LDL Cancer Research Results
LDL, LDL-cholesterol: Click to Expand ⟱
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The relationship between LDL (low-density lipoprotein) cholesterol and cancer is a complex and evolving area of research. LDL cholesterol is often referred to as "bad" cholesterol because high levels are associated with an increased risk of cardiovascular diseases.
Protumorigenic: High levels of LDL cholesterol can promote tumor growth by providing lipids that are essential for cell membrane synthesis and energy production. Additionally, LDL can influence inflammation and angiogenesis, further supporting tumor development.
Antitumorigenic: Some studies suggest that lowering LDL cholesterol through lifestyle changes or medications (like statins) may have a protective effect against certain cancers, although the evidence is not uniform across all cancer types.
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Scientific Papers found: Click to Expand⟱
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*cardioP↑, Epidemiological studies associate regular, moderate intake of blueberries and/or anthocyanins with reduced risk of cardiovascular disease, death, and type 2 diabetes, and with improved weight maintenance and neuroprotection.
*neuroP↑,
*Inflam↓, Among the more important healthful aspects of blueberries are their anti-inflammatory and antioxidant actions and their beneficial effects on vascular and glucoregulatory function
*antiOx↓,
*GutMicro↑, Blueberry phytochemicals may affect gastrointestinal microflora and contribute to host health
*Half-Life↑, However, >50% of the 13C still remained in the body after 48 h
*LDL↓, controlled study of 58 diabetic patients, blueberry intake led to a decline in LDL cholesterol, triglycerides, and adiponectin and an increase in HDL cholesterol
*adiP↓,
*HDL↑,
*CRP↓, reduction was documented in inflammatory markers, including serum high-sensitivity C-reactive protein, soluble vascular adhesion molecule-1, and plasma IL-1β
*IL1β↓,
*Risk↓, lower Parkinson disease risk was associated with the highest quintile of anthocyanin (RR: 0.76) and berry (RR: 0.77) intake
*Risk↓, Nurse's Health Study, greater intake of blueberries and strawberries was associated with slower rates of cognitive decline in older adults, with an estimated delay in decline of about 2.5 y
*cognitive↑, Cognitive performance in elderly adults improved after 12 wk of daily intake of blueberry (94) or Concord grape (95) juice.
*memory↑, Better task switching and reduced interference in memory was found in healthy older adults after 90 d of blueberry supplementation
*other↑, After 12 wk of blueberry consumption, greater brain activity was detected using magnetic resonance imaging in healthy older adults during a cognitive challenge.
*BOLD↑, Similarly, during a memory test, regional blood oxygen level-dependent activity detected by MRI (99) was enhanced in the subjects taking blueberry, but not in those taking placebo.
*NO↓, 50–200 mg/d bilberry showed a dose-dependent decrease in neurotoxic NO and malondialdehyde, combined with an increase in neuroprotective antioxidant capacity due to glutathione, vitamin C, superoxide dismutase, and glutathione peroxidase
*MDA↓,
*GSH↑,
*VitC↑,
*SOD↑,
*GPx↑,
*eff↓, The percentage loss of blueberry anthocyanins during −18°C storage was 12% after 10 mo of storage
*eff↓, Freeze-dried blueberry powder loses anthocyanins in a temperature-dependent manner with a half-life of 139, 39, and 12 d when stored at 25, 42, and 60°C, respectively
*eff↓, Blueberries are low in ascorbic acid and high in anthocyanins (187), and notably anthocyanins are readily degraded by ascorbic acid
*eff↝, Shelf-stable blueberry products like jam (196), juice (197), and extracts (198) can lose polyphenolic compounds when stored at ambient temperature whereas refrigeration mitigates losses.
*Risk↓, It can be safely stated that daily moderate intake (50 mg anthocyanins, one-third cup of blueberries) can mitigate the risk of diseases and conditions of major socioeconomic importance in the Western world.
*LDL↓, Indeed, clinical studies on healthy subjects have evidenced that standardized garlic treatment (900 mg/day) significantly reduces total cholesterol (TC) and low-density lipoprotein cholesterol (c-LDL).
*antiOx↑, Multiple studies have focused on allicin therapeutic potential as an antioxidant (inducing antioxidant product production),
AntiCan↑, anticancer (triggering cancer cells apoptosis and inhibiting tumor growth),
*cardioP↑, cardioprotective (decreasing angiogenesis and inducing vasorelaxation)
*BP↓, Conversely, aged garlic extract supplementation was shown to be more effective than the placebo in lowering systolic blood pressure
*Weight↓, Garlic powder supplementation (800 mg/daily) resulted in a significant decrease in body weight and body fat mass (
NK cell↑, Actually, aged garlic administration in patients with advanced cancer of the digestive system led to an improvement of natural killer (NK) cell activity but did not cause improvement in QoL
*AntiDiabetic↑, Actually, daily garlic allicin supplementation (0.05–1.5 g) displayed a positive and sustained role in blood glucose, total cholesterol (TC), and high/low density lipoprotein (HDL-c/LDL-c) regulation in type 2 diabetes mellitus (T2DM) management
*GSH↑, 2-month application of coated garlic powder tablets (900 mg with alliin and allicin contents of 1.3% and 0.6%, respectively), the glutathione (GSH) concentration significantly increased in circulating human erythrocytes
GSH↓, allicin reacts with GSH
Bacteria↓, Antimicrobial
LDL↓, reduction without altering HDL
ROS↑, antioxidant at low doses
NRF2↑,
cognitive↑, by activating the Nrf2-system
memory↑, by activating the Nrf2-system
BP↓, via H2S generation
RNS↓,
Apoptosis↑, Despite statins’ ability to induce apoptosis or autophagy, arrest cell cycle, or modulate favorable epigenetic reprogramming, their efficacy is highly context-dependent
TumAuto↑,
TumCCA↑,
BioAv↓, Challenges such as statin resistance, low bioavailability and pharmacokinetic variability further complicate their application in oncology.
eff↑, including nanoparticle-based drug delivery systems and combination therapies with chemotherapy, radiotherapy or immunotherapy, appear to help overcome these limitations.
HMGCR↓, statins reduce cholesterol levels by targeting HMGCR
LDL↓,
cardioP↑, statins have become a cornerstone in the management of hypercholesterolemia and the prevention of cardiovascular diseases [23], [24], [25], [26].
AntiTum↑, Notably, while research suggests that statins possess anti-tumor effects, evidence remains conflicting and highly context-dependent
ChemoSen↑, suggest that statins can sensitize cancer cells to chemotherapy and radiotherapy, potentially improving treatment outcomes,
RadioS↑,
toxicity↓, Statins are widely regarded as safe and well-tolerated. However, like any medication, they are not without potential side effects, though these are generally mild [232].
