Apoptosis Cancer Research Results
Apoptosis, Apoptosis: Click to Expand ⟱
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| 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.
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Scientific Papers found: Click to Expand⟱
*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].
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
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
*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.
*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
*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
*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
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.
*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
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in-vitro, |
GBM, |
U87MG |
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in-vitro, |
GBM, |
U251 |
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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.
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Review, |
AD, |
NA |
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Review, |
Park, |
NA |
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*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
*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↓,
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in-vitro, |
Nor, |
NRK52E |
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in-vivo, |
NA, |
NA |
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*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.
*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
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
BC, |
T47D |
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in-vitro, |
Nor, |
MCF10 |
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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
*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).
*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.
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Review, |
AD, |
NA |
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Review, |
Stroke, |
NA |
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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↓,
*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↑,
*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↓,
*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↓,
*cardioP↑, BCP mitigated cardiac markers and lipid peroxidation whereas intensified antioxidant capacity.
*lipid-P↓,
*antiOx↑,
*NRF2↑, BCP activated Nrf2, with subsequent HO1 and NQO1 amplification.
*HO-1↑,
*NQO1↑,
*TLR4↓, inhibited TLR4/NFκB pathways with subsequent enhanced anti-oxidative capacity and diminished inflammatory and apoptosis responses.
*NF-kB↓,
*Inflam↓,
*Apoptosis↓,
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in-vivo, |
Nor, |
NA |
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in-vivo, |
Stroke, |
NA |
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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
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in-vitro, |
Nor, |
HUVECs |
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in-vitro, |
Nor, |
MEF |
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*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
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
*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↑,
*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↓,
*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↓,
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Review, |
Var, |
NA |
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Park, |
NA |
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AD, |
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AntiCan↑, Numerous experimental studies demonstrated pharmacological properties of α-Bisabolol including anticancer, antinociceptive, neuroprotective, cardioprotective, and antimicrobial.
*neuroP↑,
*cardioP↑,
*AntiBio↑,
*BioAv↑, Given the polypharmacological effects and pleiotropic properties, along with favorable pharmacokinetics, and dietary availability and safety, α-Bisabolol can be used as a dietary agent, nutraceutical or phytopharmaceutical agent or as an adjuvant wit
*toxicity↓,
*BioAv↑, integrated in many cosmetic formulations due to its skin soothing effects, well documented dermal absorption
*motorD↑, improvement in locomotor activity, a reduction in the expression of thiol and a reinstate of the activity of mitochondrial complex-I.
*SOD↑, α-Bisabolol also increased the mRNA level of antioxidants proteins such as superoxide dismutase (SOD), catalase (CAT), and the keap1 gene product.
*Catalase↑,
*Keap1↑,
*MDA↓, α-Bisabolol attenuated oxidative insult by reducing malondialdehyde (MDA), restoring depleted glutathione (GSH) and improving SOD and CAT activity.
*GSH↑,
*IL1β↓, attenuated neuroinflammation by reducing glial cells activation and subsequent release of proinflammatory cytokines (IL-1β, IL-6 and TNF-α) and mediators (iNOS and COX-2).
*IL6↓,
*TNF-α↓,
*iNOS↓,
*COX2↓,
*lipid-P↓, α-Bisabolol restored mitochondrial function by preventing mitochondrial lipid peroxidation, cytochrome-C release and most importantly preserving Complex-I activity
*Cyt‑c↓,
*ROS↓, The study concluded that α-Bisabolol safeguarded against the induced upsurge of ROS and nitrite.
*MMP↑, α-Bisabolol treatment also restored mitochondrial membrane potential (MMP) validating its antioxidant effect.
*antiOx↑,
*AChE↓, showed a significant reduction in AChE activity and an ability to avert Ach depletion.
*Apoptosis↓, α-Bisabolol protected cells from Aβ triggered apoptosis by reducing Bax and Caspase-3 and increasing Bcl-2 activity.
