mtDam Cancer Research Results
mtDam, mitochondrial damage: Click to Expand ⟱
| Source: |
| Type: |
Mitochondrial damage can lead to a shift from oxidative phosphorylation to glycolysis, a process known as the Warburg effect. This shift can provide cancer cells with a selective advantage, allowing them to grow and proliferate more rapidly.
Mitochondrial Damage can also lead to cell death of cancer cells.
|
Scientific Papers found: Click to Expand⟱
*cardioP↑, Review of the pharmacological effects of astragaloside IV and its autophagic mechanism in association with inflammation - PMC
*MitoP↑, The mechanism included promotion of mitophagy, which reduced generation of mitochondrial ROS and accumulation of damaged mitochondria[31].
*ROS↓, AS-IV can reduce ROS-mediated autophagosome accumulation and myocardial injury caused by I/R[21]
*mtDam↓,
*neuroP↓, Ischemic stroke MCAO in SD rats; OGD/R in HT22 cells A neuroprotective role (-) apoptosis (+) autophagy
TumAuto↓, For NSCLC cells treated with cisplatin, AS-IV inhibited the increased autophagy of proteins Beclin1 and LC3 I/II
*AntiDiabetic↑, Protective effect of AS-IV on diabetes
*antiOx↑, Allicin, the main biologically active compound derived from garlic, has been shown to exert various anti-oxidative and anti-apoptotic activities in in vitro and in vivo studies.
*Apoptosis↓, allicin treatment significant increased cell viability, and decreased LDH release and apoptotic cell death after 6-OHDA exposure
*LDH↓,
ROS↓, Allicin also inhibited ROS generation
*lipid-P↓, reduced lipid peroxidation and preserved the endogenous antioxidant enzyme activities.
*mtDam↓, These protective effects were associated with suppressed mitochondrial dysfunction,
*MMP↓, as evidenced by decreased MMP collapse and cytochrome c release,
*Cyt‑c↓,
*ATP∅, preserved mitochondrial ATP synthesis,
*Ca+2↝, and the promotion of mitochondrial Ca(2+) buffering capacity
*neuroP↑, allicin treatment can exert protective effects against PD related neuronal injury through inhibiting oxidative stress and mitochondrial dysfunction with dynamic changes.
| - |
in-vitro, |
Park, |
SH-SY5Y |
|
|
|
*neuroP↑, Neuroprotective effects of Withania somnifera
*Inflam↓, including inflammation and oxidative stress reduction, memory and cognitive function improvement.
*ROS↓,
*cognitive↑,
*memory↑,
*GPx↑, significantly increased glutathione peroxidase activity
*Prx↓, KSM-66, had peroxiredoxin-1 and VGF levels significantly lower than the untreated control
*ATP↑, rescue of mitochondria with 0.5 mg/ml KSM-66 extract showed an increase in ATP levels.
*Vim↓, Pre-treatment with KSM-66 decreased level of vimentin
*mtDam↓, KSM-66 attenuates 6-OHDA-induced mitochondrial dysfunction in SH-SY5Y cells
*eff↑, BA significantly improved post‐ischemic cardiac function, reduced infarct size and apoptotic cell death, decreased oxidative stress, and improved the mitochondrial state.
*ROS↓,
*mtDam↓,
*AMPK↑, Furthermore, BA markedly increased AMPK activation, Nrf2 nuclear translocation, and the levels of NAD(P)H quinone dehydrogenase and heme oxygenase‐1.
*NRF2↑,
*NADPH↑,
*HO-1↑,
*cardioP↑, berbamine (BA)‐induced cardioprotective effects
*CB2 / CNR2↑, selective cannabinoid receptor 2 (CB2) agonist
*Bacteria↓, numerous pharmacological activities such as antibacterial (e.g., Helicobacter pylori), antioxidant, anti-inflammatory, analgesic (e.g., neuropathic pain), anti-neurodegenerative and anticancer properties.
*antiOx↑,
*Inflam↓,
*NP/CIPN↓,
*neuroP↑,
AntiCan↑,
*ROS↓, β-caryophyllene in reducing oxidative stress and mitochondrial dysfunction, and its possible links with neuroprotection.
*mtDam↓,
*GSH↑, β-caryophyllene (50 mg/kg/day, i.p. for 4 weeks) ↑ GSH, SOD and CAT. Inhibit lipid peroxidation. ↓ IL-1β, IL-6, and TNF-α levels. ↓ COX-2 and iNOS expression.
*SOD↑,
*Catalase↑,
*lipid-P↓,
*IL1β↓,
*IL6↓,
*TNF-α↓,
*COX2/PTGS2↓,
*iNOS↓,
*NRF2↑, β-caryophyllene (34, 102 and 306 mg/kg/day, p.o.). ↑ Nrf2 and HO-1 expression. Restored SOD and CAT activity and expression.
*HO-1↑,
*AChE↓, Syzygium aromaticum (L.) Merr. and L.M. Perry (0.05 mL/kg and 0.1 mL/kg) ↓ AChE activity, lipid peroxidation levels
*mtDam↓, CAP ameliorated mitochondrial damage, facilitated the nuclear translocation of NRF2, thereby promoting the expression of downstream antioxidant response elements, HO-1, Trx, GSS and NQO1 in GES-1 cells.
*NRF2↑,
*HO-1↑,
*Trx↑,
*GSS↑,
*NQO1↑,
*Keap1↓, CAP could directly bind to KEAP1 and inhibit the interaction between KEAP1 and NRF2.
