol supplementation significantly improved the weight gain and growth rate of animals with colon cancer
*chemoP↑, reduction in oxidative stress damage (higher levels of GSH, GPx, GR, SOD and CAT), suggesting that carvacrol presents chemopreventive effects
ROS↑, In vitro, carvacrol and thymol increased the generation of reactive oxygen species in 24.63% (n = 17) of the studies, a fact that is also observed in chemotherapeutics

4481- Chit,    Antioxidant Properties and Redox-Modulating Activity of Chitosan and Its Derivatives: Biomaterials with Application in Cancer Therapy
- Review, Var, NA
*BioAv↑, It is known that chitosan exhibits versatile biological properties, including biodegradability, biocompatibility, and a less toxic nature.
*toxicity↓,
*antiOx↑, Because of its antioxidant, antibacterial, anticancer, anti-inflammatory, and immunostimulatory activities, the biopolymer has been used in a wide variety of pharmaceutical, biomedical, food industry, health, and agricultural applications and has bee
AntiCan↑,
*Inflam↓,
*ROS↓, Many in vitro and in vivo studies have shown that chitosan exhibits redox-regulatory activity due to inhibition of ROS production, prevention of lipid oxidation by significantly reduced serum free fatty acids, and malondialdehyde concentrations
*lipid-P↓,
MDA↓,
selectivity↑, hitosan exerts an inhibitory effect on the proliferation of MDA-MB-231, MCF-7, and T47D breast cancer cells in a dose- and time-dependent manner, while being non-toxic to fibroblast L929 normal cells.
MMP↓, exposure of MDA-MB-231 cells to chitosan led to depolarization of the mitochondrial membrane, increase of ROS generation, DNA oxidation, and S phase cell cycle arrest.
ROS↑,
TumCCA↑,
MDA↑, in vitro, chitosan nanoparticles showed high antitumor activities, which were accompanied with an increase in MDA level and a decrease in GSH level in tumor tissues.
GSH↓,
ChemoSen↑, Possible Mechanism for Sensitizing Cancer Cells Toward Chemotherapeutics

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

1585- Citrate,    Sodium citrate targeting Ca2+/CAMKK2 pathway exhibits anti-tumor activity through inducing apoptosis and ferroptosis in ovarian cancer
- in-vitro, Ovarian, SKOV3 - in-vitro, Ovarian, A2780S - in-vitro, Nor, HEK293
Apoptosis↑,
Ferroptosis↑,
Ca+2↓, Sodium citrate chelates intracellular Ca2+
CaMKII ↓, inhibits the CAMKK2/AKT/mTOR/HIF1α-dependent glycolysis pathway, thereby inducing cell apoptosis.
Akt↓,
mTOR↓,
Hif1a↓,
ROS↑, Inactivation of CAMKK2/AMPK pathway reduces Ca2+ level in the mitochondria by inhibiting the activity of the MCU, resulting in excessive ROS production.
ChemoSen↑, Sodium citrate increases the sensitivity of ovarian cancer cells to chemo-drugs
Casp3↑,
Casp9↑,
BAX↑,
Bcl-2↓,
Cyt‑c↑, co-localization of cytochrome c and Apaf-1
GlucoseCon↓, glucose consumption, lactate production and pyruvate content were significantly reduced
lactateProd↓,
Pyruv↓,
GLUT1↓, sodium citrate decreased both mRNA and protein expression levels of glycolysis-related proteins such as Glut1, HK2 and PFKP
HK2↓,
PFKP↓,
Glycolysis↓, sodium citrate inhibited glycolysis of SKOV3 and A2780 cells
Hif1a↓, HIF1α expression was decreased significantly after sodium citrate treatment
p‑Akt↓, phosphorylation of AKT and mTOR was notably suppressed after sodium citrate treatment.
p‑mTOR↓,
Iron↑, ovarian cancer cells treated with sodium citrate exhibited higher Fe2+ levels, LPO levels, MDA levels, ROS and mitochondrial H2O2 levels
lipid-P↑,
MDA↑,
ROS↑,
H2O2↑,
mtDam↑, shrunken mitochondria, an increase in mitochondrial membrane density and disruption of mitochondrial cristae
GSH↓, (GSH) levels, GPX activity and expression levels of GPX4 were significantly reduced in SKOV3 and A2780 cells with sodium citrate treatment
GPx↓,
GPx4↓,
NADPH/NADP+↓, significant elevation in the NADP+/NADPH ratio was observed with sodium citrate treatment
eff↓, Fer-1, NAC and NADPH significantly restored the cell viability inhibited by sodium citrate
FTH1↓, decreased expression of FTH1
LC3‑Ⅱ/LC3‑Ⅰ↑, sodium citrate increased the conversion of cytosolic LC3 (LC3-I) to the lipidated form of LC3 (LC3-II)
NCOA4↑, higher levels of NCOA4
eff↓, test whether Ca2+ supplementation could rescue sodium citrate-induced ferroptosis. The results showed that Ca2+ dramatically reversed the enhanced levels of MDA, LPO and ROS triggered by sodium citrate
TumCG↓, sodium citrate inhibited tumor growth by chelation of Ca2+ in vivo

3624- Cro,    Crocus Sativus L. (Saffron) in Alzheimer's Disease Treatment: Bioactive Effects on Cognitive Impairment
- Review, AD, NA
*AChE↓, aqueous and methanolic saffron extract presented a moderate activity as AChE inhibitor (up to 30%),
*memory↑, f 50-200 mg/kg of crocin enhanced memory impairment
*cognitive↑, crocin (30 mg/kg) for 3 weeks significantly improved cognitive impairment caused by intracerebroventricular injection of STZ,
*MDA↑, improved cognitive tasks and produced a significant decrease of malondialdehyde (MDA) levels and increase of total thiol content and glutathione peroxidase (GPx) activity in STZ-lesioned rats
*Thiols↑,
*GPx↑,
*antiOx↑, crocetin is only one and strong antioxidant, providing protection in rescuing cell viability, blocking reactive oxygen species (ROS) production and reducing caspase-3 activation
*ROS↓, crocin can prevent oxidative stress damage to hippocampus, memory and learning impairments
*Casp3↓,
*neuroP↑, neuroprotective effects of crocin against AD
*SOD↑, increase the levels of glutathione peroxidase, superoxide dismutase, acetylcholine and choline acetyltransferase,
*Ach↑,
*ChAT↑,
*BBB↑, shown that crocetin, able to pass through BBB, inhibits fibril Aβ formation,
*Aβ↓,
*tau↓, inhibitory effects of crocin on tau protein neurofibrillary tangles in AD.
*cognitive↑, (15 mg twice a day) or a capsule of placebo (two capsules a day) for 16 weeks. The results of this study indicated that saffron produces a significant improvement in cognitive performance
*Inflam↓, anticholinergic, anti-inflammatory and antioxidant features