*BAX↓,
*Casp3↓,
*Bcl-2↑,
*BACE↓, α-Bisabolol inhibitory activity on BACE1 and found a decrease in BACE1 activity following α-Bisabolol treatment
*BChE↓, AChE, BuChE, β-secretase actions were decreased significantly in cells pretreated with α-Bisabolol
*eff↑, The compound clearly illustrated a potent anti-AchE activity of 95.869% similar to the activity of donepezil, a standard drug. I
*Aβ↓, The compound also disaggregated Aβ25–35 peptide and protected against its induced toxicity by increasing neuro2a cells viability [
*ATP↑, figure 2
RadioS↑, α-Bisabolol and Anticancer Effects, figure 3
Cyt‑c↑,
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↑,
PARP↑,
BAX↑,
BID↑,
NF-kB↑,
Fas↑,
EGFR↑,
TIMP2↑,
XIAP↓,
COX2↓,
Bak↓,
Bcl-2↓,
P53↑, The expression of p53 (a transcription factors whose products might lead to apoptosis), NF-κB and Fas was increased following α-Bisabolol treatment, indicating their function in mediating α-Bisabolol-induced apoptosis in the cancer cell line.
HER2/EBBR2↓,
FGF↓,
CEA↓,
Akt↓,
TumCCA↑, α-Bisabolol suppresses the cellular proliferation at G2/M cell cycle phase.
*Imm↑, reported that α-Bisabolol boosted the immunity response by T-cell subsets (CD4 and CD8) supplementation in treated mice.
*CD4+↑,
*CD8+↑,
*BBB↑, ↑ BBB penetration
*Pain↓, α-Bisabolol based mouthwash to that of chlorhexidine in reducing pain during brushing
*cardioP↑, α-Bisabolol and Cardioprotection, figure 5
*TBARS↓, rats co-treated with α-Bisabolol showed reduced LOOH and TBARS and increased SOD, CAT and GSH.
*SOD↑,
*Catalase↑,
*GSH↑,
*AntiBio↑, α-Bisabolol demonstrated an antibacterial effect against Staphylococcus aureus, Escherichia coli and Pseudomonas aeruginosa as well as a synergism against S. aureus, when combined with the antibiotic norfloxacin and against E. coli when combined with
*AntiFungal↑, ↓ fungal growth
*GastroP↑, α-Bisabolol and Gastroprotection. oral administration of α-Bisabolol was realized to attenuate gastric damage and to provide cytoprotection in stomach.
*RenoP↑, The nephroprotective effects of α-Bisabolol and the underlying mechanisms are summarized in Table 10.
*creat↓, ↓ creatinine, urea, uric acid
*uricA↓,
*Inflam↓, Anti-Inflammatory Effects of α-Bisabolol
*iNOS↓, ↓ iNOS, COX-2, TNF-α, p65 PGE2, nitrite, IL-6, ↓ MMP13
*COX2↓,
*TNF-α↓,
*IL6↑,
*MMP13↓,
TumCG↓, α-Bisabolol hinders the growth of MCF-7 human breast cancer cells and decipher its molecular mechanisms of reducing cell proliferation and promoting apoptosis.
TumCP↓,
Apoptosis↓,
ROS↑, This treatment led to the suppression of cell growth, an elevation in the generation of reactive oxygen species (ROS) and the initiation of apoptosis.
Bcl-2↓, cell treated with α-Bisabolol exhibited reduced levels of the cell survival gene Bcl-2, alongside elevated levels of the pro-apoptotic genes Bax, Bad, Caspase-3, Caspase-9, and cytochrome c.
BAX↑,
BAD↑,
Casp3↑,
Casp9↑,
Cyt‑c↑,
NF-kB↓, Meanwhile, NF-κB, p-PI3K, and p-Akt proteins were downregulated in α-Bisabolol treated cells.
p‑PI3K↓,
p‑Akt↓,
*lipid-P↓, BSB treatment efficiently attenuates lipid peroxidation, preventing the depletion of antioxidants.
*antiOx↑,
*Apoptosis↓, Additionally, BSB treatment was observed to inhibit apoptosis and have a positive impact on cellular signaling pathways, regulating inflammation and preserving histological integrity.
*Inflam↓,
| - |
in-vitro, |
Lung, |
A549 |
|
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- |
in-vitro, |
Cerv, |
HeLa |
|
|
|
TumCG↑, caffeine promoted the growth of cancer cells treated with paclitaxel
TumCMig↓,
Apoptosis↓,
ac‑α-tubulin↑,
| - |
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],
*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
| - |
Review, |
Var, |
NA |
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- |
Review, |
Stroke, |
NA |
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- |
Review, |
Diabetic, |
NA |
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- |
Review, |
Park, |
NA |
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*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↓,
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.