*ROS↓, Capsaicin protects GES-1 from oxidative stress
*PKM2↓, Previous studies have demonstrated that CAP can directly bind to and inhibit the activity of PKM2 and LDHA, subsequently attenuating inflammatory response
*LDHA↓,
*Inflam↓,
*memory↑, Three months of treatment with CAW improved spatial and contextual memory as well as executive function in 5xFAD mice.
*Aβ↓, This improvement was accompanied by increased antioxidant gene expression and a decrease in Aβ plaque burden relative to untreated 5xFAD animals.
*NRF2↑, These results suggest that prolonged CAW exposure could be beneficial in Alzheimer’s disease and that these effects likely involve NRF2 activation.
*toxicity↓, This excellent safety profile supports the classification of Centella asiatica as a Class 1 herb (one that can be safely consumed when used appropriately) by the Botanical Safety Handbook
*neuroP↑, Extracts of Centella asiatica have been shown to have neuroprotective effects in models of neurodegenerative conditions including AD
*ROS↓, We and other have shown that the water extract of Centella asiatica (CAW) can protect against Aβ cytotoxity, activate NRF2 and reduce oxidative damage as well as improve mitochondrial function in both cell and animal models of AD
*mtDam↓,
*cognitive↑, CAW has been shown to possess cognitive enhancing effects
NQO1↑, CAW treatment did robustly increase the expression of NRF2 and its antioxidant target genes HMOX1 and NQO1 in the cortex of female 5xFAD mice relative to WT control mice
HO-1↑,
*cognitive↑, Our group has previously shown that a water extract of Centella asiatica (CAW) elicits cognitive-enhancing effects in animal models of aging and Alzheimer’s disease, including a dose-related effect of CAW on memory in the 5xFAD mouse model of ß-amylo
*mtDam↓, improving mitochondrial function, reducing oxidative stress, and increasing synaptic density).
*ROS↓,
*NAD↑, upregulation of nicotinamide adenine dinucleotide in the brain and modulation of brain-derived neurotrophic factor.
*BDNF↑, Based on the observed effects of CAW on glycerophospholipid metabolism, one potential novel mechanism of action underlying CAW’s cognitive benefits may be BDNF modulation.
*memory↑, we found that the improvements in memory seen in WT and 5xFAD mice treated with CAW
*cognitive↑, Mechanisms underlying CAW's cognitive effects extend beyond reversing metabolic effects of Aβ accumulation.
*Dose↝, oral administration of a CA water extract (CAW) at 200 mg per kg of body weight per day (mg/kg/d) for 5 weeks improved cognitive deficits in both the Tg2576 23 and 5XFAD24,25 transgenic mouse models of AD.
*memory↑, improved learning and memory of Tg2576 mice in the Morris water maze paradigm without altering Aβ levels in the cortex in vivo or inhibiting acetylcholinesterase enzyme in vitro.
*AChE∅,
*mtDam↓, CAW in vitro improves antioxidant response, ameliorates mitochondrial dysfunction, and increases dendritic arborization.
*antiOx↑,
TumCG↓, significance of chaetocin‐induced cell growth inhibition by the expression of G2/M phase arrest and reactive oxygen species (ROS) dependent apoptosis in A549 lung cancer cells.
TumCCA↑,
ROS↑,
DNAdam↑, chaetocin could produce ROS and nuclear damage against A549 lung cancer cells.
CD47↓, chaetocin exhibits a significant level of CD47 that down‐regulates the expression of CD47 at mRNA levels.
*toxicity↓, PBMC biocompatibility study revealed that chaetocin is non‐toxic to normal cells.
MMP↓, Chaetocin‐induced apoptosis by mitochondrial membrane potential damage
Casp3↑, Chaetocin‐induced caspase‐3 and protein cleavage lead to the cell death process in A549 cells.
mtDam↓, 40% of cells were exposed to mitochondrial damage in a dose‐dependent manner. I
| - |
in-vivo, |
AD, |
NA |
|
|
|
- |
in-vivo, |
Park, |
NA |
|
|
|
*neuroP↑, Chicoric acid attenuated neuron damage in d-gal-treated mice as revealed through histological examination in the hippocampus region of the mouse brain.
*TNF-α↓, The levels of inflammatory mediators, such as TNF-α and IL-1β, as well as malondialdehyde levels, were markedly reduced after chicoric acid treatment.
*IL1β↓,
*MDA↓,
*Catalase↑, activity of CAT and the level of GSH were significantly elevated in serum by chicoric acid
*GSH↑,
*NRF2↑, chicoric acid treatment noticeably activated the Nrf2 antioxidative defense system
*mtDam↓, reversing mitochondrial dysfunction, decreasing inflammation, and neuron apoptosis caused by oxidative stress.
*Inflam↓,
*Apoptosis↓,
*ROS↓, chicoric acid significantly quenched intracellular ROS to the normal level
*cognitive↑, suggested that chicoric acid supplementation ameliorated cognitive impairment induced by d-gal and SH-SY5Y cell apoptosis induced by H2O2
*Aβ↓, chicoric acid inhibited d-gal-induced Aβ1-42 accumulation in hippocampus of mice brain.
*BDNF∅, suggesting chicoric acid treatment did not restore the expression of BDNF in the hippocampus of aging mice.
*APP↓, chicoric acid treatment markedly decreased the expression of APP and BACE1 in the whole brain, which partly explains the inhibition by chicoric acid of Aβ1-42 accumulation in the cortex and hippocampus.