6176- Cu,    Copper Oxide Nanoparticles Induced Mitochondria Mediated Apoptosis in Human Hepatocarcinoma Cells
- in-vitro, Liver, HepG2
ROS↑, found to induce cytotoxicity in HepG2 cells in dose-dependent manner, which was likely to be mediated through reactive oxygen species generation and oxidative stress.
P53↑, Tumor suppressor gene p53 and apoptotic gene caspase-3 were up-regulated due to CuO NPs exposure.
MMP↓, Decrease in mitochondrial membrane potential with a concomitant increase in the gene expression of bax/bcl2 ratio suggested that mitochondria mediated pathway involved in CuO NPs induced apoptosis.
Bax:Bcl2↑,
Apoptosis↑,
*Bacteria↓, Due to their antimicrobial properties CuO NPs are also employed in textiles, paints, plastics and food containers
MDA↑, MDA level, an end product of membrane LPO was significantly higher in cells exposed to CuO NPs in the concentration
GSH↓, CuO NPs significantly reduced the intracellular level of GSH in a dose-dependent manner
eff↓, Results showed that NAC abolished almost fully the harmful effect of CuO NPs at all concentrations studied
Casp3↑, caspase-3 were significantly up-regulated

6177- Cu,    Toxicity of copper oxide nanoparticles: a review study
- Review, Nor, NA
*ROS↑, The literature evidences that the CuO NPs exposure to the living systems results in reactive oxygen species generation, oxidative stress, inflammation, cytotoxicity, genotoxicity and immunotoxicity.
*Inflam↑,
*toxicity↑,
lipid-P↑, A549 cells that leads to high level of lipid peroxidation and ROS production while lower level of antioxidant (GSH) in HepG2
GSH↓,
MDA↑, They observed that MDA, a lipid peroxidation marker and antioxidant enzymes like SOD and CAT significantly increased followed by reduction in GSH level
*SOD↓, Lower level of GSH and inhibition of SOD and CAT activities by CuO NPs contributing to oxidative damages was also observed in embryo and while change in zebrafish physiology
*Catalase↓,

3751- CUR,  Gala,    A Novel Galantamine-Curcumin Hybrid as a Potential Multi-Target Agent against Neurodegenerative Disorders
- in-vivo, AD, NA
*AChE↓, AChE inhibitor galantamine (GAL) and the antioxidant polyphenol curcumin (CU) showed high AChE inhibition in vitro.
*MDA↑, 25% reduction in AChE activity, as well as a 28% and 73% increase in the levels of MDA and GSH, respectively
*GSH↑,
*BBB↑, Accordingly, GAL and CU have intermediate BBB permeability

1410- CUR,    Curcumin induces ferroptosis and apoptosis in osteosarcoma cells by regulating Nrf2/GPX4 signaling pathway
- vitro+vivo, OS, MG63
tumCV↓,
Apoptosis↑,
TumCG↓,
NRF2↓, after treatment with curcumin, Nrf2 and GPX4 levels were significantly decreased
GPx4↓,
HO-1↓,
xCT/SLC7A11↓, SLC7A11
ROS↑, our results revealed that after treatment with curcumin, ROS and MDA levels were significantly increased while GSH levels were decreased
MDA↑,
GSH↓,

414- CUR,    Transcriptome Investigation and In Vitro Verification of Curcumin-Induced HO-1 as a Feature of Ferroptosis in Breast Cancer Cells
- in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231
Ferroptosis↑,
Iron↑,
ROS↑,
lipid-P↑,
MDA↑,
GSH↓,
HO-1↑, Curcumin upregulates a variety of ferroptosis target genes related to redox regulation, especially heme oxygenase-1 (HO-1).
NRF2↑,
GPx↓,
ROS↑,
Iron↑, curcumin caused marked accumulation of intracellular iron
GPx4↓,
HSP70/HSPA5↑,
ATFs↑, ATF4
CHOP/DDIT3↑, DDIT3
MDA↑,
FTL↑, Curcumin upregulated FTL (encoding ferritin light chain), FTH1
FTH1↑,
BACH1↑,
REL↑, v-rel reticuloendotheliosis viral oncogene homolog A
USF1↑,
NFE2L2↑,

6212- CUR,  Rad,    Radiosensitization and Radioprotection by Curcumin in Glioblastoma and Other Cancers
- Review, Var, NA
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↓,