*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↓,
*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↓,
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↓,
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↝,
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↑,
| - |
Review, |
AD, |
NA |
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- |
Review, |
Stroke, |
NA |
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*cognitive↑, All the studies showed a positive effect of citicoline on cognitive functions.
*Ach↑, (CDP) choline. It increases the intrasynaptic concentration of acetylcholine and promotes phospholipid synthesis and neuronal repair, as shown in different studies in animals [
*Apoptosis↓, it can inhibit apoptosis associated with cerebral ischemia and several models of neurodegeneration, as demonstrated in studies in vitro or in animals
*neuroP↑, It has neuroprotective properties, as shown in studies performed in vitro or in animal models, that have been shown in different patterns of cognitive impairment, Parkinson’s disease or dementia
*memory↑, it improved human psychomotor vigilance, arousal and visual working memory with significant amelioration of oxidative stress after two weeks of being administered in healthy volunteers
| - |
Review, |
Nor, |
NA |
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- |
Review, |
Var, |
NA |
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- |
Review, |
AD, |
NA |
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*antiOx↑, Chrysin exhibits a range of biological activities, including antioxidant, anti-inflammatory, anticancer, neuroprotective, and anxiolytic effects.
*Inflam↓,
AntiCan↑,
*neuroP↑, exhibits neuroprotective effects in neurological disorders such as epilepsy, neuronal apoptosis, neuroinflammation [80], anxiety [81], depression [82], multiple sclerosis [83], Parkinson’s disease, Alzheimer’s disease, cognitive deficits,
*ROS↓, facilitate the neutralization of free radicals
*BioAv↓, Despite its therapeutic potential, chrysin’s bioavailability is significantly limited due to poor aqueous solubility and rapid metabolism in the gastrointestinal tract and liver, which reduces its systemic efficacy.
*BioAv↑, Ongoing research aims to enhance chrysin’s bioavailability through the development of delivery systems such as lipid-based carriers and nanoparticles.
*cardioP↑, Chrysin exerts cardioprotective effects by modulating certain cellular signaling pathways involved in inflammation, oxidative stress [66]
*COX2↓, it suppresses cyclooxygenase-2 (COX-2), an enzyme involved in prostaglandin synthesis that promotes inflammation
*TNF-α↓, inhibits phosphorylation and degradation of IκB-α, as well as the translocation of NF-κB, and reduces levels of TNF-α and IL-1β by inhibiting NF-κB expression
*IL1β↓,
*NF-kB↓,
*lipid-P↓, Chrysin protects against ROS by reducing lipid peroxidation levels in the liver and increasing both enzymatic and non-enzymatic antioxidant levels
*Apoptosis↓, chrysin counteracted oxidative stress, reduced neuronal apoptosis, and increased expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) [80].
*NRF2↑,
*HO-1↑,
*MDA↓, In rat models, chrysin was shown to lower serum corticosterone and malondialdehyde (MDA) levels while increasing glutathione (GSH), superoxide dismutase (SOD), glutathione peroxidase (Gpx), glutathione reductase (GR), and catalase (CAT).
*GSH↑,
*SOD↑,
*GPx↑,
*GSR↑,
*Catalase↑,
*5HT↑, Moreover, chrysin increased serotonin (5-HT) levels and reduced the activity of indoleamine 2,3-dioxygenase.
*Casp3↓, It also decreased the expression of caspases-3 and -9 [97,98].
*Casp9↓,
TumCCA↑, it causes cell cycle arrest in cancer cells, reduces expression of MAPK and PI3K/Akt signaling pathways, and disrupts overall cell proliferation
MAPK↓,
PI3K↓,
Akt↓,
TumCP↓,
TET1↑, chrysin promoted TET1 and 5-hydroxymethylcytosine expression, which stimulated apoptosis and disrupted the migration of gastric cancer cells
TLR4↓, Chrysin’s effects in lung cancer include decreasing the expression of TLR4 and Myd88 in the signaling cascade from activated receptor to the cell interior.