*BACE/β-secretase↓,
*DRP1/DNM1L↓, Resveratrol was shown to regulate mitochondrial fusion/fission dynamics through increasing the expression of MFN2 and OPA1 while decreasing the expression of DRP1 and FIS1
*FIS1↓,
*MFN2↑, Resveratrol also increased OPA1 and MFN2 expression to promote mitochondrial fusion in the hippocampus of SAMP8 mice, a model of dementia
*OPA1↑,
*DRP1/DNM1L↓, curcumin can reduce mitochondrial fission by decreasing the expression of DRP1 and FIS1, and enhance fusion by increasing the expression of OPA1, MFN1 and MFN2 in the brains of SAMP8 mice
*FIS1↓,
*OPA1↑,
*MFN1↑,
*MFN2↑,
*DRP1/DNM1L↓, quercetin was found to regulate mitochondrial dynamics by inhibiting the expression of DRP1 and FIS1 and at the same time increasing the expression of MFN1 and MFN2 in the rat hippocampus, thereby improving hypoxia-induced memory deficits
*FIS1↓,
*MFN1↑,
*MFN2↑,
*memory↑,
*mtDam↓, EGCG was found to protect mitochondrial function by down-regulating the expression of DRP1 and FIS1 in the brain
*DRP1/DNM1L↓,
*FIS1↓,
*mtDam↓, Mitochondrial function and cell viability were elevated in curcumin treated cells.
*eff↓,
*eff↑, Further, the protective effects of curcumin were stronger in pretreated SHSY5Y cells than in post-treated cells, indicating that curcumin works better in prevention than treatment in AD-like neurons.
*FIS1↓, significantly increased in Drp1, by 2.0 fold (p=0.004), and in Fis1, by 2.1 fold (
*lipid-P↓, lipid peroxidation were found ( p=0.002) in Aβ treated relative to untreated cells (figure 4). However, sig-
nificantly decreased levels were found in the curcumin treated cells ( p=0.02) relative to untreated cells.
*ATP↑, Significantly increased levels of ATP were found in cells treated with curcumin
| - |
vitro+vivo, |
Nor, |
HUVECs |
|
|
|
- |
vitro+vivo, |
Diabetic, |
NA |
|
|
|
*BloodF↑, Formononetin (FMN), a phytoestrogen from Astragalus roots, is traditionally used to enhance blood function and microcirculation; however, its mechanism remains unclear.
*Ferroptosis↓, FMN effectively reduced ferroptosis markers in HG-treated HUVECs,
*eff↓, and Erastin treatment abolished this protective effect.
*mtDam↓, block ferroptosis through two mechanisms: restoration of mitochondrial integrity and reactivation of the xCT/GPX4 antioxidant system
*xCT/SLC7A11↑,
*GPx4↑,
*Wound Healing↑, When we tested FMN in diabetic mice, wound closure rates improved substantially, the expression of xCT and GPX4 was increased, and CD31 expression in wound vessels increased, which matched what we observed in vitro.
*CD31/PECAM-1↑,
*mt-ROS↓, mitigation of mitochondrial reactive oxygen species (mtROS) accumulation through xCT/GPX4 activation.
TumCCA↑, Among the anticancer mechanisms of fucoidan are cell cycle arrest, apoptosis evocation, and stimulation of cytotoxic natural killer cells and macrophages.
Apoptosis↑,
NK cell↑,
chemoP↑, Fucoidan also protects against toxicity associated with chemotherapeutic drugs and radiation-induced damage.
TumCG↓, fucoidan slows tumor growth, kills cancer cells, and interacts with cancer chemotherapy drugs.
*Inflam↓, fucoidan has countless superior biological activities, which include anti-inflammatory, antioxidant, anticlotting, antithrombotic, antiviral, anti-angiogenesis, and anti-Helicobacter pylori activities
*antiOx↑,
*AntiThr↑,
*AntiViral↑,
angioG↓,
ChemoSen↑, Furthermore, LMWF complexed with tamoxifen, cisplatin, or paclitaxel shows cell growth inhibition, cellular apoptosis, and arrest of the cell cycle in the human breast cancer cell line MCF-7/ MDA-MB-231.
ROS↑, The study revealed that in breast cancer cells, phosphorylation of different proteins, elevation the reactive oxygen species (ROS) levels, and reduced glutathione (GSH) levels were all crucial in cancer cell apoptosis
GSH↓,
mtDam↓, reatment with fucoidan leads to increased levels of ROS in cells, along with mitochondrial damage and mitochondrial membrane potential (MMP) depolarization.
MMP↓,
DNMT3B↓, inhibition of its downstream target DNA methyltransferase 3B (DNMT3B) by the administration of a fixed dose of fucoidan
TumCG↓, Oral administration of fucoidan (5 mg/kg) effectively inhibited tumor growth in mice grown with B16 melanoma cells.
Dose↝, fucoidan (5 mg/kg) effectively inhibited tumor growth in mice
Dose↝, Twenty patients with advanced cancer were selected for the study, in which oral fucoidan (4 g daily) was administered for at least four weeks. After two consecutive weeks of ingestion, there was a significant reduction in the levels of key proinflamm
QoL∅, but no significant change was observed in patients’ quality of life, including the experience of fatigue
fatigue∅,
Dose↝, 300 mg fucoidan is safe and well tolerated by humans
*antiOx↑, hydrogen has shown great anti-oxidative stress and anti-inflammatory effect in many cerebral disease models
*Inflam↓,
*AMPK↑, hydrogen-rich water can stimulate AMPK-Sirt1-FoxO3a pathway which could play a role in anti-oxidative
stress,
*SIRT1↑,
*FOXO↑,
*mtDam↓, diminishing mitochondrial damage and acting as a neuroprotective agent, and neutralize ROS induced by Aβ
*neuroP↑,
*ROS↓,
*p38↓, hydrogen water
could suppress the activation of phospho-p38 and JNK
*cognitive↑, Currently, Hou et al.50 reported that hydrogen-rich water could improve cognition function in female transgenic AD mice by reducing the decline in brain estrogen levels
*BDNF↑, reducing the decline in brain estrogen levels, estrogen receptor (ER) β, and the expression of brain-derived neuro-trophic factor (BDNF)
*memory↑, Li et al.71 found that hydrogen-rich saline could reduce
learning and memory impairments and neural inflammation
which were induced by Aβ in rats
*lipid-P↓, Moreover, hydrogen-rich saline suppressed lipid peroxidation products, inflammatory factor like interleukin-6 and TNF-α, and the activation of astrocytes
*IL6↓,
*TNF-α↓,
*JNK↓, protective effect of hydrogen-rich saline may be due to inhibition of the activation of JNK
and NF-κB
*NF-kB↓,
*NLRP3↓, Hydrogen-rich water inhibit NLRP3, and weaken the oestrogen-ERβ-BDNF signalling pathway.
