Apoptosis Cancer Research Results

Apoptosis, Apoptosis: Click to Expand ⟱

Source:

Type: type of cell death

Situation in which a cell actively pursues a course toward death upon receiving certain stimuli.
Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not die.

Scientific Papers found: Click to Expand⟱

5296-

5-HTP,

Serotonergic Regulation in Alzheimer’s Disease

Review,

AD,

*Risk↓, There is evidence that damage or dysfunction of the 5-HT system contributes to the development of AD, and different subtypes of 5-HT receptors are a potential target for the treatment of AD
*5HT↓, Serotonin is an antioxidant that inhibits the generation of ROS, malondialdehyde and carbonyls, prevents thiol oxidation, reduces the degradation of 2-deoxy-D-ribose, and prevents apoptosis
*ROS↓,
*MDA↓,
*Apoptosis↓,
*Mood↑, Serotonin deficiency may be responsible for the increase in aggressive behavior and depression often observed in patients with AD.
*other↑, Exercise and a Mediterranean diet increase 5-HT and BDNF levels, thereby improving mood and cognition.
*other↑, In particular, the evidence suggests that sulforaphane’s beneficial effects can be mainly ascribed to its peculiar ability to activate the Nrf2/ARE pathway [271].

1900-

AF,

Potential Anticancer Activity of Auranofin

Review,

Var,

TrxR↓, Auranofin inhibits the activity of thioredoxin reductase (TrxR
ROS↑, TrxR inhibition leads to an increase in cellular oxidative stress and induces apoptosis
Apoptosis↓,
TumCP↓, TrxR1 knockdown also inhibits cancer cell proliferation and DNA replication
eff↑, cytotoxicity of cisplatin is increased in cells expressing high levels of TrxR1 compared with cells expressing low levels

2656-

AL,

Allicin Protects PC12 Cells Against 6-OHDA-Induced Oxidative Stress and Mitochondrial Dysfunction via Regulating Mitochondrial Dynamics

in-vitro,

Park,

PC12

*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.

245-

AL,

Allicin: a promising modulator of apoptosis and survival signaling in cancer

Review,

Var,

Fas↑,
Bcl-2↓,
BAX↑,
PI3k/Akt/mTOR↝, Allicin can inhibit excessive autophagy by activating the PI3K/Akt/mTOR and MAPK/ERK/mTOR signaling pathways.
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↓,
*toxicity↓, Allicin-loaded nano-formulations efficiently induce apoptosis in cancer cells while minimizing toxicity to normal cells
Cyt‑c↑, allicin induces the release of cytochrome c from the mitochondria

3433-

ALA,

Alpha lipoic acid promotes development of hematopoietic progenitors derived from human embryonic stem cells by antagonizing ROS signals

*ROS↓, However, in more mature hPSC‐derived hematopoietic stem/progenitor cells, ALA reduced ROS levels and inhibited apoptosis.
*Apoptosis↓,
*Hif1a↑, up‐regulating HIF1A in response to a hypoxic environment.
*FOXO1↑, ALA also up‐regulated sensor genes of ROS signals, including HIF1A, FOXO1, FOXO3, ATM, PETEN, SIRT1, and SIRT3, during the process of hPSCs derived hemogenic endothelial cells generation
*FOXO3↑,
*ATM↑,
*SIRT1↑,
*SIRT3↑,
*CD34↑, Flow cytometry analysis indicated that ALA improved the production of CD34+ CD43+ CD45+ hematopoietic stem/progenitor cells significantly

3551-

ALA,

Alpha lipoic acid treatment in late middle age improves cognitive function: Proteomic analysis of the protective mechanisms in the hippocampus

in-vivo,

AD,

mice

*cognitive↑, ALA improves cognitive function in ageing mice.
*Apoptosis↓, ALA downregulates apoptosis, and neuroinflammatory associated proteins in ageing mice.
*Inflam↓,
*antiOx↑, Alpha lipoic acid (ALA), a powerful antioxidant, has the potential to relieve age-related cognitive impairment and neurodegenerative disease.
*BioAv↝, Alpha lipoic acid (ALA) is a sulfur-containing and both water-soluble and lipid-soluble coenzyme involved in the energy metabolism of carbohydrates, proteins and lipids
*neuroP↑, neuroprotective action of alpha lipoic acid has been demonstrated in a number of cellular or animal models of Parkinson's disease (PD), AD and amyotrophic lateral sclerosis (ALS) due to its antioxidative and anti-inflammatory properties

5324-

ALC,

The anti-wasting effects of L-carnitine supplementation on cancer: experimental data and clinical studies

Review,

Var,

*cachexia↓, The results of this process favored L-carnitine supplementation in patients with cancer-related cachexia.
*Apoptosis↓, inhibiting apoptosis or reversing inflammatory processes.
*Inflam↓,
QoL↑, This treatment increased plasma-free carnitine concentrations and significantly improved fatigue, which was assessed using the functional assessment of cancer therapy, fatigue, and quality of life questionnaire, as well as quality-of-life measu
Dose↝, placebo-controlled trial, in which 2 g per day of LC was administrated orally for four weeks among eligible patients.
Weight↑, advanced pancreatic cancer received either LC (4 g/day orally) or a placebo for 12 weeks. The results showed that body mass index, nutritional status (body cell mass and body fat), and quality-of-life parameters increased
OS↝, There was an insignificant increase in overall survival, a decline in length of hospital stays, and decrease in fatigue among the LC-treated patients.
fatigue↓,
eff↝, some dietary factors, such as food intake restriction and intake of LC and certain micronutrients (vitamin C, vitamin B6, and iron, which are required as cofactors for endogenous LC biosynthesis) may have some effects on the efficacy of LC sup

1440-

AMQ,

Lysosomotropism depends on glucose: a chloroquine resistance mechanism

in-vitro,

BC,

4T1

eff↑, Importantly, we found that the related compound, amodiaquine, was more potent than CQ for cell killing and not susceptible to interference from glucose starvation.
Apoptosis↓,
Necroptosis↑,
eff↓, Unexpectedly, further withdrawal of glucose, in the context of serum starvation, fully rescued the effect of CQ
ChemoSen↑, CQ markedly enhanced the sensitivity of 4T1 cells to doxorubicin
eff↓, Inhibition of glycolysis with 2DG also rescued cells from CQ.

3886-

Api,

Neuroprotective effects of apigenin against inflammation, neuronal excitability and apoptosis in an induced pluripotent stem cell model of Alzheimer’s disease

in-vitro,

AD,

*Inflam↓, apigenin has potent anti-inflammatory properties with the ability to protect neurites and cell viability by promoting a global down-regulation of cytokine and nitric oxide (NO) release in inflammatory cells.
*neuroP↑, demonstrate the broad neuroprotective action of apigenin against AD pathogenesis in a human disease model.
*NO↓,
*Apoptosis↓, Apigenin reduces apoptosis in sporadic AD and control neurons

5133-

ART/DHA,

Dihydroartemisinin Exerts Anti-Tumor Activity by Inducing Mitochondrion and Endoplasmic Reticulum Apoptosis and Autophagic Cell Death in Human Glioblastoma Cells

in-vitro,

GBM,

U87MG

in-vitro,

GBM,

U251

AntiTum↑, (DHA) has been shown to exhibit anti-tumor activity in various cancer cells.
tumCV↓, Our results proved that DHA treatment significantly reduced cell viability in a dose- and time-dependent manner by CCK-8 assay.
Apoptosis↓, DHA induced apoptosis of GBM cells through mitochondrial membrane depolarization, release of cytochrome c and activation of caspases-9.
MMP↓,
Cyt‑c↑,
Casp9↑,
CHOP↑, Enhanced expression of GRP78, CHOP and eIF2α and activation of caspase 12 were additionally confirmed that endoplasmic reticulum (ER) stress pathway of apoptosis
GRP78/BiP↑,
eIF2α↑,
Casp12↑,
ER Stress↑, DHA Induced Apoptosis through Mitochondria and Endoplasmic Reticulum (ER) Stress Pathways of Apoptosis in Human GBM Cells
TumAuto↑, ER stress and mitochondrial dysfunction were involved in the DHA-induced autophagy.
ROS↑, Further study revealed that accumulation of reactive oxygen species (ROS) was attributed to the DHA induction of apoptosis and autophagy.