*cardioP↑, atorvastatin is FDA-approved for the prevention of cardiovascular events in patients with cardiac risk factors and abnormal lipid profiles.[1]
*LDL↓, patients should be prescribed high-intensity statin therapy to achieve a ≥50% reduction in low-density lipoprotein cholesterol (LDL-C) and reduce the risk of major adverse cardiovascular events (MACE).
HMG-CoA↓, Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase.[12]
Half-Life↝, Atorvastatin is rapidly absorbed after oral administration with a peak plasma concentration at 1 to 2 hours. The half-life of atorvastatin is about 14 hours, while its active metabolites have a half-life of about 20 to 30 hours.
BioAv↓, The bioavailability is low at 14% due to extensive first-pass metabolism.
Dose↝, Atorvastatin is available as atorvastatin calcium tablets in strengths of 10, 20, 40, and 80 mg. It is also available as an oral suspension in a strength of 20 mg/5 mL.[20]
lipid-P↓, Statins exhibit “pleiotropic” properties that are independent of their lipid-lowering effects.
TumCG↓, preclinical evidence suggests that statins inhibit tumor growth and induce apoptosis in specific cancer cell types.
Apoptosis↑,
ChemoSen↑, statins show chemo-sensitizing effects by impairing Ras family GTPase signaling.
RAS↓,
HMG-CoA↓, Statins are potent, competitive inhibitors of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase (HMGCR).
HMGCR↓,
LDL↓, Statins reduce blood plasma cholesterol levels by decreasing de novo cholesterol biosynthesis and by inducing changes in low density lipoprotein (LDL) receptor expression [2].
toxicity↓, Due to the well-established safety profile of statins, such studies are less expensive than the development of novel drugs.
Risk↓, statin use in cancer patients was associated with reduced cancer-related mortality. The risk of cancer death was significantly lower in postmenopausal women
P21↑, Other proposed mechanisms leading to an increase of p21 levels include the release of promoter-associated histone deacetylase and inhibition of histone deacetylase
HDAC↓,
Bcl-2↓, Statins trigger the intrinsic apoptosis pathway and decrease Bcl-2 protein expression [[154], [155], [156]], increase Bax and BIM protein expression [[156], [157], [158], [159]], and activate several caspases
BAX↑,
BIM↑,
Casp↑,
cl‑PARP↑, thereby increasing cleaved PARP-1 levels.
MMP↓, different tumor cell lines (breast, brain, and lung) showed that simvastatin-induced apoptosis is dependent on decreasing mitochondrial membrane potential and increasing reactive oxygen species (ROS) production
ROS↑,
angioG↓, Statins inhibit angiogenesis and metastasis
TumMeta↓,
PTEN↑, n breast cancer xenografts, simvastatin prevented tumor growth by reducing Akt phosphorylation and BclXL transcription, while simultaneously increasing the transcription of pro-apoptotic/anti-proliferative PTEN
eff↑, In mice, the administration of a combination of celecoxib and atorvastatin was more effective than each individual treatment, and effectively prevented prostate cancer progression from androgen dependent to androgen independent
OS↑, Long-term statin use may improve survival in GBM patients treated with temozolomide chemotherapy
Remission↑, statin use during or after chemotherapy is not associated with improved disease-free-, recurrence-free-, or overall survival in stage II colon cancer patients
*AChE↓, Berberine (9) has gained considerable attention due to its wide pharmacological potentials and several biological properties, such as acetylcholinesterase and butyrylcholinesterase inhibitory, antioxidant, monoamine oxidase oxidase,
*Aβ↓, amyloid-b peptide level-reducing, cholesterol- lowering and renoprotective activities
*LDL↓,
*RenoP↑,
*BChE↓,
*eff↑, Above all, the berberine-pyrocatechol hybrid (14) showed a strong AChE inhibitor activity (IC50 of 123 ± 3 nM)
[34]
*BACE↓, Curcumin: inhibite the rBACE1 activity [42]. In addition, it has made good inhibitory effect on acetylcholinesterase activity
*AChE↓, EGCG promoted brain health, prevented AD progression, and inhibited the AChE activity [52,53].
*eff↑, EGCG could enhance the effect of huperzine A on inhibiting AChE.
*antiOx↑, multiple activities of berberine, including antioxidant, acetylcholinesterase and butyrylcholinesterase inhibitory,
*AChE↓, inhibit AChE with an IC50 of 0.44 μM
*BChE↓, BChE inhibitor and the corresponding IC50 was estimated to be 3.44 μM
*MAOA↓, inhibitory activity on MAO-A with an IC50 value of 126 μM
*Aβ↓, monoamine oxidase inhibitory, amyloid-b peptide level-reducing and cholesterol-lowering activities.
*LDL↓, effectively reduce serum cholesterol and LDL-cholesterol levels in hyperlipidemic hamsters and human hypercholesterolemic patients
*ROS↓, First, it was reported that berberine can scavenge reactive oxygen species (ROS) and reactive nitrogen species (RNS)
*RNS↓,
*lipid-P↓, Secondly, berberine can inhibit lipid peroxidation
*Dose↝, berberine can inhibit AChE with an IC50 of 0.44 μM
*MAOB↓, inhibition of berberine against MAO-B: IC50 was estimated to be 98.4 μM
*memory↑, beneficial effect of berberine in ameliorating memory dysfunction in a rat model of streptozotocin-induced diabetes
*toxicity↓, Berberine is generally considered to be non-toxic at doses used in clinical situations and lacks genotoxic, cytotoxic or mutagenic activity
*BBB↑, Berberine can be administered orally [67] and pass through the blood-brain barrier
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eff↑, Inhibition of ACLY using bempedoic acid used in combination with palbociclib reduced cell viability in a panel of breast and pancreatic cancer cell lines.
Apoptosis↑, Mechanistically, palbociclib inhibited cell proliferation, whereas bempedoic acid stimulated apoptosis.
TumCI↓, ACLY inhibition blocked cell invasion, when used alone or in combination with palbociclib.
ACLY↓, In 2019, an inhibitor of ACLY, bempedoic acid (BA), was FDA-approved to reduce levels of low-density lipoprotein cholesterol in patients (21).
LDL↓,
eff↑, The present study aimed to determine the combined effect of ACLY inhibition using BA and CDK4/6 inhibition using Palb on the proliferation and EMT/invasion of cancer cells.