6223- CUR,    Curcumin Rewires the Tumor Metabolic Landscape: Mechanisms and Clinical Prospects
- Review, Var, NA
Ferroptosis↑, including the induction of ferroptosis by regulating the SLC7A11/GPX4 axis
GutMicro↑, and modulating gut microbiota metabolism. I
Akt↓, it inhibits pro-tumorigenic signals such as Akt/mTOR, NF-κB, Wnt/β-catenin, and STAT3, thereby blocking tumor proliferation, invasion, and metastasis
mTOR↓,
NF-kB↓,
Wnt↓,
β-catenin/ZEB1↓,
STAT3↓,
TumCP↓,
TumCI↓,
TumMeta↓,
AMPK↑, activates tumor-suppressive and cytoprotective pathways, including AMPK, p53, and nuclear factor erythroid 2-related factor 2 (Nrf2), which induce cell cycle arrest and apoptosis
P53↑,
NRF2↑,
TumCCA↑,
Apoptosis↑,
Casp↑, activation of the Caspase cascade
GPx4↓, as well as ferroptosis by inhibiting the solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4) axis [5]
DNMTs↓, inhibiting epigenetic regulatory mechanisms such as DNMTs and HDACs.
HDAC↓,
VEGF↓, inhibiting VEGF signaling and enhances the immune microenvironment by improving T cell and NK cell function
Imm↑,
NK cell↑,
Warburg↓, Curcumin effectively reverses the Warburg effect and interferes with glucose metabolism by targeting HIF-1α and inhibiting key enzymes, including hexokinase 2 (HK2), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA)
Hif1a↓,
HK2↓,
PKM2↓,
LDHA↓,
GLUT1↓, as well as the functions of glucose transporter 1 (GLUT1) and monocarboxylate transporters (MCTs) [12].
MCT1↓,
AMPK↑, curcumin activates signaling pathways such as AMPK, downregulates fatty acid synthase (FASN) and stearoyl-CoA desaturase (SCD1),
FASN↓,
SCD1↓,
GLS↓, Curcumin extensively intervenes in amino acid metabolism by inhibiting the activity of glutaminase (GLS), ornithine decarboxylase (ODC), and other enzymes,
Apoptosis↑, inducing apoptosis through mechanisms such as disrupting the electron transport chain, reducing membrane potential, and promoting the generation of reactive oxygen species (ROS)
ETC↓,
MMP↓,
ROS↑,
lipid-P↑, curcumin induces lipid peroxidation and collapses redox homeostasis, thereby activating the ferroptosis program [
ChemoSen↑, blocking invasion and metastasis, and enhancing chemosensitivity.
PDK1↓, In hypoxic pancreatic cancer cells, curcumin downregulates the expression of GLUT1, HK2, LDHA, and PDK1 by inhibiting the Beclin1/HIF-1α axis, which results in reduced ATP production and inhibited cell proliferation [
Beclin-1↓,
ATP↓,
Glycolysis↓, inhibiting glycolysis
GlucoseCon↓, decreased glucose uptake and increased lactate production
lactateProd↑,
MMPs↓, reduces MMP, GSH, and G6PD activities
GSH↓, inhibition of SLC7A11 to limit GSH synthesis, thereby triggering the collapse of the antioxidant defense system
G6PD↓,
OXPHOS↓, downregulate OXPHOS and glycolysis activities
SREBP2↓, curcumin treatment leads to a marked downregulation of the mRNA expression of SREBP and its target genes. inhibiting the expression of NPC1L1, SREBP-2, and HNF1α
COX2/PTGS2↓, curcumin exerts anti-tumor effects by downregulating the expression of NF-κB, COX-2, and AP-1
AP-1↓,
NADH↓, decreased GPx4 and FSP1 expression, induced ferroptosis by inhibiting GSH-GPx4 and FSP1-CoQ 10-NADH pathways
NRF2↑, it inhibits GPX4 and activates Nrf2 and heme oxygenase-1 (HO-1). This results in an abnormal accumulation of intracellular Fe2+, ROS, lipid peroxides, and malondialdehyde (MDA), along with a depletion of GSH
HO-1↑,
Iron↑,
MDA↑,
*ROS↓, studies have demonstrated that the topical application of curcumin on the skin exerts antitumor effects by synergistically downregulating COX-2 and ODC activities, alleviating oxidative damage, and concurrently inhibiting inflammatory proliferation i
*Inflam↓,

6210- CUR,    Potential Roles and Mechanisms of Curcumin and its Derivatives in the Regulation of Ferroptosis
Ferroptosis↑, curcumin is a ferroptosis inducer with excellent anticancer efficacy, although it also exhibits organ protective and reparative effects by acting as a ferroptosis inhibitor.
*Ferroptosis↓,
ROS↑, Accumulated intracellular iron is the trigger for ferroptosis as it can produce highly reactive free radicals via the Fenton reaction, which can lead to ferroptosis
Fenton↑,
*IronCh↑, ability of curcumin to chelate iron and regulate oxidation predicts that curcumin may have a role in regulating ferroptosis,
GPx4↓, Curcumin and its derivative EF24 repress GPX4 expression and increase MDA and ROS levels to exert a pro-ferroptosis effect in osteosarcoma cells
MDA↑,
GSH↓, reduction in GSH content and L-OOH levels was measured in curcumin-treated TNBC cells
*NRF2↑, protective effects against ferroptosis-induced damage to cells107. Through activation of the Nrf2/HO-1 pathway, curcumin can both restrict high glucose-induced neuronal (N2a) cell injury
*HO-1↑,

6695- DFC,    Inhibition of lactate dehydrogenase A by diclofenac sodium induces apoptosis in HeLa cells through activation of AMPK
- in-vitro, Cerv, HeLa
other↝, Cancer cells exhibit a unique metabolic preference for the glycolytic pathway over oxidative phosphorylation for maintaining the tumor microenvironment.
Glycolysis↓, Diclofenac (DCF), a nonsteroidal anti-inflammatory drug, has been shown to exhibit anticancer effects by interfering with the glucose metabolism pathway.
LDHA↓, DCF binds to LDHA adjacent to the substrate binding site and inhibits its activity in a dose-dependent and allosteric manner in HeLa cells.
Hypoxia↓, Thus, DCF inhibits the hypoxic microenvironment and induces apoptosis-mediated cell death.
Apoptosis↑,
lactateProd↓, DCF-induced LDHA inhibition alters pyruvate, lactate, NAD+, and ATP production in cells, and this could be a possible mechanism through which DCF inhibits glucose uptake in cancer cells.
ATP↓, DCF-induced ATP deprivation leads to mitochondria-mediated oxidative stress, which results in DNA damage, lipid peroxidation, and apoptosis-mediated cell death.
mt-ROS↑,
DNAdam↑,
lipid-P↑,
AMPK↑, Reduction in intracellular ATP levels additionally activates the sensor kinase, adenosine monophosphate-activated protein kinase (AMPK), which further downregulates phosphorylated ribosomal S6 kinase (p-S6K), leading to apoptosis-mediated cell death.
p‑S6K↓,
TumCP↓, DCF inhibits proliferation in HeLa cells
Dose↝, HeLa cells with an IC50 dose of 175 ± 4.86 μm on 24 h of incubation
selectivity↑, DCF did not significantly affect the viability of normal cervical cells at 175 μm (IC50 dose in HeLa cells), where the IC50 value was found to be greater than 1 mm concentration of DCF (
i-MDA↑, The result showed that DCF treatment in HeLa cells led to a significant increase in MDA levels, suggesting an increased level of lipid peroxidation
mtDam↑, Many reports suggest that there is a strong correlation between the inhibition of LDHA and the induction of oxidative stress (ROS production) via mitochondrial damage