3670-

Ash,

Neurodegenerative diseases and Withania somnifera (L.): An update

Review,

AD,

Review,

Park,

*Apoptosis↓, protective effects of Ashwagandha were accomplished by restoring mitochondrial and endothelial function, mitigation of apoptosis, inflammation and oxidative stress mechanisms.
*Inflam↓,
*ROS↓,
*neuroP↑, uggest the use of Withania somnifera (L.) against neurodegenerative disease

3672-

Ash,

Critical review of the Withania somnifera (L.) Dunal: ethnobotany, pharmacological efficacy, and commercialization significance in Africa

Review,

NA,

*cardioP↑, W. somnifera extracts are confirmed to have a significant cardioprotection effect based on the myocardial and antioxidant histopathological evaluations
*antiOx↑,
*ROS↓, reduced oxidative stress,
*neuroP↑, most reported neuroprotective mechanisms of W. somnifera extracts against several neurodegenerative diseases include the restoration of mitochondrial function concurrent with the mitigations of oxidative stress, inflammation, and apoptosis
*Inflam↓,
*Apoptosis↓,

3170-

Ash,

Withaferin A protects against hyperuricemia induced kidney injury and its possible mechanisms

in-vitro,

Nor,

NRK52E

in-vivo,

NA,

mice

*RenoP↑, WFA ameliorated renal damage, improved kidney function, and decreased levels of creatinine, BUN, UA, and XOD in PO-induced hyperuricemic mice.
*hepatoP↑,
*creat↓,
*BUN↓,
*uricA↓,
*Apoptosis↓, WFA markedly inhibited renal apoptosis, accompanied by changes of apoptosis-related proteins.
*α-SMA↓, Notably reduced α-SMA expression was observed after WFA administration, with WFA 10 mg/kg group presenting the most significant inhibitory effect.

3164-

Ash,

Withaferin A alleviates fulminant hepatitis by targeting macrophage and NLRP3

*hepatoP↑, Withania Somnifera, is a hepatoprotective agent
*IKKα↓, WA also inhibits inflammation by directly inhibiting IκκB activity46,47 or NLRP3 inflammasome activation in vitro in immune cells
*NLRP3↓,
*NRF2↑, WA probably protects against FH by targeting the macrophage and/or hepatocyte stress via activating NRF2, AMPKα
*AMPK↑,
*Inflam↓, Thus, WA potently protects against GalN/LPS-induced hepatotoxicity and inflammation
*Apoptosis↓, WA suppressed hepatic apoptosis in vivo
*cl‑Casp3↓, attenuate the increase of cleaved CASP3 and cleaved PARP1
*cl‑PARP1↓,
*NLRP3↓, WA prevented GalN/LPS-induced FH partially by inhibiting activation of the NLRP3 inflammasome
*ROS↓, fig 7
*ALAT↓,
*AST↓,
*GSH↑, (GSH) levels were significantly depleted by ~50% 6 h after GalN/LPS administration and were recovered to levels comparable with that of control mice by WA treatment

4818-

ASTX,

MEL,

Effect of astaxanthin and melatonin on cell viability and DNA damage in human breast cancer cell lines

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

T47D

in-vitro,

Nor,

MCF10

TumCD↑, Astaxanthin increases the melatonin-induced cell death in breast cancer cells
DNAdam↑, Astaxanthin-melatonin combination and DNA damages in breast cancer cells
*antiOx↑, strong anti-oxidative, anti-tumoral, and anti-inflammatory effects.
*AntiTum↑,
Inflam↓,
tumCV↓, Astaxanthin at lower doses than melatonin reduced cell viability and Bcl2 expression, induced apoptosis and DNA damage in MDA-MB-231 and T47D.
Bcl-2↓,
Apoptosis↓,
selectivity↑, Meanwhile, the effects of astaxanthin on cell cytotoxicity, apoptosis, and DNA damage in MCF10A cells are insignificant compared to MDA-MB-231 and T47D.
eff↑, Furthermore, the presence of astaxanthin increased the function of melatonin-induced cell death in breast cancer cells.
Dose↓, The results showed that very low doses of astaxanthin reduced survival rate, induced apoptosis, reduced the expression of Bcl2 proteins, and destroyed the DNA in cancerous cells

4813-

ASTX,

Astaxanthin Prevents Oxidative Damage and Cell Apoptosis Under Oxidative Stress Involving the Restoration of Mitochondrial Function

in-vitro,

AD,

*antiOx↑, Astaxanthin (ASTA), a natural compound known for its potent antioxidant properties, shows the biological activities in anti-apoptosis and antitumor.
*Apoptosis↓,
*AntiTum↑,
*ROS↓, ASTA significantly reduced H2O2-induced mitochondrial dysfunctions and restored the intracellular reactive oxygen species (ROS), mitochondrial membrane potential, and respiratory capacity.
*MMP↑, Astaxanthin depresses oxidative stress-induced depolarization of mitochondrial membrane potential and restores the mitochondrial respiratory capacity.
*neuroP↑, Oxidative stress (OS) is one of the factors that result in cell damage and the development of neurological diseases such as Alzheimer's disease (AD).

2629-

Ba,

Baicalein, a Component of Scutellaria baicalensis, Attenuates Kidney Injury Induced by Myocardial Ischemia and Reperfusion

in-vivo,

Nor,

Rats, Myocardial ischemia and reperfusion, induced by a 40-minute occlusion and a 3-hour reperfusion of the left anterior descending coronary artery

*RenoP↑, Intravenous pretreatment with baicalein (in doses of 3, 10, or 30 mg/kg), however, significantly reduced the increases in the creatinine level, renal histological damage, and apoptosis induced by myocardial ischemia and reperfusion.
*Apoptosis↓,
*TNF-α↓, In addition, the increases in the serum levels of tumor necrosis factor-α, interleukin-1, and interleukin-6, and of tumor necrosis factor-α in the kidneys were significantly reduced
*IL1↓,
*Bcl-2↑, Western blot analysis revealed that baicalein significantly increased Bcl-2 and reduced Bax in the kidneys
*BAX↓,
*Akt↑, inhibition of apoptosis, possibly through the reduction of tumor necrosis factor-α production, the modulation of Bcl-2 and Bax, and the activation of Akt and extracellular signal-regulated kinases 1 and 2.