TumCP↓, Palb inhibits proliferation, while BA induces apoptosis
LDL↓, Bempedoic acid (ETC-1002) is a small molecule intended to lower LDL-C in hypercholesterolemic patients,
AMPK↑, demonstrated that ETC-1002 treatment increased AMP-activated protein kinase (AMPK)26,
ACLY↓, ETC-1002 inhibits ACL and increases AMPK activity,
ACLY↓, Here, we show that ACLY inhibition up-regulates PD-L1 immune checkpoint expression in cancer cells
PD-L1↑,
mtDam↑, Mechanistically, ACLY inhibition causes polyunsaturated fatty acid (PUFA) peroxidation and mitochondrial damage, which triggers mitochondrial DNA leakage to activate the cGAS-STING innate immune pathway.
cGAS–STING↑, ACLY inhibition leads to cGAS-STING activation
LDL↓, bempedoic acid (BemA; also named ETC-1002) has been recently approved by U.S. Food and Drug Administration (FDA) for lowering low-density lipoprotein cholesterol
eff↑, dietary PUFA supplementation is sufficient to mimic the enhanced efficacy of PD-L1 blockade by ACLY inhibition, providing promising combinational strategies for immunotherapy-resistant tumors therapy.
*ACLY↓, Bempedoic acid, an ATP citrate lyase inhibitor, reduces low-density lipoprotein (LDL) cholesterol levels and is associated with a low incidence of muscle-related adverse events
*LDL↓, mean LDL cholesterol level at baseline was 139.0 mg per deciliter in both groups, and after 6 months, the reduction in the level was greater with bempedoic acid than with placebo by 29.2 mg per deciliter
*MusCon↓,
Dose↝, receive oral bempedoic acid, 180 mg daily, or placebo
cardioP↑, Among statin-intolerant patients, treatment with bempedoic acid was associated with a lower risk of major adverse cardiovascular events (death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, or coronary revascularization)
*Imm↑, traditional uses that include improving immune response and cardiovascular function.
*cardioP↑,
*LDL↓, Multiple clinical trials have provided evidence that different forms of orally administered bergamot can reduce total cholesterol and low-density lipoprotein cholesterol.
toxicity↓, The use of bergamot in multiple clinical trials has consistently shown that it is well tolerated in studies ranging from 30 days to 12 weeks.
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*memory↑, Carvacrol enhances memory and cognition by modulating the effects of oxidative stress, inflammation, and Aβ25-35-induced neurotoxicity in AD
*cognitive↑,
*ROS↓, reduces the production of reactive oxygen species and proinflammatory cytokine levels in PD
*Inflam↓,
*motorD↑, improves motor functions
*toxicity↓, in general, it is potentially safe for consumption
*TRPV3↑, Carvacrol is a potent agonist of transient receptor potential vanilloid 3 (TRPV3)
*other↓, mitigating oxidative stress (OS)/ADP-ribose (ADPR)-induced TRPM2 and GSK1016790A (GSK)-mediated TRPV4 activations
*antiOx↑, Essential oils, high in carvacrol, have powerful antioxidant properties [85-88] similar to vitamin E, ascorbic acid, and butyl hydroxyl toluene
*LDL↓, Low-density lipoprotein (LDL) is inhibited by carvacrol in vitro and mediates LDL oxidation within an incubation period of 12 h
*COX2↓, suppressing the expression level of cyclooxygenase-2 (COX-2),
*PPARα↑, triggering the peroxisome proliferator-activated receptors (PPAR) α and γ
*NO↓, inhibiting NO production
*AChE↓, Carvacrol's acetylcholinesterase inhibitory action is 10 times higher than thymol's, even though the two compounds have a relatively similar structure
*eff↑, carvacrol nanoemulsion treatment has shown more notable effects compared to carvacrol oil.
*SOD↑, increases superoxide dismutase (SOD) and catalase (CAT) activity
*Catalase↑,
*neuroP↑, neuroprotective effects of carvacrol against cognitive impairments and its potential in AD are shown in Fig. (2)
*BioAv↝, In rabbits, 1.5 g of orally administered carvacrol is progressively absorbed from the intestines, with approximately 30% of the whole dose remaining in the gastrointestinal system and 25% eliminated via urine after 22 h of administratio
*BBB↑, carvacrol in the brain tissues as it easily crosses the blood-brain barrier owing to its low molecular weight (150.2 g/mol) and higher lipophilicity
*BioAv↑, liposomal encapsulation [136], and solid lipid nanoparticles [137], were developed and found bioavailable on oral administration. These formulations exhibit improved solubility, stability, and bioavailability and enhance drug accumulation in the tiss
*LDL↓, chitosan group significantly reduced total and LDL cholesterol (F=4.21, P=0.02, and F=3.46, P=0.04, respectively) compared with placebo.
*Weight↝, As a dietary supplement, chitosan has been claimed to control obesity and to lower serum cholesterol.
*LDL↓, In man, dietary chitosan has been reported to reduce serum total cholesterol levels by 5.8-42.6% and low-density lipoprotein levels by 15.1-35.1%.
*antiOx↑, Antioxidant effects of cocoa may directly influence insulin resistance and, in turn, reduce risk for diabetes.
*AntiDiabetic↑,
*cognitive↑, beneficial effects on satiety, cognitive function, and mood.
*AntiAg↑, Bordeaux and colleagues found that, among healthy participants in a platelet function study, those who had consumed chocolate before testing (n=141) had reduced platelet activity compared to nonconsumers.
*AntiAg↑, dark chocolate consumption decreased platelet adhesion 2 h after consumption in 22 heart transplant patients
*LDL↓, ll three significantly improved LDL and HDL levels from baseline in subjects with high LDL at the start of the study.