*Inflam↓, Hydrogen therapy AD: inflammation, energy regulation, prevents neuronal damage.
*neuroP↑,
*toxicity↓, Hydrogen therapy's low side effects make it a complement to AD treatment. Even at high concentrations, hydrogen gas is still non-toxic, and has been widely used in the diving field.
*antiOx↑, hydrogen’s role as a natural antioxidant,
*ROS↓, Hydrogen has been shown to mitigate the amount of ROS released from mitochondria, thereby reducing mitochondrial DNA peroxidation and inhibiting the expression of NOD-like receptor thermal protein domain associated protein 3 (NLRP3), caspase-1, and I
*NLRP3↓,
*IL1β↓,
*mtDam↓, curtail mitochondrial damage, thereby bolstering ATP synthesis and fortifying the electron transport chain within mitochondria
*ATP↑,
*AMPK↑, activating AMPK and amplifying the downstream antioxidant response of forkhead box O3a (FOXO3
*FOXO3↑,
*SOD1↑, It elevates the levels of intracellular antioxidant enzymes, notably superoxide dismutase 1 (SOD1) and catalase (CAT), thereby serving as a neuroprotective agent that diminishes the risk and progression of AD
*Catalase↑,
*NRF2↑, Hydrogen slows AD progression by activating the cellular endogenous antioxidant system Nrf2;
*NO↓, Reduced inflammatory markers such as ROS, Nitric oxide (NO) and Malondialdehyde (MDA)
*MDA↓,
*lipid-P↓, drinking HRW significantly reduced lipid peroxidation in the brain of SAMP8 mice.
*memory↑, HRW inhibited the decline of learning and memory impairment
*ER(estro)↓, Decreased hormone levels, estrogen receptor (ER) β, and BDNF expression improve cognitive function in female transgenic AD mice.
*BDNF↑, upsurge in BDNF levels, which further ameliorated the cognitive impairments observed in mice affected by sepsis.
*cognitive↑,
*APP↓, The expression of APP, BACE1, and SAPPβ was proficiently suppressed, thereby curtailing the overproduction of Aβ in Alzheimer's
*BACE/β-secretase↓,
*Aβ↓,
*BP∅, inhaling hydrogen gas has no effect on blood pressure and other blood parameters (such as pH, body temperature, etc.),
*BBB↑, efficiently crossing the blood-brain barrier to perform their functions.
*ROS↓, PC12 cell treated with hydroxytyrosol abated the cell apoptosis and alleviated the oxidative stress through scavenging of reactive oxygen species
*mtDam↓, alleviating mitochondria damage.
*PI3K↑, resisted the inhibition of PI3K/AKT/mTOR-HIF-1α signaling pathway caused by hypoxia
*Akt↑,
*mTOR↑,
*Hif1a↑,
*ROS↓, ISL significantly attenuated H/R-triggered production of reactive oxygen species in NMCM, reduced the expression of malondialdehyde and the activity of lactate dehydrogenase, enhanced superoxide dismutase and catalase activity,
*MDA↓,
*LDH↑,
*SOD↑,
*Catalase↑,
*NRF2↑, and increased the expression of nuclear factor E2-related factor 2 (Nrf2) and its downstream heme oxygenase 1 (HO-1), thereby mitigating oxidative stress damage.
*i-Iron↓, ISL reduced intracellular free iron accumulation, up-regulated glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11) expression, and inhibited lipid peroxidation accumulation, thereby alleviating ferroptosis.
*GPx4↑,
*xCT/SLC7A11↑,
*lipid-P↓,
*Ferroptosis↓,
*HO-1↑, ISL treatment increased the levels of HO-1, GPX4, and SLC7A11, inhibited the expression of ACSL4
*ACSL4↓,
*mtDam↓, alleviated mitochondrial damage, and ferroptosis, ultimately reducing myocardial infarction area and injury induced by I/R.
*Stroke↓,
*cognitive↑, ISO improved systemic glucose metabolism and alleviated hepatic steatosis, and reversed cognitive deficits.
*PSD95↑, ISO restored synaptic proteins (PSD-95, BDNF, soluble α-synuclein), exerted anti-apoptotic effects (increased Bcl-2/Bax ratio, decreased cleaved caspase-3), and attenuated oxidative stress and mitochondrial damage.