HER2/EBBR2↓, pyrotinib combined with chrysin, it was confirmed that adding chrysin positively enhanced the inhibition of HER2-positive breast cancer growth both in vitro and in vivo,
HK2↓, As HK-2 levels decreased, chrysin inhibited glycolysis (which impairs glucose uptake and lactate production) in the tumor and activated mitochondria-related apoptosis
Glycolysis↓,
glucose↓,
lactateProd↓,
ROS↑, chrysin was shown to promote the generation of reactive oxygen species (ROS) and reduce mTOR expression, thereby stimulating autophagy [127]
mTOR↓,
TumAuto↑,
tumCV↓, chrysin significantly reduces cell viability by inducing ER stress through stimulation of UPR, PERK, ATF4, and eIF2α
ER Stress↑,
UPR↑,
PERK↑,
ATF4↑,
eIF2α↑,
BioAv↑, Solid Lipid Nanoparticles (SLNs) High biocompatibility and low toxicity due to the use of physiological lipids.
TumCG↓, report that chrysin inhibits hepatoma cells growth and induces apoptosis in a dose-dependent manner.
Apoptosis↓,
GRP78/BiP↑, Chrysin induces GRP78 overexpression, X-box binding protein-1 splicing and eukaryotic initiation factor 2α phosphorylation, hallmarks of the unfolded protein response.
eff↑, GRP78 knockdown potentiates chrysin-induced caspase-7 cleavage in hepatoma cells and enhances chrysin-induced apoptosis.
cl‑Casp7↑,
cl‑PARP↑, Combination of EGCG potentiates chrysin-induced caspase-7 and poly (ADP-ribose) polymerase (PARP) cleavage.
eff↑, Finally, EGCG sensitizes hepatoma cells to chrysin through caspase-mediated apoptosis
UPR↑, data suggest that chrysin triggers the unfolded protein response. Chrysin induces the unfolded protein response
ER Stress↑, Chrysin can induce ER stress response in hepatoma cells, including up-regulation of GRP78 expression, induction of eIF-2α phosphorylation and XBP-1 splicing.
p‑eIF2α↑,
XBP-1↝,
Proteasome↓, Chrysin is a known proteasome inhibitor [27]
| - |
Review, |
Park, |
NA |
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- |
Review, |
Stroke, |
NA |
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|
|
*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
| - |
in-vivo, |
AD, |
NA |
|
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- |
in-vivo, |
Park, |
NA |
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|
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*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↓,
*antiOx↑, Chicoric acid (CA) is a natural antioxidant with promising hepatoprotective activity.
*hepatoP↑,
*ROS↓, Pre-treatment with CA suppressed reactive oxygen species and lipid peroxidation and enhanced antioxidants in MTX-induced rats.
*lipid-P↓,
*TAC↑,
*NRF2↑, CA upregulated hepatic Nrf2, HO-1, NQO-1, and PPARγ, and attenuated inflammation.
*HO-1↑,
*NQO1↑,
*PPARγ↑,
*Inflam↓,
*Apoptosis↓, CA inhibited apoptosis by increasing Bcl-2 expression and suppressing Bax, cytochrome c, and caspase-3 in MTX-administered rats.
*Bcl-2↑,
*BAX↓,
*Cyt‑c↓,
*Casp3↓,
*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↓,
TumCP↓, results demonstrated that crocin significantly inhibited the proliferation, migration, and invasion of GC cells while promoting apoptosis.
TumCMig↓,
TumCI↓,
Apoptosis↓,
antiOx↓, crocin treatment were predominantly enriched in pathways associated with oxidative stress and ferroptosis
Ferroptosis↑,
NRF2↑, crocin facilitated the translocation of Nrf2 from the nucleus to the cytoplasm.
P53↑, crocin suppresses lung adenocarcinoma cell proliferation by upregulating p53, inducing cell cycle arrest and apoptosis, and increasing sensitivity to chemotherapeutic agents such as cisplatin and pemetrexed
TumCCA↑,
ChemoSen↑,
EMT↓, crocin inhibits the migration, invasion, and epithelial-mesenchymal transition of GC cells through the miR-320/KLF5/HIF-1α signaling pathway
Hif1a↓,
ROS↑, Ferroptosis, a regulated form of iron-dependent cell death, is characterized by the accumulation of intracellular iron, elevated reactive oxygen species (ROS) production,
tumCV↓, while crocin restrained the HCT-116 cells vitality, proliferation and the expression of Ki-67, while inducing apoptosis in a concentration-dependent manner.