*HDL↑, in another trial, HDL increased by 11.4% and 13.7% when subjects consumed dark chocolate and polyphenol-enriched dark chocolate
*BP↓, A relationship between cocoa consumption and reduced BP was first observed in the Zutphen Elderly Study. A 2010 study found that a daily dose of 1052 mg cocoa flavanols was required to reduce 24-h ambulatory BP
*eff↓, Rimbach et al. noted that beneficial effects on BP, FMD, and platelet aggregation have not been found in all human trials (67, 73). Further, improvements are often small when they are observed
*ROS↓, Cocoa intake increases serum antioxidant capacity, protecting the endothelium from oxidative stress and endogenous ROS
*NF-kB↓, suppressed pro-inflammatory cytokine expression and histamine release, downregulated nuclear factor kappa B (NF-kB), cyclooxygenase 2 (COX-2), and inducible nitric oxide synthase (iNOS)
*COX2↓,
*iNOS↓,
angioG↓, upregulated apoptotic pathways [28], inhibited angiogenesis [29] and metastasis formation
TOP1↓, suppressed DNA topoisomerases [31] and histone deacetylase [32], downregulated tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β)
HDAC↓,
TNF-α↓,
IL1β↓,
cardioP↑, promoted protective signaling pathways in the heart [34], kidney [35] and brain [8], decreased cholesterol level
RenoP↑,
neuroP↑,
LDL↓,
BioAv↑, bioavailability of chrysin in the oral route of administration was appraised to be 0.003–0.02% [55], the maximum plasma concentration—12–64 nM
eff↑, Chrysin alone and potentially in combination with metformin decreased cyclin D1 and hTERT gene expression in the T47D breast cancer cell line
cycD1/CCND1↓,
hTERT/TERT↓,
MMP-10↓, Chrysin pretreatment inhibited MMP-10 and Akt signaling pathways
Akt↓,
STAT3↓, Chrysin declined hypoxic survival, inhibited activation of STAT3, and reduced VEGF expression in hypoxic cancer cells
VEGF↓,
EGFR↓, chrysin to inhibit EGFR was reported in a breast cancer stem cell model [
Snail↓, chrysin downregulated MMP-10, reduced snail, slug, and vimentin expressions increased E-cadherin expression, and inhibited Akt signaling pathway in TNBC cells, proposing that chrysin possessed a reversal activity on EMT
Slug↓,
Vim↓,
E-cadherin↑,
eff↑, Fabrication of chrysin-attached to silver and gold nanoparticles crossbred reduced graphene oxide nanocomposites led to augmentation of the generation of ROS-induced apoptosis in breast cancer
TET1↑, Chrysin induced augmentation in TET1
ROS↑, Pretreatment with chrysin induced ROS formation, and consecutively, inhibited Akt phosphorylation and mTOR.
mTOR↓,
PPARα↓, Chrysin inhibited mRNA expression of PPARα
ER Stress↑, ROS production by chrysin was the critical mediator behind induction of ER stress, leading to JNK phosphorylation, intracellular Ca2+ release, and activation of the mitochondrial apoptosis pathway
Ca+2↑,
ERK↓, reduced protein expression of p-ERK/ERK
MMP↑, Chrysin pretreatment led to an increase in mitochondrial ROS creation, swelling in isolated mitochondria from hepatocytes, collapse in MMP, and release cytochrome c.
Cyt‑c↑,
Casp3↑, Chrysin could elevate caspase-3 activity in the HCC rats group
HK2↓, chrysin declined HK-2 combined with VDAC-1 on mitochondria
NRF2↓, chrysin inhibited the Nrf2 expression and its downstream genes comprising AKR1B10, HO-1, and MRP5 by quenching ERK and PI3K-Akt pathway
HO-1↓,
MMP2↓, Chrysin pretreatment also downregulated MMP2, MMP9, fibronectin, and snail expression
MMP9↓,
Fibronectin↓,
GRP78/BiP↑, chrysin induced GRP78 overexpression, spliced XBP-1, and eIF2-α phosphorylation
XBP-1↓,
p‑eIF2α↑,
*AST↓, Chrysin administration significantly reduced AST, ALT, ALP, LDH and γGT serum activities
ALAT↓,
ALP↓,
LDH↓,
COX2↑, chrysin attenuated COX-2 and NFkB p65 expression, and Bcl-xL and β-arrestin levels
Bcl-xL↓,
IL6↓, Reduction in IL-6 and TNF-α and augmentation in caspases-9 and 3 were observed due to chrysin supplementation.
PGE2↓, Chrysin induced entire suppression NF-kB, COX-2, PG-E2, iNOS as well.
iNOS↓,
DNAdam↑, Chrysin induced apoptosis of cells by causing DNA fragmentation and increasing the proportions of DU145 and PC-3 cells
UPR↑, Also, it induced ER stress via activation of UPR proteins comprising PERK, eIF2α, and GRP78 in DU145 and PC-3 cells.
Hif1a↓, Chrysin increased the ubiquitination and degradation of HIF-1α by increasing its prolyl hydroxylation
EMT↓, chrysin was effective in HeLa cell by inhibiting EMT and CSLC properties, NF-κBp65, and Twist1 expression
Twist↓,
lipid-P↑, Chrysin disrupted intracellular homeostasis by altering MMP, cytosolic Ca (2+) levels, ROS generation, and lipid peroxidation, which plays a role in the death of choriocarcinoma cells.
CLDN1↓, Chrysin decreased CLDN1 and CLDN11 expression in human lung SCC
PDK1↓, Chrysin alleviated p-Akt and inhibited PDK1 and Akt
IL10↓, Chrysin inhibited cytokines release, TNF-α, IL-1β, IL-10, and IL-6 induced by Ni in A549 cells.
TLR4↓, Chrysin suppressed TLR4 and Myd88 mRNA and protein expression.
NOTCH1↑, Chrysin inhibited tumor growth in ATC both in vitro and in vivo through inducing Notch1
PARP↑, Pretreating cells with chrysin increased cleaved PARP, cleaved caspase-3, and declined cyclin D1, Mcl-1, and XIAP.
Mcl-1↓,
XIAP↓,
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*antiOx↑, Cinnamon is known to have antioxidant, antibacterial, anti-inflammatory, and other therapeutic properties.
*Inflam↓,
*cardioP↑, natural remedy to treat serious diseases such as type 2 diabetes, chronic digestion problems, cardiovascular diseases, and even cancer and Alzheimer’s disease.
angioG↓, cinnamon extract (CE) displays anticancer activity5 and inhibits angiogenesis by blocking vascular endothelial growth factor (VEGF) 2 signaling
VEGF↓,
*LDL↓, , and low-density lipoprotein cholesterol (7–27%) for patients who consumed 1 g, 3 g, or 5 g of cinnamon for 40 days.
COX2↓, treatment of melanoma cell lines with CE also induced a decrease in Cox-2 and HIF-1α expression in the tumor tissues that mediate the potent antitumor activity of cinnamon
Hif1a↓,
*Aβ↓, A study found that Cinnamon (肉桂 ròu guì) extract (CEppt) inhibits the formation of toxic Aβ oligomers and prevents the toxicity of Aβ on neuronal PC12 cells.
*tau↓, he extract of the whole cinnamon effectively inhibited the aggregation of human tau in vitro, and this could be attributed to both proanthocyanidin timer and cinnamaldehyde in CE
*toxicity↓, In one study, the intake of up to 6 g/d of C. cassia for > 40 days did not show any adverse effects.
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*AntiAge↑, supplementation positively affects mitochondrial deficiency syndrome and the symptoms of aging based mainly on improvements in bioenergetics.