6759- DHA,  doxoR,    Differential sensitization of cancer cells to doxorubicin by DHA: a role for lipoperoxidation
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF7
ChemoSen↑, In MDA-MB-231, doxorubicin efficacy enhancement by DHA was linked to an increase in malondialdehyde level, a final product of lipid peroxidation.
i-MDA↑, DHA elicited by itself a 3.7-fold malondialdehyde level increase, additive to that induced by doxorubicin.
lipid-P↑,
ROS↑, These data indicate that the differential effect of DHA among cells on drug toxicity results from a differential oxidative response to doxorubicin.

3215- EGCG,    Epigallocatechin gallate modulates ferroptosis through downregulation of tsRNA-13502 in non-small cell lung cancer
- in-vitro, NSCLC, A549 - in-vitro, NSCLC, H1299
TumCP↓, EGCG resulted in a notable suppression of cell proliferation, as evidenced by a reduction in Ki67 immunofluorescence staining
Ki-67↓,
GPx4↓, EGCG treatment led to a decrease in the expression of glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) while increasing the levels of acyl-CoA synthetase long-chain family member 4 (ACSL4).
ACSL4↑,
Iron↑, accompanied by an increase in intracellular iron, malondialdehyde (MDA), and reactive oxygen species (ROS), alongside ultrastructural alterations characteristic of ferroptosis.
MDA↑,
ROS↑,
Ferroptosis↑,
eff↑, The cooperative effect of metformin and EGCG-activated Nrf2/HO-1 signaling pathway, facilitated by SIRT1-mediated Nrf2 deacetylation, enhances the susceptibility of NSCLC to EGCG modulation by promoting reactive oxygen species (ROS) generation and a
NRF2↑,
HO-1↑,

7046- GA,    Gallic acid: A promising anti-non-small cell lung cancer compound targeting early growth response protein-1 for apoptosis and ferroptosis
- in-vitro, NSCLC, A549 - in-vitro, NSCLC, H1299
TumCP↓, GA suppressed NSCLC cell proliferation, induced cell cycle arrest, and inhibited cell migration and invasion.
TumCCA↑,
TumCMig↓,
TumCI↓,
Apoptosis↑, GA simultaneously facilitated apoptosis and ferroptosis through EGR1 in NSCLC cells.
Ferroptosis↑,
THBS1↓, downregulating thrombospondin-1 via EGR1, inhibiting transforming growth factor beta 1/Smad2/3 signaling pathway.
EGR1↓,
TGF-β1↓,
SMAD2↓,
SMAD3↓,
GPx4↓, characterized by reduced GPX4 expression, increased reactive oxygen species and malondialdehyde accumulation, altered mitochondria, and iron overload.
ROS↑,
i-MDA↑,
i-Iron↑,

3771- H2,    Molecular Hydrogen Neuroprotection in Post-Ischemic Neurodegeneration in the Form of Alzheimer’s Disease Proteinopathy: Underlying Mechanisms and Potential for Clinical Implementation—Fantasy or Reality?
- Review, AD, NA - Review, Stroke, NA
*cognitive↑, hydrogen improves cognitive and neurological deficits and prevents or delays the onset of neurodegenerative changes in the brain.
AntiCan↑, Chinese National Health and Medical Commission in 2020 recommended the use of inhaled hydrogen in addition to oxygen therapy for anti-cancer, anti-inflammatory and anti-oxidant treatments
*Inflam↓,
*antiOx↑,
*ROS↓, Hydrogen has been suggested as a new complementary therapy against stroke, which, e.g., reduces oxidative stress,
*neuroP↑, Molecular Hydrogen Neuroprotection in Post-Ischemic Brain Injury
*SOD↑, molecular hydrogen significantly increases SOD and GSH-Px activity, reduces malondialdehyde levels and infarct volume, relieves cerebral edema, improves neurological outcomes and alleviates cognitive deficits
*GPx↑,
*MDA↑,
*BBB↑, Molecular hydrogen has been shown to protect the permeability of the blood-brain barrier after focal and global cerebral ischemia
*OS↑, It was documented that hydrogen therapy significantly improved the 7-day survival rate of mice after global brain ischemia, from 8.3 to 50%
*Ca+2↓, In addition, hydrogen lowered the increased levels of intracellular Ca2+ caused by glutamate toxicity
*APP↓, Taken together, these results indicate that treatment with hydrogen-rich water prevents proteolysis of the amyloid protein precursor towards amyloid
*p‑tau↓, hydrogen-rich water significantly inhibited the phosphorylation of the tau protein