2626-

Ba,

Molecular targets and therapeutic potential of baicalein: a review

Review,

Var,

Review,

AD,

Review,

Stroke,

AntiCan↓, anticancer, antidiabetic, antimicrobial, antiaging, neuroprotective, cardioprotective, respiratory protective, gastroprotective, hepatic protective, and renal protective effects
*neuroP↑,
*cardioP↑, Cardioprotective action of baicalein
*hepatoP↑,
*RenoP↑, baicalein’s capacity to lessen cisplatin-induced nephrotoxicity is probably due, at least in part, to the attenuation of renal oxidative and/or nitrative stress
TumCCA↑, Baicalein induces G1/S arrest in lung squamous carcinoma (CH27) cells by downregulating CDK4 and cyclin D1, as well as upregulating cyclin E
CDK4↓,
cycD1/CCND1↓,
cycE/CCNE↑,
BAX↑, SGC-7901 cells showed that when baicalein was administered, Bcl-2 was downregulated and Bax was increased
Bcl-2↓,
VEGF↓, Baicalein inhibits the synthesis of vascular endothelial growth factor (VEGF), HIF-1, c-Myc, and nuclear factor kappa B (NF-κB) in the G1 and S phases of ovarian cancer cell
Hif1a↓,
cMyc↓,
NF-kB↓,
ROS↑, Baicalein produced intracellular reactive oxygen species (ROS) and activated BNIP3 to slow down the development and hasten the apoptosis of MG-63,OS cell
BNIP3↑,
*neuroP↑, Baicalein exhibits neuroprotective qualities against amyloid (AN) functions by preventing AN from aggregating in PC12 neuronal cells to cause A𝛽-induced cytotoxicity
*cognitive↑, baicalein encourages non-amyloidogenic processing of APP, which lowers the generation of A𝛽 and enhances cognitive function
*NO↓, baicalein effectively reduced NO generation and iNOS gene expression
*iNOS↓,
*COX2↓, Baicalein therapy significantly decreased the expression of COX-2 and iNOS, as well as PGE2 and NF-κB, indicating a protective effect against cerebral I/R injury.
*PGE2↓,
*NRF2↑, Baicalein therapy markedly elevated nuclear Nrf2 expression and AMPK phosphorylation in the ischemic cerebral cortex
*p‑AMPK↑,
*Ferroptosis↓, Baicalein suppressed ferroptosis associated with 12/15-LOX, hence lessening the severity of post-traumatic epileptic episodes generated by FeCl3
*lipid-P↓, HT22 cells were damaged by ferroptosis, which is mitigated by baicalein may be due to its lipid peroxidation inhibitor
*ALAT↓, Baicalin lowers the raised levels of hepatic markers alanine transaminase (ALT), aspartate aminotransferase (AST)
*AST↓,
*Fas↓, Baicalin has also been shown to suppress apoptosis, decrease FAS protein expression, block the caspase-8 pathway, and decrease Bax protein production
*BAX↓,
*Apoptosis↓,

3678-

BBR,

Network pharmacology study on the mechanism of berberine in Alzheimer’s disease model

Review,

AD,

*APP↓, BBR were decreased in the mRNA and protein expression of APP and presenilin 1 while PPARG was increased with a reduction in the NF-κB pathway.
*PPARγ↑, upregulated PPARG with decreasing its downstream NF-ΚB pathway
*NF-kB↓,
*Aβ↓, BBR played a protective role in the AD mice model via blocking APP processing and amyloid plaque formation.
*cognitive↑, berberine significantly reduced amyloid accumulation and improved cognitive impairment in APP/PS1 mice
*antiOx↑, via anti-oxidative stress, anti-neuroinflammation, inhibition of neuronal cell apoptosis, etc
*Inflam↓,
*Apoptosis↓,
*BioAv↑, BBR was found to be metabolized to dihydro-berberine by intestinal bacteria, whose bioavailability was five times higher than that of BBR
*BioAv↝, oral bioavailability (OB, >30%),
*BBB↑, blood-brain barrier (BBB, >0.3)
*motorD↑, BBR treated 5×FAD mice ameliorated their behavior activity including in locomotor activity and cognitive function compared to control.
*NRF2↑, BBR enhanced cellular antioxidant capacity, regulated antioxidant-related pathways such as Nrf2 and HO-1, and thereby reduced oxidative stress damage
*HO-1↑,
*ROS↓,
*p‑Akt↑, BBR significantly increased the phosphorylation levels of AKT and ERK
*p‑ERK↑,

3680-

BBR,

Network pharmacology reveals that Berberine may function against Alzheimer’s disease via the AKT signaling pathway

in-vivo,

AD,

3 × Tg AD mice

*Akt↑, Akt1 mRNA expression levels were significantly decreased in AD mice and significantly increased after BBR treatment (p < 0.05).
*neuroP↑, BBR may exert a neuroprotective effect by modulating the ERK and AKT signaling pathways.
*p‑ERK↑, Besides, AKT and ERK phosphorylation decreased in the model group, and BBR significantly increased their phosphorylation levels.
*Aβ↓, BBR has therapeutic potential in the treatment of AD by targeting amyloid beta plaques, neurofibrillary tangles, neuroinflammation, and oxidative stress
*Inflam↓,
*ROS↓,
*BioAv↑, oral bioavailability (OB) = 36.86%, drug-likeness (DL) = 0.78,
*BBB↑, blood brain barrier (BBB) = 0.57,
*Half-Life↝, half-life (HL) = 6.57. BBR half-life (t1/2) is in the mid-elimination group.
*memory↑, BBR improves the performance of memory and recognition tasks in AD mice
*cognitive↑,
*HSP90↑, Among the core targets, Akt1 (t = −5.01, p = 0.002), Hsp90aa1 (t = −3.66, p = 0.011), Hras (t = −2.99, p = 0.024) and Igf1 (t = 3.75, p = 0.019) mRNA levels were significantly increased after BBR treatment
*APP↓, BBR reduces Aβ levels by modulating APP processing and ameliorates Aβ pathology by inhibiting the mTOR/p70S6K signaling pathway
*mTOR↓,
*P70S6K↓,
*CD31↑, it promotes the formation of brain microvessels by enhancing CD31, VEGF, N-cadherin, Ang-1 and inhibits neuronal apoptosis (Ye et al., 2021).
*VEGF↑,
*N-cadherin↑,
*Apoptosis↓,

3682-

BBR,

Berberine Improves Cognitive Impairment by Simultaneously Impacting Cerebral Blood Flow and β-Amyloid Accumulation in an APP/tau/PS1 Mouse Model of Alzheimer’s Disease

in-vitro,

AD,

mouse

*cognitive↑, results showed that BBR ameliorated cognitive deficits in 3×Tg AD mice, reduced the Aβ accumulation, inhibited the apoptosis of neurons
*Aβ↓,
*Apoptosis↓,
*CD31↑, promoted the formation of microvessels in the mouse brain by enhancing brain CD31, VEGF, N-cadherin, Ang-1.
*VEGF↑,
*N-cadherin↑,
*angioG↑,
*neuroP↑, berberine is effective to 3×Tg AD mice, has a neuroprotective effect,
*p‑tau↓, lowering Aβ levels, inhibiting the phosphorylation of Tau protein, anti-oxidation, inhibiting the activity of AchE and MAO, and regulating lipids, hypoglycemic.
*antiOx↑,
*AChE↓,
*MAOB↓,
*lipid-P↓,

2724-

BetA,

Down-regulation of NOX4 by betulinic acid protects against cerebral ischemia-reperfusion in mice

in-vivo,

Nor,

mice

in-vivo,

Stroke,

AntiTum↑, Betulinic acid is mainly known for its anti-tumor and anti-inflammatory activities.
*Inflam↓,
*ROS↓, Our previous study showed that betulinic acid could decrease the reactive oxygen species (ROS) production by regulating the expression of NADPH oxidase.
*NOX4↓, Pre-treatment with betulinic acid (50 mg/kg/day for 7 days via gavage) prior to MCA occlusion prevented the ischemia/reperfusion-induced up-regulation of NOX4 and ROS production.
*Apoptosis↓, treatment with betulinic acid could markedly blunt the ischemia/reperfusion-induced neuronal apoptosis
neuroP↑, betulinic acid protects against cerebral ischemia/reperfusion injury in mice

2739-

BetA,

Glycolytic Switch in Response to Betulinic Acid in Non-Cancer Cells

in-vitro,

Nor,

HUVECs

10 µM

in-vitro,

Nor,

MEF

*Glycolysis↑, BA elevates the rates of cellular glucose uptake and aerobic glycolysis in mouse embryonic fibroblasts with concomitant reduction of glucose oxidation.
*GlucoseCon↑, BA increases cellular glucose uptake
*Apoptosis↓, Without eliciting signs of obvious cell death BA leads to compromised mitochondrial function, increased expression of mitochondrial uncoupling proteins (UCP) 1 and 2, and liver kinase B1 (LKB1)-dependent activation AMP-activated protein kinase.
*UCP1↓,
*AMPK↑, AMPK activation accounts for the increased glucose uptake and glycolysis which in turn are indispensable for cell viability upon BA treatment.
GLUT1↑, The expression of glucose transporter GLUT1 was elevated upon BA treatment for 16 h
mt-ROS↑, We observed increased production of mitochondrial ROS (Fig. 4A) and elevated expression of uncoupling proteins UCP1 and UCP2 in BA-treated MEF