*cardioP↑, Cardiovascular disease and inflammation are alleviated by the antioxidant effect of CoQ10
*Inflam↓, Administration of CoQ10 in doses ranging from 60 to 500 mg/day for a 1-week to 4-month intervention period significantly decreased production of inflammatory cytokines
*antiOx↑,
*lipid-P↓, The concentrations of CoQ10 in the plasma of elderly people are positively correlated with levels of physical activity and cholesterol concentrations (Del Pozo-Cruz et al., 2014a,b), as well as with lower lipid oxidative damage.
*QoL↑, Older individuals given a combination of selenium and CoQ10 over a 4-year period reported an improvement in vitality, physical performance, and quality of life
*neuroP↑, health benefits in elderly people by preventing chronic oxidative stress associated with cardiovascular and neurodegenerative diseases
*Dose↝, the highest dose for CoQ10 supplementation is 1200 mg daily according to well-designed randomized, controlled human trials, although doses as high as 3000 mg/day have been used in shorter clinical trials
*BP↓, These authors interpreted the results to indicate a significant reduction in systolic blood pressure without improvements in other CVD risk factors, such as diastolic blood pressure, total cholesterol, LDL- and high-density lipoprotein (HDL)-choleste
*IGF-1↑, elderly healthy participants who received selenium and CoQ10 supplementation for over 4 years, an increase in insulin-like growth factor 1 (IGF-1) and postprandial insulin-like growth factor-binding protein 1 (IGFBP-1) levels
*IGFBP1↑,
*eff↑, A combination of CoQ10 with red yeast rice, berberina, policosanol, astaxanthin, and folic acid significantly decreased total cholesterol, LDL-cholesterol, triglycerides, and glucose in the blood while increasing HDL-cholesterol levels
*LDL↓,
*HDL↑,
*eff↑, 60 patients suffering from statin-associated myopathy were enrolled in a 3-month study to test for efficacy of CoQ10 and selenium treatment. A consistent reduction in their symptoms, including muscle pain, weakness, cramps, and fatigue was observed
*other↑, Because of its capacity to reduce the side-effects of statins, CoQ10 has been proposed to prevent and/or slow the progression of frailty and sarcopenia in the elderly chronically treated with statins.
*RenoP↑, experiments performed on rats showed a promising protective effect of ubiquinol in the kidneys
*ROS↓, 65 patients undergoing hemodialysis, supplementation with high amounts of CoQ10 (1200 mg/day) lowered F2-isoprostane plasma levels indicative of a reduction in oxidative stress
*TNF-α↓, low grade inflammation, respond well to CoQ10 supplementation with significant decrease in TNF-α plasma levels without having an effect on C-reactive protein and IL-6 production
*IL6↓, Another study reported that CoQ10 therapy in doses ranging from 60 to 300 mg/day caused no significant decrease in C-reactive protein while eliciting a significant reduction in IL-6 levels
*other↝, Preclinical studies demonstrated that CoQ can preserve mitochondrial function and reduce the loss of dopaminergic neurons in the case of Parkinson's disease
*other∅, There was no improvement observed in oxidative stress or neurodegeneration markers in a randomized clinical trial in Alzheimer's Disease patients with CoQ10 supplementation at a dose of 400 mg/day for 16 weeks
*antiOx↑, Curcumin, a natural compound with potent antioxidant and anti-inflammatory properties
*Inflam↓,
*AntiAge↑, Its potential anti-aging properties are due to its power to alter the levels of proteins associated with senescence, such as adenosine 5′-monophosphate-activated protein kinase (AMPK) and sirtuins
*AMPK↑,
*SIRT1↑,
*NF-kB↓, preventing pro-aging proteins, such as nuclear factor-kappa-B (NF-κB) and mammalian target of rapamycin (mTOR)
*mTOR↓,
*NLRP3↓, Moreover, curcumin, by inhibiting the NF-κB pathway, can directly restrain the assembly or even inhibit the activation of the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome
*NADPH↓, by inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and elevating the activity of antioxidant enzymes and consequently lowering reactive oxygen species (ROS)
*ROS↓,
*COX2↓, (COX-2), granulocyte colony-stimulating factor (G-CSF), and monocyte chemotactic protein-1 (MCP-1) can be decreased by curcumin
*MCP1↓,
*IL1β↓, by decreasing IL-1β, IL-17, IL-23, TNF-α, and myeloperoxidase, enhancing levels of IL-10, and downregulating activation of NF-κB
*IL17↓,
*IL23↓,
*TNF-α↓,
*MPO↓,
*IL10↑,
*lipid-P↓, curcumin showed a significant decline in lipid peroxidation and increased superoxide dismutase levels, in addition to a reduction in Aβ aggregation and tau hyperphosphorylation through the regulation of GSK3β, Cdk5, p35, and p25
*SOD↑,
*Aβ↓,
*p‑tau↓,
*GSK‐3β↓,
*CDK5↓,
*TXNIP↓, Curcumin also has an inhibitory role on the thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome pathway
*NRF2↑, well as upregulation of Nrf2, NAD(P)H quinine oxidoreductase 1 (NQO1), HO-1, and γ-glutamyl cysteine synthetase (γ-GCS) in brain cells.
*NQO1↑,
*HO-1↑,
*OS↑, significant improvement in OS, and a positive evolution in memory and spatial learning
*memory↑,
*BDNF↑, Besides that, it promoted neurogenesis through increasing brain-derived neurotrophic factor (BDNF) levels
*neuroP↑, Curcumin can promote neuroprotection
*BACE↓, Figure 7
*AChE↓, figure 7
*LDL↓, and reduced total cholesterol and LDL levels.
*Inflam↓, known to have protective effects, including anti-inflammatory, antioxidant, anti-arthritis, pro-healing, and boosting memory cognitive functions.
*antiOx↑,
*memory↑,
*Aβ↓, curcumin prevents Aβ aggregation and crosses the blood-brain barrier,
*BBB↑,
*cognitive↑, curcumin ameliorates cognitive decline and improves synaptic functions in mouse models of AD
*tau↓, curcumin's effect on inhibition of A and tau,copper binding ability, cholesterol lowering ability, anti-inflammatory and modulation of microglia, acetylcholinesterase (AChE) inhibition, antioxidant properties,
*LDL↓,
*AChE↓,
*IL1β↓, Curcumin reduced the levels of oxidized proteins and IL1B in the brains of APP mice
*IronCh↑, Curcumin binds to redox-active metals, iron and copper
*neuroP↑, Curcumin, a neuroprotective agent, has poor brain
bioavailability.
*BioAv↝,
*PI3K↑, They found that curcumin significantly upregulates phosphatidylinositol 3-kinase (PI3K), Akt, nuclear factor E2-related factor-2 (Nrf2), heme oxygenase 1, and ferritin expression
*Akt↑,
*NRF2↑,
*HO-1↑,
*Ferritin↑,
*HO-2↓, and that it significantly downregulates heme oxygenase 2, ROS, and A40/42 expression.