7560- HYP,    Hyperoside: A Review of Its Structure, Synthesis, Pharmacology, Pharmacokinetics and Toxicity
- Review, Nor, NA - Review, AD, NA
*RenoP↓, Thirdly, long-term use of hyperoside is toxic to the kidneys, but the damage is reversible
Casp3↑, Up-regulates caspase-3, caspase-8, Bax, p53 and MDA contents; decreases GSH, SOD and CAT activities; decreases VEGF and Bcl-2 levels; and inhibits cell growth. HeLa 100 μmol/L
Casp8↑,
MDA↑,
GSH↓,
SOD↓,
Catalase↓,
VEGF↓,
Bcl-2↓,
TumCG↓,
p‑Akt↓, Down-regulates BMP-7 expression, AKT phosphorylation and PI3K expression; induces cell cycle arrest; and inhibits cell proliferation. Human HepG2 5, 10, 20, 40 and 80 μM
PI3K↓,
TumCCA↑,
TumCP↓,
BMP7/OP1↓,
*ZO-1↑, up-regulates ZO-1 and claudin5 protein expression; maintains the integrity of the blood–brain barrier; and may protect neural function in CIR-injured mice. CIR injury induced by MCAO in mice 50 mg/kg
*BBB↝,
*p‑Akt↑, increases the phosphorylation of AKT and GSK-3β; alleviates early brain injury after subarachnoid haemorrhage; and promotes nerve function recovery in rats.
*GSK‐3β↑,
*SOD↑, increases SOD and CAT activities and GSH content; increases SIRT1 gene expression; down-regulates NF-κB mRNA
*Catalase↑,
*GSH↑,
*SIRT1↑,
*NF-kB↓,
*IL1β↓, Down-regulates IL-1β, IL-6, IL-8, TNF-α, ROS, MDA, Bax and caspase-3 levels; increases CAT, SOD and GSH activities; up-regulates Bcl-2, BDNF, TrkB, SIRT1 and NGF expression; reduces LPS-induced inflammation, oxidative stress and apoptosis; and protec
*IL6↓,
*IL8↓,
*TNF-α↓,
*ROS↓,
*MDA↓,
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BDNF↑,
*TrkB↑,
*NGF↑,
*Apoptosis↓,
*cardioP↑, Cardioprotective Activity of Hyperoside.
*AST↓, Decreases the levels of AST, CK, CK-MB and c-TnT in rats; the rate of cardiomyocyte apoptosis;
*hepatoP↑, Hepatoprotective Activity of Hyperoside.
*AST↓, Decreases liver index, AST, ALT, MDA and Bach1 complex levels and alleviates the pathological damage of acute liver injury mice.
*ALAT↓,
*MDA↓,
*BACH1↓,
*neuroP↑, Brain-Protective Activity of Hyperoside.
*Stroke↓, Down-regulates TNF-α, IL-1β, IL-6, ICAM-1, VCAM-1, TLR4, COX-2, NF-κB, caspase-3, caspase-9, Bax and Bcl-2 expression and prevents CIR injury. Middle cerebral artery occlusion/reperfusion rat model
*ICAM-1↓,
*VCAM-1↓,
*TLR4↓,
*COX2/PTGS2↓,
*RenoP↑, Renal-Protective Activity of Hyperoside.
*NLRP3↓, Suppresses NLRP3, caspase-1 and ASC expression and prevents acute kidney injury induced by lipopolysaccharide. Mouse acute kidney injury model
*Casp1↓,
*ASC↓,
*BioAv↓, low oral bioavailability
*BioAv↑, hyperoside is compatible with other traditional Chinese medicines and they can improve its bioavailability and oral absorption.
*toxicity↓, Firstly, an acute toxicity test of hyperoside showed that its LD50 > 5000 mg/kg

7803- IBC,    Isobavachalcone induces hepatotoxicity in zebrafish embryos and HepG2 cells via the System Xc--GSH-GPX4 signaling pathway in ferroptosis response
- in-vivo, Nor, NA - in-vitro, NA, HepG2
*hepatoP↓, However, IBC causes some hepatotoxicity, and the mechanism of toxicity is unclear.
*ALAT↑, exposure to IBC increased zebrafish embryo mortality and decreased hatchability. Meanwhile, IBC induced liver injury and increased expression of ALT and AST activity.
*AST↑,
*ROS↑, IBC caused the increase of ROS and MDA the decrease of CAT, GSH, and GSH-Px; the increase of Fe2+ content; and the changes of ferroptosis related genes (acsl4, gpx4, and xct) and iron storage related genes (tf, fth, and fpn) in zebrafish embryos.
*MDA↑,
*Catalase↓,
*GSH↓,
*GPx↓,
*i-Iron↑,

7871- isoO,  Cisplatin,    Isoorientin reverses lung cancer drug resistance by promoting ferroptosis via the SIRT6/Nrf2/GPX4 signaling pathway
- vitro+vivo, Lung, NA
ChemoSen↑, combination of isoorientin (IO) and DDP treatment resulted in a significant decrease in the viability of drug-resistant cells, a substantial increase in intracellular iron, malondialdehyde (MDA) and ROS concentrations
i-Iron↑,
i-MDA↑,
*i-ROS↑,
GSH↓, a notable decrease in glutathione concentration, and the occurrence of ferroptosis in cells, as revealed by in vitro and in vivo experiments.
Ferroptosis↑,
NRF2↓, there was a decrease in the expression of nuclear factor-erythroid factor 2-related factor 2 (Nrf2), glutathione peroxidase 4 (GPX4), and sirtuin 6 (SIRT6) proteins, and an increase in cellular ferroptosis.
GPx4↓,
SIRT6↓,

1924- JG,    Juglone triggers apoptosis of non-small cell lung cancer through the reactive oxygen species -mediated PI3K/Akt pathway
- in-vitro, Lung, A549
TumCMig↓, substantially suppressed the migration and invasion of these two lung cancer cells
TumCI↓,
TumCCA↑, juglone arrested the cell cycle, induced apoptosis, increased the cleavage of caspase 3
Apoptosis↑,
cl‑Casp3↑,
BAX↑, protein expression of Bax and Cyt c
Cyt‑c↑,
ROS↑, juglone treatment considerably increased intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) levels
MDA↑,
GPx4↓, suppressed glutathione peroxidase 4 (GPX4) and superoxide dismutase (SOD) activities
SOD↓,
PI3K↓, inhibited the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway
Akt↓,
eff↓, N-acetylcysteine (a ROS scavenger) partially reversed the positive effects of juglone in terms of migration, invasion, ROS production, apoptosis, and PI3K/Akt pathway-associated protein expression