2744-

BetA,

Betulin and betulinic acid: triterpenoids derivatives with a powerful biological potential

Review,

Var,

Apoptosis↓, Various studies have demonstrated that BE is able to induce apoptosis in numerous cancer cell lines (
TumCCA↑, 10 uM concentration, BE arrests cell cycle of murine melanoma B164A5 cells in S phase.
Casp9↑, BE is involved in the sequential activation of caspase-9, caspases 3 and 7, and cleaving of poly(ADP-ribose) polymerase (PARP) (Potze et al. 2014).
Casp3↑,
Casp7↑,
cl‑PARP↑,
MMP↓, mitochondrial membrane potential loss (Li et al. 2010; Potze et al. 2014).
ROS↑, increased reactive oxygen species (ROS) production
TOP1↓, BA was also shown to inhibit the proliferation of topoisomerases and therefore express anti-proliferative activity
NF-kB↓, BA was demonstrated to inhibit activating of NF-kB

5663-

BNL,

Osthole/borneol thermosensitive gel via intranasal administration enhances intracerebral bioavailability to improve cognitive impairment in APP/PS1 transgenic mice

in-vivo,

AD,

mice

*ZO-1↓, Mechanisms showed that borneol as a “courier” opened up intercellular space and loosened the tight junctions of the nasal mucosa by suppressing ZO-1 and occludin expression
*cl‑Casp3↓, Osthole assisted by borneol demonstrated significantly improved efficiency in suppressing cleaved caspase-3 expression, increasing the Bcl-2/Bax ratio
*Bax:Bcl2↓,
*MDA↓, reducing malondialdehyde levels, inhibiting neuron apoptosis, and decreasing Aβ levels by inhibiting BACE1 expression to alleviate cognitive impairment in APP/PS1 mice
*Apoptosis↓,
*Aβ↓,
*BACE↓,
*cognitive↑,
*BioAv↑, our study demonstrated that the intracerebral bioavailability of osthole profoundly improved with intranasal administration of osthole/borneol
memory↑, our study demonstrated that the intracerebral bioavailability of osthole profoundly improved with intranasal administration of osthole/borneol
P-gp↓, This may be caused by a higher dose of BO inhibiting the action of the P-gp transporter in intestinal mucosa and CYP450 metabolism in the liver.
BioEnh↑,

3507-

Bor,

Boron inhibits apoptosis in hyperapoptosis condition: Acts by stabilizing the mitochondrial membrane and inhibiting matrix remodeling

*MMP↑, n the presence of boron, there was a significant and dose-dependent increase in MMP, which inhibited mitochondrial remodeling to the condensed state and hence the release of Cyt c and initiation of apoptosis.
*Cyt‑c↓, Boron inhibits the release of mitochondrial Cyt c and activation of Casp
*Apoptosis↓, Boron inhibits apoptosis.
*Casp3↓,
*NO↓, Nitric oxide (NO) and iNOS levels decrease in boron treated hyperapoptosis cultures.
*iNOS↓,

3510-

Bor,

Boron Affects the Development of the Kidney Through Modulation of Apoptosis, Antioxidant Capacity, and Nrf2 Pathway in the African Ostrich Chicks

in-vivo,

Nor,

ostrich chicks

*RenoP↑, Our results revealed that low doses of boron (up to 160 mg) had positive effect, while high doses (especially 640 mg) caused negative effect on the development of the kidney
*ROS↓, The low doses regulate the oxidative and enzyme activity in the kidney.
*antiOx↑, boron at low doses upregulated the expression of genes involved in the antioxidant pathway
*Apoptosis↓, low levels of boron (up to 160 mg) inhibited the cell apoptosis, regulate the enzyme activity, and improved the antioxidant system, thus may encourage the development of the ostrich chick's kidney
*NRF2↑, maximum localization of Nrf2 in 80 mg/L BA dose group
*HO-1↑, As the boron concentration increased, the expression of Nrf2, GCLc, and HO-1 genes upregulated
*MDA↓, In comparison to those of the group 1, MDA content (lipid peroxidation marker) was significantly decreased by 26.02 and 48.12% in the 40 and 80 mg/L BA groups
*lipid-P↓,
*GPx↓, GSH-PX activity of ostrich chick kidney tissue was slightly increased in the 40 and 80 mg/L BA groups,
*Catalase↑, supplementation of low doses of boron in the ostrich drinking water has resulted in stimulation of antioxidant capacity of GR, CAT, and SOD significantly.
*SOD↑,
*ALAT↓, boron supply in low doses (especially 80 mg/L BA) showed decrease levels in the activity of ALT, AST, and ALP.
*AST↓,
*ALP↓,

1207-

CA,

PacT,

Caffeine inhibits the anticancer activity of paclitaxel via down-regulation of α-tubulin acetylation

in-vitro,

Lung,

A549

patients receiving treatment with taxanes, such as paclitaxel, should avoid consuming caffeinated beverages or foods.

in-vitro,

Cerv,

HeLa

TumCG↑, caffeine promoted the growth of cancer cells treated with paclitaxel
TumCMig↓,
Apoptosis↓,
ac‑α-tubulin↑,

5869-

CA,

Carnosic Acid Induces Antiproliferation and Anti-Metastatic Property of Esophageal Cancer Cells via MAPK Signaling Pathways

in-vitro,

ESCC,

KYSE150

TumCP↓, CA dose-dependently inhibited cell proliferation, apoptosis, migration, and colony formation.
Apoptosis↓,
TumCMig↓,
TumCCA↑, CA arrested the cell cycle at G2/M phase, promoted cell apoptosis, induced DNA damage, and inhibited the MAPK signaling pathways.
DNAdam↑, CA Provokes Strong DNA Damage Response
MAPK↓,
γH2AX↑, CA dose-dependently increased the expression of γ-H2AX.
TumMeta↓, CA Inhibits Metastasis and Invasion of KYSE-150 Cells via Suppressed MAPK Signaling Pathway
TumCI↓,
P21↑, capabilities of CA to activate p21-mediated signaling pathway [25] and induced apoptosis and production of reactive oxygen species (ROS) [28],
ROS↑,
EMT↓, inhibited the EMT [29],
ChemoSen↑, enhanced the anticancer effects of other compounds [26],

5830-

CAP,

Inhibition of pyroptosis and apoptosis by capsaicin protects against LPS-induced acute kidney injury through TRPV1/UCP2 axis in vitro

in-vitro,

Nor,

HK-2

*IL1β↓, capsaicin ameliorated LPS-induced cytotoxicity in vitro and attenuated the release of interleukin (IL)-1β and IL-18.
*IL18↓,
*TRPV1↑, Molecularly, capsaicin activated transient receptor potential cation channel subfamily V member 1 –mitochondrial uncoupling protein 2 axis and inhibited caspase-1-mediated pyroptosis
*ROS↓, capsaicin alleviated LPS-induced ROS production and mitochondrial membrane potential disruption and inhibited apoptosis.
*MMP↑,
*Apoptosis↓,
*RenoP↑, These findings suggest that capsaicin shows a protective effect in in vitro acute kidney injury model.
*Inflam↓, Capsaicin ameliorates LPS-induced cytotoxicity and inflammation response in HK-2 cells
*UCPs↑, Capsaicin alleviates LPS-induced pyroptosis in HK-2 cells by activating TRPV1/UCP2 axis