*ROS↓,
*Ach↑, significant increase in brain ACh, glutathione, paraoxenase, and BCL2 levels with respect to untreated group associated with significant decrease in brain AChE activity,
*GSH↑,
*Bcl-2↑,
*ChAT↑, nvestigation revealed that the selected treatments
caused marked increase in ChAT positive cells.
Risk↓, IF has shown potential for reducing cancer risk and enhancing therapeutic efficacy by sensitizing tumor cells to chemotherapy and radiotherapy.
ChemoSen↑, intermittent fasting (IF) may enhance the effectiveness of chemotherapy and targeted therapies by activating autophagy. IF enhances the effectiveness of chemotherapy, including drugs such as cisplatin, cyclophosphamide, and doxorubicin
RadioS↑, disease stabilization, improved response to radiotherapy patients with glioma
*Dose↝, 16:8—16 h of fasting with an 8 h eating window;
*Dose↝, 5:2—consuming a standard number of calories for 5 days and reducing intake to 25% of daily requirements for 2 days;
*Dose↝, Eat–Stop–Eat—complete fasting for 24–48 h.
*LDL↓, IF during Ramadan (approximately 18 h of fasting for 29–30 days) reduces LDL cholesterol levels and increases HDL cholesterol in women, as well as reducing inflammatory markers such as CRP and TNF-α
*CRP↓,
*TNF-α↓,
TumAuto↓, Intermittent fasting activates autophagy as an adaptive mechanism to nutrient deprivation, which may modulate tumor development and treatment
GLUT1↓, fasting reduces the expression of glucose transporters GLUT1/2, which slow down cancer metabolism and increase the susceptibility of cancer cells to oxidative stress
GLUT2↓,
glucose↓, studies on cell and animal models have shown that intermittent fasting reduces glucose and insulin-like growth factor (IGF-1) levels [103], as well as insulin [104,105], resulting in the inhibition of the mTOR kinase pathway (PI3K/Akt/mTOR), suppress
IGF-1↓,
Insulin↓,
mTOR↓,
mTORC1↓, suppression of mTORC1 [22], and activation of AMPK through increased ADP/ATP ratio in cells, which supports autophagy and induces apoptosis
AMPK↑,
Warburg↓, Moreover, IF counteracts the Warburg effect by promoting oxidative phosphorylation, leading to an increase in the production of reactive oxygen species (ROS) and enhanced oxidative stress in cancer cells [106,108], causing DNA damage and the activati
OXPHOS↑,
ROS↑,
DNAdam↑,
JAK1↓, fasting reduces the production of adenosine by cancer cells, inhibiting the activation of the JAK1/STAT pathway, thereby reducing cancer cell proliferation
STAT↓,
TumCP↓,
QoL↑, reduction in IGF-1 levels, improved quality of life patients with multiple cancer types
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Risk↓, Intermittent fasting (IF) has emerged as a potential adjunctive strategy in cancer prevention, mitigation, and treatment.
TumCMig↓,
IGF-1↓, IF may reduce cancer risk, including its effects on insulin-like growth factor 1 suppression, autophagy induction, and chronic inflammation reduction.
TumAuto↑,
Inflam↓, IF has been shown to reduce chronic inflammation,13,40 a risk factor for various cancers
ChemoSen↑, we discuss IF’s potential to enhance the efficacy of conventional cancer therapies by sensitizing cancer cells, promoting apoptosis, and reducing treatment-related side effects.
Apoptosis↑,
chemoP↑, IF has shown potential in protecting healthy tissues during chemotherapy.
*glucose↓, Fasting has been shown to enhance metabolic health by improving insulin sensitivity, lowering blood sugar levels, and reducing the risk of type 2 diabetes.
*AntiDiabetic↑,
*cardioP↑, Recent studies support the cardioprotective effect of IF by reducing cholesterol levels, lowering blood pressure, and improving cardiovascular health
*LDL↓,
*BP↓,
*neuroP↑, IF may reduce the risk of neurodegenerative diseases, enhance cognitive function, and improve memory
*cognitive↑,
*memory↑,
*OS↑, some studies have suggested that IF may extend lifespan and improve overall health
*QoL↑,
Imm↑, In the context of cancer prevention, IF may directly affect the function of immune cells, reducing their production of inflammatory cytokines and promoting a more anti-inflammatory environment.5
TumCG↓, Evidence suggests that FMDs can effectively slow tumor growth by altering cancer cell metabolism, enhance the efficacy of traditional cancer therapies by reducing side effects, and potentially bolster antitumor immune surveillance
ChemoSideEff↓, IF may also help alleviate common side effects such as fatigue, nausea, and weight loss associated with cancer treatments
QoL↑, Results showed that chemotherapy-induced QoL decline was significantly less pronounced during fasting periods compared to non-fasting periods
*LDL↓, ellagic acid treatment improved the levels of blood lipid metabolism with a 4.7% decline in total cholesterol, 7.3% decline in triglycerides, 26.5% increase in high-density lipoprotein, and 6.5% decline in low-density lipoprotein.
*HDL↑,
*BDNF↑, ellagic acid increased plasma BDNF by 21.2% in the overweight group and showed no effects on normal-weight participants
*cognitive↑, ellagic acid has a potential to restore cognitive performance related to mild age-related declines
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Beclin-1↑, EGCG not only regulates autophagy via increasing Beclin-1 expression and reactive oxygen species generation,
ROS↑,
Apoptosis↑, Apoptosis is a common cell function in biology and is induced by endoplasmic reticulum stress (ERS)
ER Stress↑,
*Inflam↓, EGCG has health benefits including anti-tumor [15], anti-inflammatory [16], anti-diabetes [17], anti-myocardial infarction [18], anti-cardiac hypertrophy [19], anti-atherosclerosis [20], and antioxidant
*cardioP↑,
*antiOx↑,
*LDL↓, These effects are mainly related to (LDL) cholesterol inhibition, NF-κB inhibition, MPO activity inhibition, decreased levels of glucose and glycated hemoglobin in plasma, decreased inflammatory markers, and reduced ROS generation
*NF-kB↓,
*MPO↓,
*glucose↓,
*ROS↓,
ATG5↑, EGCG induced autophagy by enhancing Beclin-1, ATG5, and LC3B and promoted mitochondrial depolarization in breast cancer cells.