1921- JG,    Juglone induces ferroptotic effect on hepatocellular carcinoma and pan-cancer via the FOSL1-HMOX1 axis
- in-vitro, PC, NA - vitro+vivo, PC, NA
TumCG↓, Juglone suppressed HCC growth via ferroptosis in vitro and in vivo
Ferroptosis↑,
ROS↑, evidenced by increased levels of iron, lipid peroxidation (LPO), reactive oxygen species (ROS), malondialdehyde (MDA)
Iron↑,
lipid-P↑,
MDA↑,
GSH↓, decreased levels of glutathione (GSH)
FOSL1↑, induce ferroptosis in pan-cancer by activating the FOSL1-HMOX1 axis
HO-1↑, HMOX1

1275- LT,    Mechanism of luteolin induces ferroptosis in nasopharyngeal carcinoma cells
- in-vitro, Laryn, NA
Ferroptosis↑,
MDA↑,
Iron↑,
SOD↓,
GSH↓,
GPx4↓,
SOX4↓,
GDF15↓,

4231- Lut,    Luteolin and its antidepressant properties: From mechanism of action to potential therapeutic application
- Review, AD, NA
*PSD95↑, upregulating the expression of synaptophysin, postsynaptic density protein 95, brain-derived neurotrophic factor, B cell lymphoma protein-2, superoxide dismutase, and glutathione S-transferase; and decreasing the expression of malondialdehyde, caspa
*BDNF↑,
*SOD↑,
*GSTA1↑,
*MDA↑,
*Casp3↓,
*Mood↑, antidepressant effects of luteolin are mediated by various mechanisms, including anti-oxidative stress, anti-apoptosis, anti-inflammation, anti-endoplasmic reticulum stress, dopamine transport, synaptic protection, hypothalamic–pituitary–adrenal axi
*antiOx↑,
*Apoptosis↓,
*Inflam↓,
*ER Stress↓,

4803- Lyco,    Enhanced cytotoxic and apoptosis inducing activity of lycopene oxidation products in different cancer cell lines
- in-vitro, Pca, PC3 - in-vitro, BC, MCF7 - in-vitro, Melanoma, A431 - in-vitro, Liver, HepG2 - in-vitro, Cerv, HeLa - in-vitro, Lung, A549
tumCV↓, The decreased cell viability with depleted GSH and increased MDA levels were observed when treated with COL products than control, LYC and AOL
GSH↓,
MDA↑,
ROS↑, In addition, COL products increased ROS levels and percent apoptosis.
Apoptosis↑,

1204- MET,    Metformin induces ferroptosis through the Nrf2/HO-1 signaling in lung cancer
- in-vitro, Lung, A549 - in-vitro, Lung, H1299
MDA↑,
ROS↑,
Iron↑, iron ions
GSH↓,
T-SOD↓,
Catalase↓,
GPx4↓,
xCT/SLC7A11↓,
NRF2↓,
HO-1↓,

4103- MF,    Comparing the Effects of Long-term Exposure to Extremely Low-frequency Electromagnetic Fields With Different Values on Learning, Memory, Anxiety, and β-amyloid Deposition in Adult Rats
- in-vivo, NA, NA
*Dose↝, 1, 100, 500, and 2000 microtesla (μT), 50 Hz frequency for one h/day for two months,
*memory↑, Exposure to ELF-EMF had an anxiogenic effect on rats, promoted memory, and induced oxidative stress.
*ROS↑, exposure to the magnetic fields caused a significant increase (P<0.05) in TOS in the serum of 100, 500, and 2000 μT, compared with the control group
*MDA↑, Our results declared that the exposure to the magnetic fields caused a significant increase (P<0.05) in the levels of MDA in groups 1, 100, 500, and 2000 μT, in comparison to the control group

3498- MF,    Effect of Static Magnetic Field on Oxidant/Antioxidant Parameters in Cancerous and Noncancerous Human Gastric Tissues
- in-vitro, GC, NA
*SOD↑, SMF causes increase in SOD activity and decrease in MDA level in the noncancerous tissue.
*MDA↓,
SOD↓, However, it decreases SOD and glutathione peroxidase (GSH-Px) activities and increases MDA level and catalase (CAT) activity in the cancerous tissue.
GPx↓,
MDA↑,
Catalase↑,

1273- Myr,    Myricetin Induces Ferroptosis and Inhibits Gastric Cancer Progression by Targeting NOX4
- vitro+vivo, GC, NA
Ferroptosis↑, (iron and ROS are critical for ferroptosis)
MDA↑,
Iron↑,
GSH↓,
NOX4↑, increased NOX4 expression in tumor tissue (is an enzyme that produces reactive oxygen species (ROS), particularly hydrogen peroxide (H₂O₂).)
NRF2↓,
GPx4↓,