*BDNF↑,
*Bax:Bcl2↓,
*cl‑Casp3↓,
*ROS↓,
*mtDam↓,
*GSK‐3β↓, Mechanistically, ISO inhibited GSK3β activity, promoted Nrf2 nuclear accumulation, upregulated HO-1 expression, and reduced tau phosphorylation at Ser396
*NRF2↑,
*HO-1↑,
*p‑tau↓,
*neuroP↑, ISO exerts a neuroprotective effect in TDACD model by inhibiting oxidative stress via GSK3β/Nrf2 pathway, and highlight ISO as a potential therapeutic candidate for TDACD.
| - |
in-vitro, |
Liver, |
HepG2 |
|
|
|
- |
in-vitro, |
CRC, |
HT-29 |
|
|
|
- |
in-vitro, |
Lung, |
A549 |
|
|
|
ChemoSen↑, The antiproliferation of DOX on Hela, HepG2, HT-29, and A549 cells could be increased synergistically when cotreated with ISO in vitro. I
TumCP↓,
chemoP↑, ISO could also improve the survival rate of DOX-injured cardiomyocytes by reducing reactive oxygen species, maintaining mitochondrial function, and inhibiting apoptosis.
*ROS↓,
*mtDam↓,
*Apoptosis↓,
*cardioP↑, In mice receiving DOX, a protective effect on myocardial tissue, which was reflected by improved survival state of mice receiving chemotherapy, was observed.
*NRF2↑, ISO upregulated Nrf2 and TGF-β3 by downregulating the phosphorylation levels of JNK and p38 proteins on the MAPK pathway and the Akt and Stat3 expression levels.
*TGF-β↑,
*p‑JNK↓,
*p‑p38↓,
*MAPK↝,
*Akt↝,
*STAT3↝,
*Apoptosis↓, isoquercitrin (ISO) display the most effective anti‐cytotoxic activities via inhibiting STZ‐induced apoptosis, mitochondria dysfunction and oxidative stress.
*mtDam↓,
*ROS↓,
*Diff↑, ISO largely rescues STZ‐induced differentiation inhibition and enhances neurite outgrowth of Neuro2a (N2a) cells in vitro.
*cognitive↑, oral administration of ISO protects hippocampal neurons from STZ‐induced neurotoxicity and significantly improves the cognitive and behavioural impairment in STZ‐induced AD rats.
*Apoptosis↓, Isoquercitrin and quercetin significantly inhibited Glu-induced oxidative cell death by restoring intracellular reactive oxygen species (ROS) levels and mitochondrial superoxide generation, Ca2+ dysregulation, mitochondrial dysfunction,
*ROS↓,
*SOD2↑,
*Ca+2↓, isoquercitrin and quercetin significantly restored Glu-induced ROS generation and Ca2+ increase in a concentration-dependent manner
*mtDam↓,
*NRF2↑, These two compounds significantly increased the expression levels of nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) in the presence or absence of Glu treatment.
*HO-1↑,
*other↑, These findings suggest that isoquercitrin and quercetin are the active principles representing the protective effects of DMLE, and these effects were mediated by the Nrf2/HO-1 pathway.
*AIF↓, Glu significantly increased nuclear levels of AIF, whereas isoquercitrin or quercetin reversed Glu-induced nuclear translocation of AIF.
*LC3‑Ⅱ/LC3‑Ⅰ↓, decreased the LC3AB-II/-I ratio to a level lower than Glu alone.
*eff↑, Combination of Isoquercitrin and Quercetin Synergistically Inhibited Glu-Induced Cell Death
*NRF2↑, After LYC intervened in the body, it activated Nrf2 nuclear translocation and its downstream HO-1 and NQO1 antioxidant signaling pathways
*HO-1↑, Lycopene activates Nrf2-HO-1 antioxidant pathway to inhibit oxidative stress injury induced by AAI exposure in NRK52E cells
*NQO1↑,
*ROS↓, LYC inhibited ROS production by renal tubular epithelial cells, and alleviated mitochondrial damage.
*mtDam↓,
*Bcl-2↑, LYC was able to up-regulate the expression of Bcl-2, down-regulate Bax expression and inhibit the activation of cleaved forms of Caspase-9 and Caspase-3, which finally attenuated the apoptosis
*BAX↓,
*Casp9↓,
*Casp3↓,
*Apoptosis↓,
*RenoP↑, Interestingly, there was a significant improvement in damaged renal tissue in mice with AAN after lycopene intervention
*lipid-P↓, lycopene significantly decreased the expression of AAI-induced lipid peroxidation product (MDA), and increased the expression of antioxidant enzyme systems (T-AOC, SOD, and GSH-PX)
*SOD↑,
*GPx↑,
*Inflam↓, Lycopene improves inflammatory responses in the kidneys of AAN mice
*TNF-α↓, TNF-α, IL-6, IL-10, was increased and the expression of IL-12 was decreased in the kidneys of model mice compared with the control group. However, LYC intervention reversed the expression of these genes in a dose-dependent manner
*IL6↓,
*IL10↓,
*Inflam↓, main activity profile of lycopene includes antiatherosclerotic, antioxidant, anti-inflammatory, antihypertensive, antiplatelet, anti-apoptotic, and protective endothelial effects, the ability to improve the metabolic profile, and reduce arterial stif
*antiOx↑, It is a much more potent antioxidant than alpha-tocopherol (10 × more potent) or beta-carotene (twice as potent)
*AntiAg↑, lycopene, protecting against myocardial infarction and stroke, is its antiplatelet activity
*cardioP↑, favorable effect in patients with subclinical atherosclerosis, metabolic syndrome, hypertension, peripheral vascular disease, stroke and several other cardiovascular disorders
*SOD↑, Lycopene modulates also the production of antioxidant enzymes, such as superoxide dismutase and catalase
*Catalase↑,
*ROS↓, By reducing oxidative stress and reactive oxygen species, lycopene increases the bioavailability of nitric oxide (NO), improves endothelium-dependent vasodilation and reduces protein, lipids, DNA, and mitochondrial damage (
*mtDam↓,
*cardioP↑, Lycopene exerts a cardioprotective effect against atrazine induced cardiac injury due to its anti-inflammatory effect, by blocking the NF-kappa B pathway and NO production
*NF-kB↓,
*NO↓,
*COX2/PTGS2↓, downregulation of cyclooxygenase 2,
*LDL↓, significant reductions in total and LDL cholesterol were revealed only at doses of, at least, 25 mg lycopene/day
*eff↑, It was noticed that lycopene can potentiate the antiplatelet effect of aspirin, which requires low lycopene diet
*ER Stress↓, Lycopene protects the cardiomyocytes by relieving ERS
*BioAv↑, Lycopene is very bioavailable in the presence of oil, especially in monounsaturated oils, other dietary fats and processed tomato products
*eff↑, Lycopene can increase the antioxidant properties of vitamin C, E, polyphenols and beta-carotene in a synergistic way
*MMPs↓, figure 3, secretion of MMPs
*COX2/PTGS2↓,
*RAGE↓,
*antiOx↑, Lycopene is an antioxidant protecting from oxidative stress-induced cell damage
*ROS↓, Lycopene inhibited apoptosis by reducing ROS, and by inhibiting mitochondrial dysfunction and NF-κB-target gene Nucling expression in neuronal cells.