LC3B↑,
MMP↑,
lactateProd↓, 20 mg kg−1 EGCG significantly decreased glucose, lactic acid, and vascular endothelial growth factor (VEGF) levels
VEGF↓,
Zeb1↑, (20 uM) inhibited the proliferation through activating autophagy via upregulating ZEB1, WNT11, IGF1R, FAS, BAK, and BAD genes and inhibiting TP53, MYC, and CASP8 genes in SSC-4 human oral squamous cells [
Wnt↑,
IGF-1R↑,
Fas↑,
Bak↑,
BAD↑,
TP53↓,
Myc↓,
Casp8↓,
LC3II↑, increasing the LC3-II expression levels and induced apoptosis via inducing ROS in mesothelioma cell lines,
NOTCH3↓, but also could reduce partially Notch3/DLL3 to reduce drug-resistance and the stemness of tumor cells
eff↑, In combination therapies, low-intensity pulsed electric field (PEF) can improve EGCG to affect tumor cells; ultrasound (US) with tumor cells is the application of physical stimulation in cancer therapy.
p‑Akt↓, 20 μM EGCG increased intracellular ROS levels and LC3-II, and inhibited p-Akt in PANC-1 cells
PARP↑, 100 μM EGCG increased LC3-II, activated caspase-3 and PARP, and reduced p-Akt in HepG2
*Cyt‑c↓, EGCG protected neuronal cells against human viruses by inhibiting cytochrome c and Bax translocations, and reducing autophagy with increased LC3-II expression and decreased p62 expression
*BAX↓,
*memory↑, EGCG restored autophagy in the mTOR/p70S6K pathway to weaken memory and learning disorders induced by CUMS
*neuroP↑, Finally, EGCG increased the neurological scores through inhibiting cell death
*Ca+2?, EGCG treatment, [Ca2+]m and [Ca2+]i expressions were reduced and oxyhemoglobin-induced mitochondrial dysfunction lessened.
GRP78/BiP↑, MMe cells with EGCG treatment improved GRP78 expression in the endoplasmic reticulum, and induced EDEM, CHOP, XBP1, and ATF4 expressions, and increased the activity of caspase-3 and caspase-8.
CHOP↑, GRP78 accumulation converted UPR of MMe cells into pro-apoptotic ERS
ATF4↑,
Casp3↑,
Casp8↑,
UPR↑,
*OS↑, Dietary intake of epicatechin promoted survival in the diabetic mice (50% mortality in diabetic control group vs. 8.4% in epicatechin group after 15 wk of treatment),
*Inflam↓, reduced systematic inflammation markers and serum LDL cholesterol,
*LDL↓,
*AntiAge↑, epicatechin may be a novel food-derived, antiaging compound.
*GSH↑, In addition, the GSH concentration and total SOD activity in the livers of the db+EC group were significantly greater,
*SOD↑,
*AMPKα↑, Epicatechin improves AMPKα activity in the liver and skeletal muscle of diabetic mice.
*Weight∅, whereas blood pressure, blood glucose, food intake, and body weight gain were not significantly altered.
*Inflam↓, gingerol and shogaol classes of compounds, might exert several beneficial effects including anti-inflammatory, antioxidant, and cholesterol lowering properties
*antiOx↑,
*LDL↓,
*AntiAg↑, previous clinical trials report few side-effects, mostly minor in nature (e.g. mild nausea, heartburn).[1] Of these reported side effects, potentially the most significant is an antiplatelet effect.
*AntiAg∅, In contrast, two studies reported that 2–3.6g of ginger had no effect on measures of platelet aggregation in health adults.
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*antiOx↑, antioxidative properties as it directly neutralizes hydroxyl radicals and reduces peroxynitrite level
*NRF2↑, activates Nrf2 and HO-1, which regulate many antioxidant enzymes and proteasomes.
*HO-1↑,
*Inflam↓, hydrogen may prevent inflammation
*neuroP↑, prevention and treatment of various ageing-related diseases, such as neurodegenerative disorders, cardiovascular disease, pulmonary disease, diabetes, and cancer.
*cardioP↑,
*other↓, It also prevented ischemia-reperfusion (I/R) injury and stroke in a rat model
*ROS↓, H2 has been shown to exert its beneficial effects in various pathological conditions that involve free radicals and oxidative stress
*NADPH↓, figure 2, H2 Inhibits NADPH Oxidase Activity
*Catalase↑,
*GPx1↑,
*NO↓, H2 Indirectly Reduces Nitric Oxide (NO) Production
*mt-ROS↓, H2 Decreases Mitochondrial ROS
*SIRT3↑, In the kidneys, H2 suppressed the downregulated Sirt3 expression, which is the most abundant member of the sirtuin family, by reducing oxidative stress reactions
*SIRT1↑, In the liver, H2 elevated HO-1 to induce Sirt1 expression
*TLR4↓, H2 inhibits TLR4, which involves hyperglycemia in type 2 diabetes mellitus
*mTOR↓, For example, H2 inhibits mTOR, activates autophagy, and alleviates cognitive impairment resulting from sepsis
*cognitive↑,
*Sepsis↓,
*PTEN↓, It inhibits the activation of the PTEN/AKT/mTOR pathway and alleviates peritoneal fibrosis
*Akt↓,
*NLRP3↓, It also facilitates autophagy-mediated NLRP3 inflammasome inactivation and alleviates mitochondrial dysfunction and organ damage
*AntiAg↑, antiageing mechanism of H2 and the influence on ageing hallmarks are summarized in Figure 3.
*IL6↓, significantly suppressed inflammatory cytokines (IL-6, TNF-α, and IL-1β), MDA, and 8-OHdG, and improved memory dysfunction
*TNF-α↓,
*IL1β↓,
*MDA↓,
*memory↑,
*FOXO3↑, HRW can also upregulate Sirt1-Forkhead box protein O3a (FOXO3a
TumCG↓, H2 inhibits lung cancer progression
*LDL↓, Decreases oxidized LDL; improves HDL function
*BioEnh↑, Firstly, the pre-emulsification of an oil with vegetable lecithin has been shown to increase the systemic bioavailability of certain fatty acids, without increasing total plasma lipid concentrations.
*antiOx↑, different lecithin from various sources (soy, rapeseed) or with differing PL compositions have been reported to exert varying antioxidant properties
*BioEnh↑, ported higher plasma alpha-linolenic acid (ALA) concentrations in the PL-emulsified group
*LDL↓, oybean PL in patients with primary hyperlipidemia has been reported to significantly reduce blood cholesterol levels
*HDL∅, while maintaining plasmatic HDL levels
*Obesity↓, potential of lecithin on the prevention and amelioration of obesity-related metabolic disorders
eff↑, lecithin derived from olive oil compared to that of other seed oils (sunflower, corn or soybean) as a platelet aggregation factor (PAF) antagonist
GutMicro↝, importance of gut microbiota on lipid metabolism and metabolic health renders obligatory that further research on the effect of vegetable lecithin on TMAO production and gut microbiota in general be explored.