5888-

CAR,

Therapeutic application of carvacrol: A comprehensive review

Review,

Var,

Review,

Stroke,

Review,

Diabetic,

Review,

Park,

*antiOx↑, demonstrated as anti‐oxidant, anticancer, diabetes prevention, cardioprotective, anti‐obesity, hepatoprotective and reproductive role, antiaging, antimicrobial, and immunomodulatory properties.
*AntiCan↑,
*AntiDiabetic↑,
*cardioP↑,
*Obesity↓,
*hepatoP↑,
*AntiAg↑,
*Bacteria↓,
*Imm↑,
MMP2↓, anticancer ability against malignant cells via decreasing the expressions of matrix metalloprotease 2 and 9, inducing apoptosis
MMP9↓,
Apoptosis↓,
MMP↓, disrupting mitochondrial membrane, suppressing extracellular signal‐regulated kinase 1/2 mitogen‐activated protein kinase signal transduction
ERK↓,
PI3K↓, decreasing the phosphoinositide 3‐kinase/protein kinase B.
ALAT↓, decreased the concentrations of alanine aminotransferase, alkaline phosphatase and aspartate aminotransferase,
*ROS↓, Essential oils found in plants are natural anti‐oxidants that reduce cell damage caused by reactive species and prevent mutagenic and carcinogenic processes.
*Catalase↑, Carvacrol has remarkably higher anti‐oxidative and hepatoprotective properties, which improves the activity of enzymatic anti‐oxidants (catalase, superoxide dismutase, and glutathione peroxidase)
*SOD↑,
*GPx↑,
*AST↓, Carvacrol decreased the level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactic acid dehydrogenase (LDH) and improved the status of inflammation, necrosis, and coagulation in the liver
*LDH↓,
*necrosis↓,
ROS↑, prostate cancer cells via lowering cell viability, increasing the rate of reactive oxygen species, and disrupting the mitochondrial membrane potential.
TumCCA↑, Carvacrol induced cell cycle arrest at G0/G1 that declined increased CDK inhibitor p21 expression and decreased cyclin‐dependent kinase 4 (CDK4), and cyclin D1 expressions.
CDK4↓,
cycD1/CCND1↓,
NOTCH↓, carvacrol inhibited Notch signaling in PC‐3 cells via downregulating Jagged‐1 and Notch‐1
IL6↓, human prostate cancer cell lines, which significantly reduced IL‐6
chemoP↑, Carvacrol has significant protective effects in reducing the side effects of chemotherapeutics such as irinotecan hydrochloride anticancer drugs that cause induction of intestinal mucositis.
*Pain↓, Pain management
*neuroP↑, The neuroprotective role of carvacrol was examined by Guan et al. in 2019 against ischemic stroke,
*TRPM7↓, downregulating TRPM7 channels
*motorD↑, improved catalepsy, akinesia, bradykinesia, locomotor activity, and motor coordination.
*NF-kB↓, Carvacrol reduced inflammatory biomarkers, such as nuclear factor κB and cyclooxygenase‐2, and levels of nitric oxides, malondialdehyde, and glutathione create oxidative stress.
*COX2↓,
*MDA↓,

5907-

CAR,

Anti-proliferative and pro-apoptotic effect of carvacrol on human hepatocellular carcinoma cell line HepG-2

in-vitro,

Liver,

HepG2

TumCG↓, In this study, we showed that carvacrol inhibited HepG2 cell growth by inducing apoptosis
Apoptosis↓,
Casp3↓, activation of caspase-3, cleavage of PARP and decreased Bcl-2 gene expression
cl‑PARP↑,
Bcl-2↓,
p‑ERK↓, decreasing phosphorylation of ERK1/2 significantly in a dose-dependent manner, and activated phosphorylation of p38
p‑p38↑,
*Bacteria↓, carvacrol has been shown to exhibit anti-microbial, anti-mutagenic, anti-platelet, analgesic, anti-inflammatory, anti-angiogenic, anti-oxidant, anti-elastase, insecticidal, anti-parasitic,cell-protective, AChE inhibitor and anti-tumor activity
*AntiAg↑,
*Inflam↓,
*antiOx↑,
*AChE↓,
AntiTum↑,
MMP↓, classical apoptosis response, including decrease in mitochondrial membrane potential and increase in cytochrome c release from mitochondria, decrease in Bcl-2/Bax ratio, increase in caspase activity and cleavage of PARP and fragmentation of DNA,
Cyt‑c↑,
Bax:Bcl2↑,
Casp↑,
DNAdam↑,
selectivity↑, we found that carvacrol induced stronger effects on hepatocellular carcinoma cells compared to normal human fetal liver cells.

5902-

CAR,

A novel antagonist of TRPM2 and TRPV4 channels: Carvacrol

in-vitro,

Nor,

HEK293

*other↓, When OS-induced TRPM2 and GSK-induced TRPV4 activations were inhibited by the treatment of CARV
*GSH↑, upregulation of glutathione and glutathione peroxidase.
*GPx↑,
*ROS↓, The possible TRPM2 and TRPV4 blocker action of carvacrol (CARV) via the modulation oxidative stress and apoptosis in the SH-SY5Y neuronal cells.
*Apoptosis↓,

5901-

CAR,

Neuroprotective role of carvacrol in ischemic brain injury: a systematic review of preclinical evidence and proposed TRPM7 involvement

Review,

Stroke,

*neuroP↑, improved neurological scores when carvacrol was given before or shortly after injury.
*ROS↓, studies showed reduced oxidative damage (MDA, 4-HNE), increased antioxidant enzymes (SOD, CAT, GPx), lower apoptosis (cleaved caspase-3), and variable changes in TRPM7 expression.
*MDA↓,
*4-HNE↓,
*SOD↑,
*Catalase↑,
*GPx↑,
*Apoptosis↓,
*cl‑Casp3↓,
*TRPM7⇅, variable changes in TRPM7 expression
*BBB↓, Natural products such as carvacrol can cross the blood-brain barrier and have been reported to inhibit TRPM7 in vitro
*TRPM7↓,

5957-

CEL,

Celecoxib induces apoptosis by inhibiting 3-phosphoinositide-dependent protein kinase-1 activity in the human colon cancer HT-29 cell line

in-vitro,

Colon,

HT29

COX2↓, Celecoxib, a COX-2-specific inhibitor, has been shown to reduce the number of adenomatous colorectal polyps in patients with familial adenomatous polyposis.
PDK1↓, celecoxib induces apoptosis in the colon cancer cell line HT-29 by inhibiting the 3-phosphoinositide-dependent kinase 1 (PDK1) activity.
Apoptosis↓,

6014-

CGA,

Exploring the Pharmacological Potential of Chlorogenic acid as an Anti-Cancer Agent and a Call for Advance Research

Review,

Var,

AntiCan↑, chlorogenic acid (CHA) possesses several pharmacological attributes, such as anticancer, hepatoprotective, antimicrobial, immune-suppressant, antioxidant, and antidiabetic activities.
*hepatoP↑,
*Bacteria↓,
*antiOx↓,
*AntiDiabetic↑,
Apoptosis↓, It can hinder the process of cell division, trigger cell apoptosis, and suppress an increase in cancerous cell growth.
TumCG↓,
angioG↓, mechanisms include angiogenesis, invasion and migration, oxidative stress, inflammation, cell cycle arrest, and proliferation.
TumCI↓,
TumCMig↓,
ROS↝,
Inflam↝,

6068-

CHL,

Dietary chlorophyllin inhibits the canonical NF-κB signaling pathway and induces intrinsic apoptosis in a hamster model of oral oncogenesis

in-vivo,

Oral,

hamster

NF-kB↓, Dietary administration of chlorophyllin (4 mg/kg bw) suppressed the development of HBP carcinomas by inhibiting the canonical NF-κB signaling pathway by downregulating IKKβ, preventing the phosphorylation of IκB-α, and reducing NF-κB
IKKα↓,
Apoptosis↓, Inactivation of NF-κB signaling by chlorophyllin was associated with the induction of intrinsic apoptosis as evidenced by modulation of Bcl-2 family proteins
Bcl-2↑,
survivin↓, enforced nuclear localization of survivin, upregulation of apoptogenic molecules, activation of caspases, and cleavage of PARP.
Casp↑,
cl‑PARP↑,