*NF-kB↓,
*neuroP↑, Lycopene may be beneficial for preventing oxidative stress-mediated neuronal death in patients with neurodegeneration.
*MMP↓, As shown in Figure 3C, amyloid-β increased the ratio of green to red fluorescence in the cells, which reflects a decrease in MMP in amyloid β-stimulated cells
*mtDam↓, Lycopene suppressed decrease in OCR in amyloid-β-stimulated cell, suggesting that lycopene prevents mitochondrial damage induced by amyloid-β in the cells.
*OCR↓, In the present study, lycopene significantly inhibited amyloid-β-induced mitochondrial dysfunction, which was proven by its protective effect in reducing both MMP and OCR.
| - |
Review, |
Nor, |
NA |
|
|
|
- |
NA, |
AD, |
NA |
|
|
|
- |
NA, |
Diabetic, |
NA |
|
|
|
- |
NA, |
Stroke, |
NA |
|
|
|
- |
NA, |
LiverDam, |
NA |
|
|
|
- |
NA, |
Park, |
NA |
|
|
|
*mtDam↓, The mitochondrial decay, which is responsible for aging, can be reversed by the increased levels of nicotinamide adenine dinucleotide (NAD+) in the body.
*BioAv↝, NMN is a precursor of NAD+ that acts as an intermediate in NAD+ biosynthesis, while dietary supplements of NMN are found to increase the NAD+ levels in the body
*BioAv↑, molecular weight is 334.22 g/mol. It is fairly acidic and water-soluble compound. The solubility has been reported to be 1.8 mg/mL
*OS↑, plays a vital role in a variety of biological processes of the body including cell death, aging, gene expression, neuroinflammation and DNA repair, which indicating a significance role of NAD+ in longevity and health of human life
*eff↑, NMN has therapeutic effects towards a range of diseases, including age-induced type 2 diabetes, obesity, cerebral and cardiac ischemia, heart failure and cardiomyopathies
*eff↑, Alzheimer’s disease and other neurodegenerative disorders, corneal injury, macular degeneration and retinal degeneration, acute kidney injury and alcoholic liver disease
*cognitive↑, cognitive impairments, DNA damage and sirtulin gene inactivation, are brought about by aging which can be evaded by enhancing NAD+ count in the body
*DNAdam↓,
*SIRT1↑, NMN, the NAMPT reaction product, is able to be utilised to trigger the SIRT1 activity
*cardioP↑, NMN also can restore gene expression linked to circadian rhythm, inflammatory response and oxidative stress, and improve hepatic insulin sensitivity, partially by SIRT1 activation.
*ROS↓, NMN has been proven to reduce DNA damage and accumulation of ROS
*Dose↝, NMN in available commercial products vary from 50 to 150 mg/capsule, whereas some consumers take two 150 mg capsules per day
*BioAv↑, NMN was speedily absorbed in the small intestine by a specific transporter, which was encoded by the Slc12a8 gene as demonstrated in in vitro and in vivo studies
*hepatoP↑, NMN supplementation has been found to have significant recovering effects on hepatocyte functions and liver pathologies in early-stage of ethanol toxicity, instead of causing adverse effects to the liver
*eff↑, supplementation of NMN has been found to be a promising therapeutic remedy for PD
*BG↓, Oral administration of NMN increased serum bilirubin contents and decreased blood glucose, chloride and serum creatinine levels, but within the normal range.
*creat↓,
*ER Stress↓, 4-PBA attenuated ER stress and mitochondrial dysfunction induced by Dex in MC3T3-E1 cells.
*mtDam↓,
*Apoptosis↓, 4-PBA reduces apoptosis induced by Dex and ER stressors in osteoblast cells
eff↑, inhibiting ER stress. This new discovery is of great significance for molecular intervention against GC-induced osteoporosis.
| - |
Review, |
AD, |
NA |
|
|
|
- |
Review, |
Diabetic, |
NA |
|
|
|
- |
Review, |
Var, |
NA |
|
|
|
- |
in-vitro, |
Nor, |
H9c2 |
|
|
|
*antiOx↑, In this study, the antioxidant and anti-inflammatory effects of the main flavonoids of propolis (chrysin, pinocembrin, galangin, and pinobanksin) and propolis extract were researched.