6487- Nimb,    Anticancer properties of nimbolide and pharmacokinetic considerations to accelerate its development
- Review, Var, NA
TumCP↓, anti-proliferation, induction of apoptosis, inhibition of metastasis and angiogenesis, and modulation of carcinogen-metabolizing enzymes.
Apoptosis↓,
TumMeta↑,
angioG↓,
*antiOx↑, nimbolidehas been found to possess antioxidant effect and free radical scavenging activities.
*eff↑, In comparison to azadirachtin and ascorbic acid (vitamin C), nimbolide was shown to be a more potent antioxidant
Apoptosis↑, Nimbolide induces apoptosis through diverse molecular mechanism(s).
MOMP↑, Nimbolide disrupts MOMP, which promotes caspases activation leading to apoptosis.
CDK1↓, Nimbolide also reduces the level of CDKs and cyclins, causing cell cycle arrest.
TumCCA↑,
MAPK↓, Nimbolide also abrogates various signaling cascades including MAPK (ERK1/2), JAK2/STAT3 and PI3K/Akt, leading to suppression of proliferation of a wide variety of human cancer cells.
JAK2↓,
STAT3↓,
PI3K↓,
Akt↓,
TumCP↓,
*NRF2↑, Nimbolide disrupts the Nrf2-KEAP1 complex and promotes the release of Nrf2, thus increasing levels of antioxidant and detoxification enzymes.
NF-kB↓, Inhibition of the NF-κB pathway also reduces the dissociation of GSK-3β from β-catenin, hence restraining the Wnt/β-catenin
GSK‐3β↑,
Wnt↓,
β-catenin/ZEB1↓,
chemoPv↑, nimbolide showed remarkable chemopreventive property.
Bcl-xL↓, Nimbolide treatmentdecreased the expression of antiapoptotic proteins(Bcl-xL, Bcl-2, survivin, caspase inhibitor molecules) and increased the expression of proapoptotic proteins (cytochrome c, Bax, Bad, Bid, cleaved caspases) in prostate cancer cells
Bcl-2↓,
survivin↓,
Cyt‑c↑,
BAX↑,
BID↑,
cl‑Casp↑,
P53↑, nimbolide acted by up-regulation of p53 levelin HeLa cells, thereby priming these cells towards apoptosis by destabilizing the mitochondria
DR5↑, Nimbolide up-regulated the expression of both DR5 and DR4 in chronic myeloid leukemia (KBM-5), multiple myeloma (U266), embryonic kidney carcinoma (A293), pancreatic adenocarcinoma (AsPC-1), and breast adenocarcinoma (MDA-MB-231) cells
DR4↑,
ROS↑, nimbolide resulted in generation of reactive oxygen species (ROS)
lipid-P↑, ROS also induced lipid peroxidation of cellular membranes, generating toxic metabolites such as malondialdehyde (MDA) that can react with DNA to form adducts to induce apoptosis.
MDA↑,
MMP2↓, nimbolide reduced mRNA expression of MMP-2, MMP-9, uPA and uPA receptor in breast cancer cells (MCF-7)
MMP9↓,
uPA↓,
ICAM-1↓, nimbolide was shown to downregulate the expression of MMP-9, ICAM-1, and CXCR4 in colorectal cancer xenografts
CXCR4↓,
CXCR2↓, nimbolide also reduced expression of CXCL8 and CXCR2 in breast cancers, and thus abrogated angiogenesis
angioG↓,
BBB↑, nimbolide might be able to cross blood-brain barrier (BBB) and the concentration could be sufficient for nimbolide to suppress intracranial tumour cell proliferation.


Showing Research Papers: 1 to 50 of 67
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 67

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

BMP7/OP1↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 4,   Catalase↑, 2,   Fenton↑, 1,   Ferroptosis↓, 1,   Ferroptosis↑, 16,   GCLM↓, 1,   GPx↓, 3,   GPx4↓, 15,   GPx4↑, 1,   GSH↓, 29,   GSR↑, 1,   GSTA1↓, 1,   GSTs↓, 1,   H2O2↑, 2,   HO-1↓, 3,   HO-1↑, 4,   Iron↑, 12,   i-Iron↑, 2,   Keap1↑, 1,   lipid-P↑, 9,   MDA↓, 2,   MDA↑, 38,   i-MDA↑, 4,   NADH↓, 1,   NADPH/NADP+↓, 1,   NFE2L2↑, 1,   NOX4↑, 1,   NRF2↓, 7,   NRF2↑, 5,   OSI↑, 1,   OXPHOS↓, 1,   ROS↑, 35,   mt-ROS↑, 1,   SAM-e↝, 1,   SOD↓, 8,   SOD↑, 1,   SOD2↓, 1,   T-SOD↓, 1,   TAC↓, 2,   TOS↑, 2,   xCT/SLC7A11↓, 3,   xCT/SLC7A11↑, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

FTH1↓, 3,   FTH1↑, 1,   FTL↑, 1,   NCOA4↑, 2,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 5,   ETC↓, 1,   p‑MEK↓, 1,   MMP↓, 7,   mtDam↑, 2,   Raf↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACSL4↑, 2,   ALAT↓, 1,   AMPK↑, 3,   p‑AMPK↑, 1,   ATG7↑, 1,   FASN↓, 1,   G6PD↓, 1,   GLS↓, 1,   GlucoseCon↓, 2,   Glycolysis↓, 3,   HK2↓, 3,   lactateProd↓, 2,   lactateProd↑, 1,   LDH↓, 2,   LDHA↓, 2,   NAD↝, 1,   PDK1↓, 1,   PFKP↓, 1,   PI3K/Akt↝, 1,   PKM2↓, 1,   Pyruv↓, 1,   p‑S6K↓, 1,   SCD1↓, 1,   SIRT1↑, 1,   SREBP2↓, 1,   Warburg↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 7,   p‑Akt↓, 2,   Apoptosis↓, 1,   Apoptosis↑, 16,   mt-Apoptosis↑, 1,   BAX↑, 6,   Bax:Bcl2↑, 2,   Bcl-2↓, 7,   Bcl-xL↓, 2,   BID↑, 2,   Casp↑, 2,   cl‑Casp↑, 1,   Casp3↑, 12,   cl‑Casp3↑, 1,   Casp7↑, 3,   Casp8↑, 2,   Casp9↑, 3,   Cyt‑c↑, 7,   DR4↑, 1,   DR5↑, 1,   Endon↑, 1,   Ferroptosis↓, 1,   Ferroptosis↑, 16,   p‑JNK↑, 1,   MAPK↓, 3,   MAPK↝, 1,   MCT1↓, 1,   MOMP↑, 1,   survivin↓, 1,   TumCD↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

AMPKα↑, 1,   CaMKII ↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,   PhotoS↑, 1,   tumCV↓, 2,   USF1↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ATF6↑, 1,   ATFs↑, 1,   CHOP/DDIT3↑, 1,   eIF2α↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   HSP70/HSPA5↓, 1,   HSP70/HSPA5↑, 2,   HSP90↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1↓, 1,   Beclin-1↑, 2,   p‑Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 2,   p62↓, 1,   TumAuto↑, 3,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 4,   DNMTs↓, 1,   P53↑, 5,   cl‑PARP↑, 1,   cl‑PARP1↑, 1,   SIRT6↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   CDK2↓, 1,   CDK4↓, 1,   Cyc↓, 1,   cycD1/CCND1↓, 1,   P21↓, 1,   P21↑, 1,   TumCCA↑, 11,  