2794-

CHr,

An updated review on the versatile role of chrysin in neurological diseases: Chemistry, pharmacology, and drug delivery approaches

Review,

Park,

Review,

Stroke,

*neuroP↑, chrysin has protective effects against neurological conditions by modulating oxidative stress, inflammation, and apoptosis in animal models.
*ROS↓,
*Inflam↓,
*Apoptosis↓,
*IL1β↓, attenuated IL-1β and TNF-α, COX-2, iNOS, and NF-kB expression, activated JNK
*TNF-α↓,
*COX2↓,
*iNOS↓,
*NF-kB↓,
*JNK↓,
*HDAC↓, alleviated histone deacetylase (HDCA) activity, GSK-3β levels, IFNγ, IL-17,
*GSK‐3β↓,
*IFN-γ↓,
*IL17↓,
*GSH↑, increased GSH levels
*NRF2↑, Park's: Increased Nrf2, modulated HO-1, SOD, CAT, decreased MDA, inhibited NF-κB and iNOS
*HO-1↑, upregulated expression of hallmark antioxidant enzymes, including HO-1, SOD, and CAT; and decreased levels of MDA
*SOD↑,
*MDA↓,
*NO↓, Attenuated NO, increased GPx
*GPx↑,
*TBARS↓, decreased levels of TBARS, AChE, restored activities of GR, GSH, SOD, CAT and Vitamin C
*AChE↓,
*GR↑,
*Catalase↑,
*VitC↑,
*memory↑, attenuated memory impairment
*lipid-P↓, attenuated lipid peroxidation
*ROS↓, attenuated ROS

3997-

CoQ10,

Coenzyme Q and Its Role in the Dietary Therapy against Aging

Review,

AD,

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

3832-

Cro,

Traditional Chinese Medicine: Role in Reducing β-Amyloid, Apoptosis, Autophagy, Neuroinflammation, Oxidative Stress, and Mitochondrial Dysfunction of Alzheimer’s Disease

Review,

AD,

*neuroP↑, TCM known for its medicinal properties in neuropsychiatric disorders, such as depression, seizure, anxiety, and neurodegenerative disease.
*memory↑, Crocin can improve memory impairment and learning ability by reducing neuron apoptosis and Bax levels as well as increasing the expression of Bcl-2
*Apoptosis↓,
*cognitive↑, crocin alleviates malathion-induced neurological alterations and cognitive impairment by exerting its anti-apoptotic effects
*ER Stress↓, Regulate endoplasmic reticulum ,40 mg/kg

1596-

Cu,

CDT,

Unveiling the promising anticancer effect of copper-based compounds: a comprehensive review

Review,

NA,

TumCD↑, Copper and its compounds are capable of inducing tumor cell death through various mechanisms of action, including activation of apoptosis signaling pathways by reactive oxygen species (ROS), inhibition of angiogenesis, induction of cuproptosis, and p
Apoptosis↓,
ROS↑,
angioG↑,
Cupro↑,
Paraptosis↑,
eff↑, copper nanoparticles can be used as effective agents in chemodynamic therapy, phototherapy, hyperthermia, and immunotherapy.
eff↓, Elevated copper concentrations may promote tumor growth, angiogenesis, and metastasis by affecting cellular processes
selectivity↑, Copper nanoparticles also can selectively attack cancer cells and spare healthy cells This selectivity is attributed to the EPR effect, which enables nanoparticles to accumulate in tumor tissue by exploiting leaky blood vessels
DNAdam↑, Copper has been found to induce DNA damage and oxidation through the formation of ROS.
eff↑, Tumor cells suffering from oxygen deficiency often have an increased concentration of CTR-1, which facilitates the transport of copper(I) into the cells
eff↑, The results demonstrate the promising capabilities of 64CuCl2 as a valuable tool for both diagnosis and therapy in various types of cancer
eff↑, nanoparticles have remarkable properties, including a large surface area to volume ratio, excellent compatibility with living organisms, and the ability to generate ROS when exposed to an acidic tumor microenvironment
eff↑, Several studies have shown that copper nanoparticles can be used as effective agents in chemodynamic therapy (CDT)
Fenton↑, CDT is a promising treatment strategy for cancer that utilizes the in situ Fenton reaction, which is activated by endogenous substances, such as GSH and H2O2 without the need for external energy input
H2O2↑, Copper-based substrates have been developed that generate H2O2 internally and function effectively in weakly acidic tumor microenvironments (TME)
eff↑, metal peroxide nanomaterials and offers a promising strategy to improve CDT efficacy
eff↑, Copper nanoparticles can also be used in phototherapy
eff↑, Copper nanoparticles have also shown success in destroying cancer tissue by hyperthermia. This method is a local anticancer treatment in which cells are exposed to high temperatures.
RadioS↑, promising results when used in combination with radiotherapy or chemotherapy for various tumor types.
ChemoSen↑,
eff↑, copper nanoparticles are promising in cancer immunotherapy because they enhance immune-based therapies
*toxicity↝, Copper is a necessary trace mineral for the human body, but high concentrations of copper can be toxic
other↑, Extensive research has shown that cancer cells require an increased copper content to support their rapid growth compared to normal cells
eff↑, Copper nanoparticles can be used to generate heat when exposed to certain wavelengths of light or alternating magnetic fields.

2818-

CUR,

Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways

Review,

AD,

*neuroP↑, Curcumin's protective functions against neural cell degeneration due to mitochondrial dysfunction and consequent events such as oxidative stress, inflammation, and apoptosis in neural cells have been documented
*ROS↓, studies show that curcumin exerts neuroprotective effects on oxidative stress.
*Inflam↓,
*Apoptosis↓,
*cognitive↑, cognitive performance to receive the title of neuroprotective
*cardioP↑, Studies have shown that curcumin can induce cell regeneration and defense in multiple organs such as the brain, cardiovascular system,
other↑, It has been shown that chronic use of curcumin in patients with neurodegenerative disorder can cause gray matter volume increase
*COX2↓, Curcumin also decreased the brain protein levels and activity of cyclooxygenase 2 (COX-2)
*IL1β↓, inhibition of IL-1β and TNF-α production, and enhancement of Nf-Kβ inhibition
*TNF-α↓,
NF-kB↓,
*PGE2↓, hronic curcumin therapy has shown a significant decrease in lipopolysaccharide (LPS)-induced elevation of brain prostaglandin E2 (PGE2) synthesis in rats
*iNOS↓, curcumin pretreatment decreased NOS activity in the ischemic rat model
*NO↓, curcumin has been shown to decrease NOS expression and NO production in rat brain tissue
*IL2↓, IL-2 is a cytokine that is anti-inflammatory. Numerous studies have shown that curcumin increases the secretion of IL-2
*IL4↓, curcumin reduced levels of IL-4
*IL6↓, Numerous studies have shown that curcumin in neurodegenerative events attenuates IL-6 production
*INF-γ↓, curcumin reduced the production of INF-γ, as pro-inflammatory cytokine
*GSK‐3β↓, Furthermore, previous findings have confirmed that inhibition of GSK-3β or CREB activation by curcumin has reduced the production of pro-inflammatory mediators under different conditions
*STAT↓, Inhibition of GSK-3β by curcumin has been found to result in reduced STAT activation
*GSH↑, chronic curcumin therapy increased glutathione levels in primary cultivated rat cerebral cortical cells
*MDA↓, multiple doses of 5, 10, 40 and 60 mg/kg) in rodents will inhibit neurodegenerative agent malicious effects, and reduce the amount of MDA and lipid peroxidation in brain tissue
*lipid-P↓,
*SOD↑, Curcumin induces increased production of SOD, glutathione peroxidase (GPx), CAT, and glutathione reductase (GR) activating antioxidant defenses
*GPx↑,
*Catalase↑,
*GSR↓,
*LDH↓, Curcumin decreased lactate dehydrogenase, lipoid peroxidation, ROS, H2O2 and inhibited Caspase 3 and 9
*H2O2↓,
*Casp3↓,
*Casp9↓,
*NRF2↑, ncreased mitochondrial uncoupling protein 2 and increased mitochondrial biogenesis. Nuclear factor-erythroid 2-related factor 2 (Nrf2)
*AIF↓, Curcumin treatment decreased the number of AIF positive nuclei 24 h after treatment in the hippocampus,
*ATP↑, curcumin in hippocampal cells induced an increase in mitochondrial mass leading to increased production of ATP with major improvements in mitochondrial efficiency