TumCP↓,
Ki-67↓,
Apoptosis↓,
Inflam↓, inflammation- and oxidative- related factors in HCT-116 cells were largely blunted by crocin that enhanced ROS, restrained the MMP and suppressed p-JAK2/JAK2, p-STAT3/STAT3, and p-ERK/ERK expression
ROS↑,
MMP↓,
JAK2↓,
STAT3↓,
ERK↓,
MIP2↓, we found that crocin manifested an obvious inhibition of the contents of MIP-2, IL-6, MCP-1, IL-8, IL-1β, and TNF-α in HCT-116 cells in relative to the control group and the inhibitory effect of 200 μM
IL6↓,
MCP1↓,
IL8↓,
IL1β↓,
TNF-α↓,
SOD↓, oxidative stress-related factors and confirmed that the contents of SOD, CAT, and GSH in HCT-116 cells were reduced by crocin in relative to the control group and the 200 μM
Catalase↓,
GSH↓,
ROS↑, crocin exhibited a notable increase production of ROS in HCT-116 cells
mtDam↑, crocin is inducing oxidative stress and damaging the mitochondria, leading to cell death.
Showing Research Papers: 1 to 50 of 142
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 142
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↓, 1, Catalase↓, 1, Ferroptosis↑, 1, GSH↓, 1, NRF2↑, 1, ROS↓, 1, ROS↑, 11, ROS↝, 1, mt-ROS↑, 1, SOD↓, 1, TrxR↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP↓, 5, mtDam↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 1, cMyc↓, 1, glucose↓, 1, Glycolysis↓, 1, HK2↓, 1, lactateProd↓, 1, PDK1↓, 1, PI3k/Akt/mTOR↝, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 2, p‑Akt↓, 1, Apoptosis↓, 17, Apoptosis↑, 1, BAD↑, 1, Bak↓, 1, BAX↑, 4, Bax:Bcl2↑, 1, Bcl-2↓, 6, Bcl-2↑, 1, BID↑, 1, Casp↑, 2, Casp12↑, 1, Casp3↓, 1, Casp3↑, 4, Casp7↑, 1, cl‑Casp7↑, 1, Casp8↑, 2, Casp9↑, 5, Cyt‑c↑, 5, Fas↑, 2, Ferroptosis↑, 1, MAPK↓, 2, Necroptosis↑, 1, p‑p38↑, 1, Proteasome↓, 1, survivin↓, 1, TumCD↑, 1,
Kinase & Signal Transduction(tgid=6) ⓘ
HER2/EBBR2↓, 2,
Transcription & Epigenetics(tgid=7) ⓘ
tumCV↓, 4,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP↑, 1, eIF2α↑, 2, p‑eIF2α↑, 1, ER Stress↑, 3, GRP78/BiP↑, 2, PERK↑, 1, UPR↑, 2, XBP-1↝, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
BNIP3↑, 1, TumAuto↑, 2,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 3, P53↑, 2, PARP↑, 1, cl‑PARP↑, 4, γH2AX↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK4↓, 2, cycD1/CCND1↓, 2, cycE/CCNE↑, 1, P21↑, 1, TumCCA↑, 7,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
EMT↓, 2, ERK↓, 2, p‑ERK↓, 1, FGF↓, 1, mTOR↓, 1, NOTCH↓, 1, PI3K↓, 2, p‑PI3K↓, 1, STAT3↓, 1, TOP1↓, 1, TumCG↓, 4, TumCG↑, 1,
Migration(tgid=13) ⓘ
CEA↓, 1, Ki-67↓, 1, MMP2↓, 1, MMP9↓, 1, TET1↑, 1, TIMP2↑, 1, TumCI↓, 3, TumCMig↓, 4, TumCP↓, 6, TumMeta↓, 1, ac‑α-tubulin↑, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, ATF4↑, 1, EGFR↑, 1, Hif1a↓, 2, VEGF↓, 1,
Barriers & Transport(tgid=15) ⓘ