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

BRAF↑, 1,   BRAF↝, 1,   EMT↓, 3,   p‑ERK↓, 1,   FOSL1↑, 1,   FOXO3↑, 1,   GDF15↓, 1,   GSK‐3β↑, 1,   HDAC↓, 1,   IGF-1↓, 1,   mTOR↓, 6,   p‑mTOR↓, 1,   PI3K↓, 7,   PTEN↓, 1,   PTEN↝, 1,   STAT3↓, 2,   TRPM7↓, 1,   TumCG↓, 8,   Wnt↓, 2,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   AXL↓, 1,   BACH1↑, 1,   Ca+2↓, 2,   Ca+2↑, 1,   F-actin↓, 1,   Ki-67↓, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 1,   PCBP1↓, 1,   SMAD2↓, 1,   SMAD3↓, 1,   Snail↓, 1,   SOX4↓, 1,   TGF-β↓, 1,   TGF-β1↓, 1,   THBS1↓, 1,   TumCI↓, 5,   TumCMig↓, 4,   TumCP↓, 14,   TumMeta↓, 3,   TumMeta↑, 1,   uPA↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 2,   ATF4↑, 2,   EGFR↓, 1,   EGR1↓, 1,   Hif1a↓, 5,   Hypoxia↓, 1,   NO↑, 1,   REL↑, 1,   VEGF↓, 3,   VEGF↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   GLUT1↓, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2,   COX2/PTGS2↑, 1,   CXCR2↓, 1,   CXCR4↓, 1,   ICAM-1↓, 1,   IL1↓, 1,   IL1β↑, 1,   IL6↓, 1,   Imm↑, 1,   JAK2↓, 1,   NF-kB↓, 5,   NK cell↑, 1,   PSA↓, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 5,   Dose↝, 2,   eff↓, 6,   eff↑, 5,   RadioS↑, 2,   selectivity↑, 5,  

Clinical Biomarkers(tgid=22) ⓘ

AFP↓, 1,   ALAT↓, 1,   BRAF↑, 1,   BRAF↝, 1,   EGFR↓, 1,   GutMicro↑, 1,   IL6↓, 1,   Ki-67↓, 1,   LDH↓, 2,   PSA↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   chemoPv↑, 1,   TumVol↓, 3,   TumW↓, 2,   Weight↑, 1,  
Total Targets: 239

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 7,   Catalase↓, 3,   Catalase↑, 3,   Ferroptosis↓, 1,   GPx↓, 1,   GPx↑, 3,   GSH↓, 2,   GSH↑, 3,   GSH∅, 1,   GSR↑, 1,   GSTA1↑, 1,   HO-1↑, 1,   i-Iron↑, 1,   lipid-P↓, 3,   MDA↓, 3,   MDA↑, 9,   NRF2↑, 2,   ROS↓, 7,   ROS↑, 4,   i-ROS↑, 1,   SOD↓, 2,   SOD↑, 7,   Thiols↑, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 2,   ALAT↑, 1,   LDH↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↑, 1,   Apoptosis↓, 2,   BAX↓, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-2↑, 1,   Casp1↓, 1,   Casp3↓, 3,   Casp3↑, 1,   Ferroptosis↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

LC3II↑, 1,   p62↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,  

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

GSK‐3β↑, 1,  

Migration(tgid=13) ⓘ

APP↓, 1,   BACH1↓, 1,   Ca+2↓, 1,   TumCP↓, 1,   VCAM-1↓, 1,   ZO-1↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 3,   BBB↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

ASC↓, 1,   COX2/PTGS2↓, 1,   ICAM-1↓, 1,   IL1β↓, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 7,   Inflam↑, 1,   NF-kB↓, 2,   TLR4↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 2,   BDNF↑, 2,   ChAT↑, 1,   NGF↑, 1,   PSD95↑, 1,   tau↓, 1,   p‑tau↓, 1,   TrkB↑, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 3,   Dose↝, 1,   eff↓, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   ALAT↑, 1,   ALP↓, 1,   AST↓, 3,   AST↑, 1,   IL6↓, 1,   LDH↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   chemoP↑, 1,   cognitive↑, 3,   hepatoP↓, 1,   hepatoP↑, 2,   memory↑, 2,   Mood↑, 1,   neuroP↑, 3,   OS↑, 1,   radioP↑, 1,   RenoP↓, 1,   RenoP↑, 1,   toxicity↓, 6,   toxicity↑, 1,   Wound Healing↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 104

Scientific Paper Hit Count for: MDA, Serum malondialdehyde
7 Silver-NanoParticles
7 Curcumin
4 Boron
3 Magnetic Fields
3 Shikonin
2 Artemisinin
2 Copper and Cu NanoParticles
2 Juglone
2 Sulforaphane (mainly Broccoli)
1 3-bromopyruvate
1 cetuximab
1 Allicin (mainly Garlic)
1 Andrographis
1 Apigenin (mainly Parsley)
1 Ashwagandha(Withaferin A)
1 Berberine
1 Betulinic acid
1 Carvacrol
1 Thymol-Thymus vulgaris
1 chitosan
1 Chrysin
1 Citric Acid
1 Crocetin
1 Galantamine
1 Radiotherapy/Radiation
1 Diclofenac
1 Docosahexaenoic Acid
1 doxorubicin
1 EGCG (Epigallocatechin Gallate)
1 Gallic acid
1 Hydrogen Gas
1 Hyperoside
1 Isobavachalcone
1 isoorientin
1 Cisplatin
1 Luteolin
1 Lutein
1 Lycopene
1 Metformin
1 Myricetin
1 Nimbolide
1 Phenethyl isothiocyanate
1 Piperlongumine
1 Pterostilbene
1 Quercetin
1 salinomycin
1 Sulfasalazine
1 Selenium
1 Chemotherapy
1 Anti-oxidants
1 Silymarin (Milk Thistle) silibinin
1 Selenite (Sodium)
1 Thymoquinone
1 Vitamin C (Ascorbic Acid)
1 Vitexin
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#:570  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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