5070-

dietSTF,

A review of fasting effects on the response of cancer to chemotherapy

Review,

Var,

chemoP↑, Studies suggest that fasting before or during chemotherapy may induce differential stress resistance, reducing the adverse effects of chemotherapy and enhancing the efficacy of drugs.
ChemoSen↑,
*DNArepair↑, (1) repairing DNA damage in normal tissues (but not tumor cells);
*Apoptosis↓, preventing apoptosis-mediated damage to normal cells;
*CD8+↑, depleting regulatory T cells and improving the stimulation of CD8 cells;
UPR↑, accumulating unfolded proteins and protecting cancer cells from immune surveillance
eff↝, discuss how ‘fasting-mimicking diet’ as a modified form of fasting enables patients to eat a low calorie, low protein, and low sugar diet while achieving similar metabolic outcomes of fasting.
TumAuto↑, upregulating autophagy flux as a protection against damage to organelles and some cancer cells;

3206-

EGCG,

Insights on the involvement of (-)-epigallocatechin gallate in ER stress-mediated apoptosis in age-related macular degeneration

Review,

AMD,

*Ca+2↓, EGCG restores [Ca2+]i homeostasis by decreasing ROS production through inhibition of prohibitin1 which regulate ER-mitochondrial tether site and inhibit apoptosis.
*ROS↓,
*Apoptosis↓,
*GRP78/BiP↓, EGCG downregulated GRP78, CHOP, PERK, ERO1α, IRE1α, cleaved PARP, cleaved caspase 3, caspase 12 and upregulated expression of calnexinin MRPE cells
*CHOP↓,
*PERK↓,
*IRE1↓,
*p‑PARP↓,
*Casp3↓,
*Casp12↓,
*ER Stress↓,
*UPR↓, EGCG mitigates ER stress; maintain calcium homeostasis and inhibition of UPR to control the progression of AMD.

1974-

EGCG,

Protective Effect of Epigallocatechin-3-Gallate in Hydrogen Peroxide-Induced Oxidative Damage in Chicken Lymphocytes

in-vitro,

Nor,

0, 22.5, 45, and 90 μM

*ROS↓, suppressed the increase in intracellular reactive oxygen species (ROS), nitric oxide (NO),
*NO↓,
*MMP↑, preincubation of the cells with EGCG increased mitochondrial membrane potential (MMP) and reduced calcium ion ([Ca2+]i) load.
*i-Ca+2↓, EGCC Increased Mitochondrial Membrane Potential and Decreased [Ca2+]i
*HO-1↑, expression of SOD, Heme oxygenase-1 (HO-1), Catalase (CAT), GSH-PX, nuclear factor erythroid 2-related factor 2 (Nrf2), and thioredoxin-1 (Trx-1).
*Catalase↑,
*NRF2↑,
*Trx1↑,
*antiOx↑, EGCC Increased Antioxidant Capacity
*SOD↑, EGCC Decreased ROS and Increased SOD Generation
*Apoptosis↓,

2395-

EGCG,

EGCG inhibits diabetic nephrophathy through up regulation of PKM2

Study,

Diabetic,

*PKM2↑, pigallocatechin (EGCG), isolated from Green tea, increases Pyruvate kinase M2 (PKM2) expression, decreases toxic glucose metabolites, mitochondrial dysfunction and apoptosis, augments glycolytic flux and PGC-1α levels
*Apoptosis↓,
*PGC-1α↑,

2150-

Ex,

Roles and molecular mechanisms of physical exercise in cancer prevention and treatment

Review,

Var,

eff↓, Physical exercise should be considered an important intervention to prevent and treat cancer and its complications.
Dose↝, Sensitivity to physical exercise varies in different cancers; we provide evidence for the exercise type and strength in various cancers and in differing stages.
TumCP↓, nhibiting cancer cell proliferation and inducing apoptosis and regulating metabolism and the immune environment are the main mechanisms of the benefits of physical exercise in cancer prevention and treatment.
Apoptosis↓,
ChemoSen↑, Graphic Abstract
chemoP↑, Graphic Abstract

2841-

FIS,

Fisetin, an Anti-Inflammatory Agent, Overcomes Radioresistance by Activating the PERK-ATF4-CHOP Axis in Liver Cancer

in-vitro,

Nor,

RAW264.7

LPS-induced Raw264.7 cells

in-vitro,

Liver,

HepG2

10, 25, 100, and 200 μM, 24 h

in-vitro,

Liver,

Hep3B

in-vitro,

Liver,

HUH7

*Inflam↓, fisetin reduced the LPS-induced production of pro-inflammation markers, such as TNF-α, IL-1β, and IL-6, demonstrating the anti-inflammatory effects of fisetin
*TNF-α↓,
*IL1β↓,
*IL6↓,
Apoptosis↓, fisetin induced apoptotic cell death and ER stress through intracellular calcium (Ca2+) release, the PERK-ATF4-CHOP signaling pathway, and induction of GRP78 exosomes.
ER Stress↑,
Ca+2↑,
PERK↑, inducing the GRP78-PERK-ATF4-CHOP pathway in fisetin-treated radioresistant liver cancer cells.
ATF4↑, fisetin treatment of HepG2 and Hep3B cells resulted in the upregulation of ATF4 and CHOP in a time-dependent manner
CHOP↑,
GRP78/BiP↑,
tumCV↓, fisetin decreased the cell viability and increased LDH activity in HepG2, Hep3B, and Huh7 cells in a concentration-dependent manner
LDH↑,
Casp3↑, caspase-3 activity was significantly enhanced
cl‑Casp3↑, fisetin treatment significantly increased the pro-apoptotic markers, including cleaved caspase-3, caspase-8, and caspase-9
cl‑Casp8↑,
cl‑Casp9↑,
p‑eIF2α↑, fisetin treatment increased CHOP, p-eIF2α, ATF4, p-PERK, and GRP78 levels
RadioS↑, Radiation Combined with Fisetin Overcomes Radioresistance

3723-

Gb,

Can We Use Ginkgo biloba Extract to Treat Alzheimer’s Disease? Lessons from Preclinical and Clinical Studies

Review,

AD,

*memory↑, GBE displayed generally consistent anti-AD effects in animal experiments, and it might improve AD symptoms in early-stage AD patients after high doses and long-term administration.
*antiOx↑, Antioxidant properties
*Casp3↓, ↓caspase-3
*APP↓, ↓APP
*AChE↓, ↓AChE activity
*Aβ↓, ↓Aβ oligomers
*5HT↑, ↑5-HT in the striatum
*SOD↓, ↓SOD ↓MDA ↓NO
*MDA↓,
*NO↓,
*GSH↑, ↓SOD ↑GSH ↓MDA
*Bcl-2↑, ↑Bcl-2 ↓Bax
*BAX↑,
*TNF-α↓, ↓TNF-α, IL-1β, ccl-2, iNOS, and IL-10
*IL1β↑,
*iNOS↓,
*IL10↓,
*p‑tau↓, ↓tau phosphorylation
*ROS↓, ↓ROS
*MAOB↓, ↓MAO-B enzyme activity
*cognitive↑, A total of 819 patients who had been diagnosed with AD, or that had AD-like symptoms, received lower SKT scores after GBE treatment for 12 to 24 weeks
*neuroP↑, Neuroprotective Mechanism Analysis
*Apoptosis↓, GBE Inhibits Cell Apoptosis