*Inflam↓,
*ROS↓, ROS levels were decreased; SOD and CAT activities were increased; and the expression of HO-1 protein was increased by chrysin.
*SOD↑,
*Catalase↑,
*HO-1↑,
*NO↓, The results demonstrated that NO (Nitric Oxide), NOS (Nitric Oxide Synthase), and the activation of the NF-κB signaling pathway were inhibited in a dose-dependent manner
*NOS2↓,
*NF-kB↓,
*NRF2↑, it is possible that phytochemicals activate the Nrf2 pathway and inhibited the NF-κB (Nuclear factor kappa B) pathway.
*hepatoP↑, propolis has antioxidant, anti-inflammatory, anti-cancer, anti-bacterial, and hepatoprotective properties.
*MDA↓, chrysin reduced the cytotoxicity, MDA levels, and lysosomal and mitochondrial damage induced by AlP in a dose-dependent manner and increased the GSH activity induced by AlP i
*mtDam↓,
*GSH↑,
*p65↓, Similarly, galangin at 15, 30, and 60 mg/kg inhibited the expression of NF-κB p65, NOS, TNF-α, and IL-1β in a dose-dependent manner
*TNF-α↓,
*IL1β↓,
*NRF2↑, Nrf2 translocation from the cytoplasm to the nucleus was up-regulated (chrysin range of 5 μM–10 μM, pinocembrin range of 5 μM–40 μM, and propolis-extract range of 5 μg/mL–40 μg/mL)
*NRF2↓, and then down-regulated (chrysin range of 15 μM–25 μM, pinocembrin range of 40 μM–60 μM, and propolis-extract range of 40 μg/mL–100 μg/mL) following treatments with chrysin, pinocembrin, and propolis extract
*ROS⇅, Secondly, chrysin, pinocembrin, galangin, pinobanksin, and propolis extract exhibited antioxidant and pro-oxidant effects in a dose-dependent manner.
*BioAv↓, bioavailability values of galangin and chrysin in propolis extracts were determined in a study, and they were at 7.8% and 7.5%, respectively
*BioAv↑, Moreover, propolis extract has a higher bioavailability than single-flavonoid standards
*mt-ROS↓, quercetin treatment downregulated redox status, lipid droplets, and LPO release, restored damaged mitochondrial membrane potential, and repaired mtDNA damage, PGC-1α nuclear transfer, and mitochondrial dynamics.
*lipid-P↓,
*MMP↑,
*mtDam↓,
*NLRP3↓, gene and protein expressions of NLRP3, ASC, cleaved-caspase1, IL-18, IL-1β, and GSDMD-N were decreased, which effectively inhibited cell pyroptosis.
*ASC↓,
*cl‑Casp1↓,
*IL18↓,
*IL1β↓,
*GSDMD↓,
*Pyro↓,
*CYP2E1↓, Quercetin Inhibited CYP2E1 Activity to Alleviate High-Concentration Ethanol-Induced Hepatocyte Oxidative Stress and Lipid Peroxidation
*MFN1↓, Our study found that quercetin inhibited the expressions of mitochondrial fusion genes including Mfn1, Mfn2, and OPA1,
*MFN2↓,
*OPA1↓,
*DRP1/DNM1L↑, as well as increased fission genes expressions, and and the most significant change was Drp1
*AntiAge↑, Resveratrol produces changes associated with longer lifespan, including increased insulin sensitivity, reduced insulin-like growth factor-1 (IGF-I) levels, increased AMP-activated protein kinase (AMPK)
*IGF-1↓,
*AMPK↑,
*CRM↑, resveratrol opposed the effects of the high-calorie diet in 144 out of 153 significantly altered pathways.
*PGC-1α↑, activated receptor- γ coactivator 1α (PGC-1α) activity, increased mitochondrial number, and improved motor function.
*mtDam↓,
*motorD↑, Surprisingly, the resveratrol-fed HC mice steadily improved their motor skills as they aged
*hepatoP↑, At 18 months of age it was apparent that the high-calorie diet greatly increased the size and weight of livers and that resveratrol prevented these changes
*Dose↝, this study shows that an orally available small molecule at doses achievable in humans can safely reduce many of the negative consequences of excess caloric intake, with an overall improvement in health and survival.
*AMPK↑, In muscle, resveratrol activated AMPK, increased SIRT1 and PGC-1α protein levels,
*SIRT1↑, Resveratrol, which was discovered in a small-molecule screen as a potent SIRT1 activator
*PGC-1α↑,
*BP↓, Systolic blood pressure dropped and HOMA index improved after resveratrol.
*CRM↑, 30 days of resveratrol supplementation induces metabolic changes in obese humans, mimicking the effects of calorie restriction.
*Dose↝, resveratrol (150 mg/day (99%); resVida™)
*mtDam↓, Resveratrol increases AMPK activity, increases mitochondrial efficiency and respiration on fatty acid substrates.
*ALAT↓, paralleled by lower plasma ALAT values, as mentioned before, both indicating improved liver function.
*hepatoP↑,
*NLRP3↓, inhibits NLRP3 inflammasome-derived IL-1β secretion and pyroptosis in macrophages.
*mtDam↓, Resveratrol inhibits the activation step of the NLRP3 inflammasome by suppressing mitochondrial damage
*p38↑, Resveratrol also induces autophagy by activating p38, and macrophages treated with an autophagy inhibitor are resistant to the suppressive effects of resveratrol.
TumCD↑, urolithin A markedly induced cell death of OSCC via the induction of endoplasmic reticulum stress and subsequent inhibition of AKT and mTOR signaling as evidenced by decreased levels of phosphorylated mTOR and 4EBP1.