GLUT1↑, 1, P-gp↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2↓, 2, IKKα↓, 1, IL1β↓, 1, IL6↓, 2, IL8↓, 1, Inflam↓, 2, Inflam↝, 1, JAK2↓, 1, MCP1↓, 1, MIP2↓, 1, NF-kB↓, 4, NF-kB↑, 1, TLR4↓, 1, TNF-α↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 1, BioEnh↑, 1, ChemoSen↑, 3, Dose↓, 1, Dose↝, 1, eff↓, 2, eff↑, 5, eff↝, 1, RadioS↑, 1, selectivity↑, 2,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 1, CEA↓, 1, EGFR↑, 1, HER2/EBBR2↓, 2, IL6↓, 2, Ki-67↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↓, 1, AntiCan↑, 3, AntiTum↑, 3, chemoP↑, 1, fatigue↓, 1, memory↑, 1, neuroP↑, 1, OS↝, 1, QoL↑, 1, Weight↑, 1,
Total Targets: 142
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
AntiBio↑, 2,
Redox & Oxidative Stress(tgid=1) ⓘ
4-HNE↓, 1, antiOx↓, 1, antiOx↑, 16, Catalase↑, 8, Ferroptosis↓, 1, GPx↓, 1, GPx↑, 5, GSH↑, 7, GSR↑, 1, HO-1↑, 6, Keap1↑, 1, lipid-P↓, 10, MDA↓, 9, NOX4↓, 1, NQO1↑, 2, NRF2↑, 9, ROS↓, 20, SIRT3↑, 1, SOD↑, 7, TAC↑, 1, TBARS↓, 2, UCPs↑, 1, uricA↓, 2, VitC↑, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↑, 1, ATP∅, 1, MMP↓, 1, MMP↑, 4, mtDam↓, 2, UCP1↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
ALAT↓, 3, AMPK↑, 2, p‑AMPK↑, 1, BUN↓, 1, GlucoseCon↑, 1, Glycolysis↑, 1, LDH↓, 2, PPARγ↑, 2, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 2, p‑Akt↑, 1, Apoptosis↓, 33, BAX↓, 4, Bax:Bcl2↓, 1, Bcl-2↑, 3, Casp3↓, 4, cl‑Casp3↓, 3, Casp9↓, 1, Cyt‑c↓, 4, Fas↓, 1, Ferroptosis↓, 1, iNOS↓, 5, JNK↓, 1, necrosis↓, 1, TRPV1↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
Ach↑, 1, other↓, 1, other↑, 2, other↝, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↓, 1, HSP90↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
ATM↑, 1, DNAdam↓, 1, cl‑PARP1↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
CD34↑, 1, p‑ERK↑, 2, FOXO1↑, 1, FOXO3↑, 1, GSK‐3β↓, 1, HDAC↓, 1, mTOR↓, 1, P70S6K↓, 1, TRPM7↓, 2, TRPM7⇅, 1,
Migration(tgid=13) ⓘ
AntiAg↑, 2, APP↓, 3, Ca+2↝, 1, CD31↑, 2, MMP13↓, 1, N-cadherin↑, 2, ZO-1↓, 1, α-SMA↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↑, 1, Hif1a↑, 1, NO↓, 4, VEGF↑, 2,
Barriers & Transport(tgid=15) ⓘ
BBB↓, 1, BBB↑, 3, GastroP↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD4+↑, 1, COX2↓, 6, IFN-γ↓, 1, IKKα↓, 1, IL1↓, 1, IL17↓, 1, IL18↓, 1, IL1β↓, 5, IL6↓, 1, IL6↑, 1, Imm↑, 2, Inflam↓, 19, NF-kB↓, 5, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 6,
Synaptic & Neurotransmission(tgid=18) ⓘ
5HT↓, 1, 5HT↑, 1, AChE↓, 4, BChE↓, 1, BDNF∅, 1, p‑tau↓, 1,
Protein Aggregation(tgid=19) ⓘ
Aβ↓, 6, BACE↓, 3, MAOB↓, 1, NLRP3↓, 2,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
GR↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 7, BioAv↝, 2, eff↑, 1, Half-Life↝, 1,
Clinical Biomarkers(tgid=22) ⓘ
ALAT↓, 3, ALP↓, 1, AST↓, 4, creat↓, 2, IL6↓, 1, IL6↑, 1, LDH↓, 2,
Functional Outcomes(tgid=23) ⓘ
AntiAge↑, 1, AntiCan↑, 1, AntiDiabetic↑, 2, AntiTum↑, 2, cachexia↓, 1, cardioP↑, 7, cognitive↑, 9, hepatoP↑, 6, memory↑, 3, Mood↑, 1, motorD↑, 3, neuroP↑, 17, Obesity↓, 1, Pain↓, 2, RenoP↑, 6, Risk↓, 1, toxicity↓, 2,
Infection & Microbiome(tgid=24) ⓘ
AntiFungal↑, 1, Bacteria↓, 3, CD8+↑, 1,
Total Targets: 149
Scientific Paper Hit Count for: Apoptosis, Apoptosis
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
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