4247-

GI,

6-Shogaol from Dried Ginger Protects against Intestinal Ischemia/Reperfusion by Inhibiting Cell Apoptosis via the BDNF/TrkB/PI3K/AKT Pathway

vitro+vivo,

NA,

*BDNF↑, activating BDNF/TrkB/PI3K/AKT signaling pathway and inhibiting II/R-induced cell apoptosis. The outcome is further validated both in vivo and in vitro.
*TrkB↑,
*PI3K↑,
*Akt↑,
*Apoptosis↓,
*Inflam↓, dried ginger, behaviors multiple biological activities, including anti-inflammation, antioxidation, and anti-apoptosis.
*antiOx↑,

Showing Research Papers: 1 to 50 of 117
Page 1 of 3 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 117

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

4-HNE↓, 1, antiOx↓, 1, antiOx↑, 14, Catalase↑, 6, Ferroptosis↓, 1, GPx↓, 1, GPx↑, 5, GSH↑, 5, GSR↓, 1, H2O2↓, 1, HO-1↑, 4, lipid-P↓, 6, MDA↓, 8, NOX4↓, 1, NRF2↑, 7, ROS↓, 20, SIRT3↑, 1, SOD↓, 1, SOD↑, 6, TBARS↓, 1, Trx1↑, 1, UCPs↑, 1, uricA↓, 1, VitC↑, 1,

Mitochondria & Bioenergetics ⓘ

AIF↓, 1, ATP↑, 1, ATP∅, 1, MMP↓, 1, MMP↑, 4, mtDam↓, 1, PGC-1α↑, 1, UCP1↓, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 3, AMPK↑, 2, p‑AMPK↑, 1, BUN↓, 1, GlucoseCon↑, 1, Glycolysis↑, 1, LDH↓, 3, PKM2↑, 1, PPARγ↑, 1, SIRT1↑, 1,

Cell Death ⓘ

Akt↑, 3, p‑Akt↑, 1, Apoptosis↓, 34, BAX↓, 2, BAX↑, 1, Bax:Bcl2↓, 1, Bcl-2↑, 2, Casp12↓, 1, Casp3↓, 4, cl‑Casp3↓, 3, Casp9↓, 1, Cyt‑c↓, 2, Fas↓, 1, Ferroptosis↓, 1, iNOS↓, 5, JNK↓, 1, necrosis↓, 1, TRPV1↑, 1,

Transcription & Epigenetics ⓘ

other↓, 1, other↑, 2, other↝, 1,

Protein Folding & ER Stress ⓘ

CHOP↓, 1, ER Stress↓, 3, GRP78/BiP↓, 1, HSP90↑, 1, IRE1↓, 1, PERK↓, 1, UPR↓, 1,

DNA Damage & Repair ⓘ

ATM↑, 1, DNAdam↓, 1, DNArepair↑, 1, p‑PARP↓, 1, cl‑PARP1↓, 1,

Proliferation, Differentiation & Cell State ⓘ

CD34↑, 1, p‑ERK↑, 2, FOXO1↑, 1, FOXO3↑, 1, GSK‐3β↓, 2, HDAC↓, 1, mTOR↓, 1, P70S6K↓, 1, PI3K↑, 1, STAT↓, 1, TRPM7↓, 2, TRPM7⇅, 1,

Migration ⓘ

AntiAg↑, 2, APP↓, 3, Ca+2↓, 1, Ca+2↝, 1, i-Ca+2↓, 1, CD31↑, 2, N-cadherin↑, 2, ZO-1↓, 1, α-SMA↓, 1,

Angiogenesis & Vasculature ⓘ

angioG↑, 1, Hif1a↑, 1, NO↓, 7, VEGF↑, 2,

Barriers & Transport ⓘ

BBB↓, 1, BBB↑, 2,

Immune & Inflammatory Signaling ⓘ

COX2↓, 4, IFN-γ↓, 1, IKKα↓, 1, IL1↓, 1, IL10↓, 1, IL17↓, 1, IL18↓, 1, IL1β↓, 4, IL1β↑, 1, IL2↓, 1, IL4↓, 1, IL6↓, 2, Imm↑, 1, INF-γ↓, 1, Inflam↓, 16, NF-kB↓, 3, PGE2↓, 2, TNF-α↓, 5,

Synaptic & Neurotransmission ⓘ

5HT↓, 1, 5HT↑, 1, AChE↓, 4, BDNF↑, 1, p‑tau↓, 2, TrkB↑, 1,

Protein Aggregation ⓘ

Aβ↓, 5, BACE↓, 1, MAOB↓, 2, NLRP3↓, 2,

Hormonal & Nuclear Receptors ⓘ

GR↑, 1,

Drug Metabolism & Resistance ⓘ

BioAv↑, 4, BioAv↝, 2, Half-Life↝, 1,

Clinical Biomarkers ⓘ

ALAT↓, 3, ALP↓, 1, AST↓, 4, creat↓, 1, IL6↓, 2, LDH↓, 3,

Functional Outcomes ⓘ

AntiAge↑, 1, AntiCan↑, 1, AntiDiabetic↑, 2, AntiTum↑, 2, cachexia↓, 1, cardioP↑, 4, cognitive↑, 10, hepatoP↑, 5, memory↑, 4, Mood↑, 1, motorD↑, 2, neuroP↑, 16, Obesity↓, 1, Pain↓, 1, RenoP↑, 5, Risk↓, 1, toxicity↓, 1, toxicity↝, 1,

Infection & Microbiome ⓘ

Bacteria↓, 3, CD8+↑, 1,
Total Targets: 160

Scientific Paper Hit Count for: Apoptosis, Apoptosis

6 Magnetic Fields
6 Quercetin
6 Thymoquinone
6 Urolithin
5 Hydrogen Gas
5 Lycopene
4 Ashwagandha(Withaferin A)
4 Carvacrol
3 Berberine
3 Betulinic acid
3 EGCG (Epigallocatechin Gallate)
3 Resveratrol
3 Shikonin
3 Taurine
2 Allicin (mainly Garlic)
2 Alpha-Lipoic-Acid
2 Astaxanthin
2 Baicalein
2 Boron
2 Honokiol
2 Luteolin
2 Parthenolide
2 Selenium NanoParticles
2 Silymarin (Milk Thistle) silibinin
2 Vitamin K2
1 5-Hydroxytryptophan
1 Auranofin
1 Acetyl-l-carnitine
1 Amodiaquine
1 Apigenin (mainly Parsley)
1 Artemisinin
1 Melatonin
1 borneol
1 Caffeic acid
1 Paclitaxel
1 Carnosic acid
1 Capsaicin
1 Celecoxib
1 Chlorogenic acid
1 Chlorophyllin
1 Chrysin
1 Coenzyme Q10
1 Crocetin
1 Copper and Cu NanoParticles
1 chemodynamic therapy
1 Curcumin
1 diet Short Term Fasting
1 Exercise
1 Fisetin
1 Ginkgo biloba
1 Ginger/6-Shogaol/Gingerol
1 γ-linolenic acid (Borage Oil)
1 hydrogen sulfide
1 HydroxyCitric Acid
1 Orlistat
1 Huperzine A/Huperzia serrata
1 Lutein
1 Mushroom Lion’s Mane
1 nicotinamide adenine dinucleotide
1 Naringin
1 Nimbolide
1 Phenylbutyrate
1 Phenethyl isothiocyanate
1 Rosmarinic acid
1 Sulfasalazine
1 Cisplatin
1 Radiotherapy/Radiation
1 Docosahexaenoic Acid
1 Vitamin B3,Niacin

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#:14  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

Apoptosis Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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