ER Stress↑,
Akt↓,
mtDam↓,
p‑mTOR↓,
*BioAv↝, The bioavailability of urolithins widely varies with inter individual gut microbiome composition depending on the presence of several identified species like Clostridium coccoides and Eggerthellacae family
ROS↑, remarkable anticancer effect on progressive Oral squamous cell carcinoma cells due to their ability to induce ER stress, ROS, cell cycle arrest and increased apoptosis through the preferential inhibition of AKT/mTOR/ERK signaling pathway.
TumCCA↑,
Apoptosis↑,
ERK↓,
Showing Research Papers: 1 to 34 of 34
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 34
Pathway results for Effect on Cancer / Diseased Cells:
NA, unassigned(tgid=0) ⓘ
CD47↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
GSH↓, 1, HO-1↑, 1, NQO1↑, 1, ROS↓, 1, ROS↑, 3,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 2, mtDam↓, 3,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↑, 2, Casp3↑, 1, TumCD↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
TumAuto↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 1, DNMT3B↓, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
TumCCA↑, 3,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↓, 1, p‑mTOR↓, 1, TumCG↓, 3,
Migration(tgid=13) ⓘ
TumCP↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
NK cell↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 2, Dose↝, 3, eff↑, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, chemoP↑, 2, fatigue∅, 1, QoL∅, 1,
Total Targets: 30
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
Stroke↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 9, Catalase↑, 6, CYP2E1↓, 1, Ferroptosis↓, 2, GPx↑, 2, GPx4↑, 2, GSH↑, 3, GSS↑, 1, HO-1↑, 8, i-Iron↓, 1, Keap1↓, 1, lipid-P↓, 8, MDA↓, 4, MFN1↓, 1, MFN1↑, 2, MFN2↓, 1, MFN2↑, 3, NQO1↑, 2, NRF2↓, 1, NRF2↑, 13, OPA1↓, 1, OPA1↑, 2, Prx↓, 1, ROS↓, 21, ROS⇅, 1, mt-ROS↓, 2, SOD↑, 5, SOD1↑, 1, SOD2↑, 1, Trx↑, 1, xCT/SLC7A11↑, 2,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↓, 1, ATP↑, 3, ATP∅, 1, DRP1/DNM1L↓, 4, DRP1/DNM1L↑, 1, FIS1↓, 5, MMP↓, 2, MMP↑, 1, mtDam↓, 31, OCR↓, 1, PGC-1α↑, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ACSL4↓, 1, ALAT↓, 1, AMPK↑, 5, CRM↑, 2, LDH↓, 1, LDH↑, 1, LDHA↓, 1, LDL↓, 1, NAD↑, 1, NADPH↑, 1, PKM2↓, 1, SIRT1↑, 3,
Cell Death(tgid=5) ⓘ
Akt↑, 1, Akt↝, 1, Apoptosis↓, 7, BAX↓, 1, Bax:Bcl2↓, 1, Bcl-2↑, 1, cl‑Casp1↓, 1, Casp3↓, 1, cl‑Casp3↓, 1, Casp9↓, 1, Cyt‑c↓, 1, Ferroptosis↓, 2, GSDMD↓, 1, iNOS↓, 1, JNK↓, 1, p‑JNK↓, 1, MAPK↝, 1, p38↓, 1, p38↑, 1, p‑p38↓, 1, Pyro↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
AntiThr↑, 1, other↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↓, 2,
Autophagy & Lysosomes(tgid=9) ⓘ
LC3‑Ⅱ/LC3‑Ⅰ↓, 1, MitoP↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
Diff↑, 1, FOXO↑, 1, FOXO3↑, 1, GSK‐3β↓, 1, IGF-1↓, 1, mTOR↑, 1, PI3K↑, 1, STAT3↝, 1,
Migration(tgid=13) ⓘ
AntiAg↑, 1, APP↓, 2, Ca+2↓, 1, Ca+2↝, 1, CD31/PECAM-1↑, 1, MMPs↓, 1, RAGE↓, 1, TGF-β↑, 1, Vim↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
Hif1a↑, 1, NO↓, 3,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
ASC↓, 1, CB2 / CNR2↑, 1, COX2/PTGS2↓, 3, IL10↓, 1, IL18↓, 1, IL1β↓, 5, IL6↓, 3, Inflam↓, 10, NF-kB↓, 4, p65↓, 1, TNF-α↓, 5,
Synaptic & Neurotransmission(tgid=18) ⓘ
AChE↓, 1, AChE∅, 1, BDNF↑, 4, BDNF∅, 1, PSD95↑, 1, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 3, BACE/β-secretase↓, 2, NLRP3↓, 4,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
ER(estro)↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 4, BioAv↝, 2, Dose↝, 4, eff↓, 2, eff↑, 8,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, BG↓, 1, BloodF↑, 1, BP↓, 1, BP∅, 1, creat↓, 1, IL6↓, 3, LDH↓, 1, LDH↑, 1, NOS2↓, 1, RAGE↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiDiabetic↑, 1, cardioP↑, 6, cognitive↑, 10, hepatoP↑, 4, memory↑, 7, motorD↑, 1, neuroP↓, 1, neuroP↑, 9, NP/CIPN↓, 1, OS↑, 1, RenoP↑, 1, toxicity↓, 3, Wound Healing↑, 1,
Infection & Microbiome(tgid=24) ⓘ
AntiViral↑, 1, Bacteria↓, 1,
Total Targets: 156
Scientific Paper Hit Count for: mtDam, mitochondrial damage
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#:614 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
Home Page