BioAv↑, soy lecithin is best suited to be used as a major pharmacological excipient, and it is broadly used in drug delivery systems.
antiOx↑, significant role in medicine as it is an antioxidant
LDL↓, maintains cholesterol levels
memory↑, crucial neurotransmitters involved in memory recall and storage
*Inflam↓, main activity profile of lycopene includes antiatherosclerotic, antioxidant, anti-inflammatory, antihypertensive, antiplatelet, anti-apoptotic, and protective endothelial effects, the ability to improve the metabolic profile, and reduce arterial stif
*antiOx↑, It is a much more potent antioxidant than alpha-tocopherol (10 × more potent) or beta-carotene (twice as potent)
*AntiAg↑, lycopene, protecting against myocardial infarction and stroke, is its antiplatelet activity
*cardioP↑, favorable effect in patients with subclinical atherosclerosis, metabolic syndrome, hypertension, peripheral vascular disease, stroke and several other cardiovascular disorders
*SOD↑, Lycopene modulates also the production of antioxidant enzymes, such as superoxide dismutase and catalase
*Catalase↑,
*ROS↓, By reducing oxidative stress and reactive oxygen species, lycopene increases the bioavailability of nitric oxide (NO), improves endothelium-dependent vasodilation and reduces protein, lipids, DNA, and mitochondrial damage (
*mtDam↓,
*cardioP↑, Lycopene exerts a cardioprotective effect against atrazine induced cardiac injury due to its anti-inflammatory effect, by blocking the NF-kappa B pathway and NO production
*NF-kB↓,
*NO↓,
*COX2↓, downregulation of cyclooxygenase 2,
*LDL↓, significant reductions in total and LDL cholesterol were revealed only at doses of, at least, 25 mg lycopene/day
*eff↑, It was noticed that lycopene can potentiate the antiplatelet effect of aspirin, which requires low lycopene diet
*ER Stress↓, Lycopene protects the cardiomyocytes by relieving ERS
*BioAv↑, Lycopene is very bioavailable in the presence of oil, especially in monounsaturated oils, other dietary fats and processed tomato products
*eff↑, Lycopene can increase the antioxidant properties of vitamin C, E, polyphenols and beta-carotene in a synergistic way
*MMPs↓, figure 3, secretion of MMPs
*COX2↓,
*RAGE↓,
*antiOx↑, As one of the most potent antioxidants, its capacity to neutralise singlet oxygen is double that of ?-carotene, ten times greater than that of ?-tocopherol, and one hundred and twenty-five times more effective than glutathione
*ROS⇅, lycopene acts as an antioxidant in systems that produce singlet oxygen but behaves as a pro-oxidant in systems that create peroxide
*Dose↝, In low doses, it acts as an antioxidant, but at high doses, it acts as a pro-oxidant
*eff↑, In situation where there is an imbalance between antioxidant defences and ROS production, such as during inflammation or exposure to environmental toxins [91], lycopene may switch from its antioxidant role to a pro-oxidant role
*LDL↓, Wistar rats given a high-fat diet and 50mg/kg body weight of lycopene daily for 3mths had significant reductions in plasma total cholesterol, triglycerides, and lLDL levels but increased HDL cholesterol
*RenoP↑, shown to protect the kidney against chemically induced damage
*Inflam↓, evidence is plentiful demonstrating the anti-inflammatory effects of lycopene both in vitro and in vivo
neuroP↑, mice with Alzheimer's disease induced by ? amyloid, lycopene reduced oxidative stress, decreased neuronal loss, improved synaptic plasticity, and inhibited neuroinflammation
Rho↓, lycopene treatment was demonstrated to have the potential to mitigate vascular arteriosclerosis in allograft transplantation by inhibiting Rho-associated kinases
antiOx↓, Lycopene is a potent antioxidant that fights ROS and, subsequently, complications.
ROS↓,
BP↓, It reduces blood pressure via inhibiting the angiotensin-converting enzyme and regulating nitrous oxide bioavailability.
LDL↓, important role in lowering of LDL (low-density lipoproteins) and improving HDL (high-density lipoproteins) levels to minimize atherosclerosis
*toxicity∅, Lycopene is a natural substance that may be used in high doses as a dietary supplement without causing harm to human health or physiology
eff↑, Thermal food processing, particularly in the presence of cooking oils, causes lycopene to micellize and enhance its intestinal absorption rate by a factor of ten
ROS↑, As a pro-oxidant, lycopene may have both good and negative impacts in biological systems, as well as influence the course of human illnesses.
*Half-Life↑, Plasma lycopene has a half-life of 12–33 days in the human body
*BioAv↓, Tomato lycopene is not easily absorbed since it is integrated into the nutritional matrix.
*BioAv↑, Clinical research demonstrates that heat-processed tomato products absorb lycopene more quickly than raw sources, and that adding oil increases absorption
*antiOx↑, Lycopene’s ability to protect against oxidative stress has been established
*antiOx↑, Lycopene, the main pigment of tomatoes, possess the strongest antioxidant activity among carotenoids. Lycopene has unique structure and chemical properties.
TumCP↓, the anticancer of lycopene is also considered to be an important determinant of tumor development including the inhibition of cell proliferation, inhibition of cell cycle progression, induction of apoptosis, inhibition of cell invasion, angiogenesis
TumCCA↓,
Apoptosis↑,
TumCI↓,
angioG↓,
TumMeta↓,
*Risk↓, and may be associated with a decreased risk of different types of cancer.
cycD1/CCND1↓, Several studies suggested lycopene decreased cell cycle related proteins, such as cyclin D1, D3 and E, the cyclin-dependent kinases 2 and 4, bcl-2, while decreased phospho-Akt levels and increased p21, p27, p53 and bax levels and in Bax: Bcl-2 ratio
CycD3↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
Bcl-2↓,
P21↑,
p27↑,
P53↑,
BAX↑,
selectivity↑, lycopene selectively inhibited cell growth in MCF-7 human breast cancer cells but not in the MCF-10 mammary epithelial cells
MMP↓, When treating LNCaP human prostate cancer cells with lycopene, the decreased mitochondrial function could be observed.
Cyt‑c↑, release of mitochondrial cytochrome c and finally led to apoptosis
Wnt↓, Lycopene could inhibit Wnt-TCF signaling pathway in cancer cells.
eff↑, Lycopene could synergistically increase QC anticancer activity and inhibit Wnt-TCF signaling in cancer cells.
PPARγ↑, Lycopene could inhibit the growth of cancer cells by activating the PPARγ – LXRα - ABCA1 pathway and decreasing cellular total cholesterol levels
LDL↓,
Akt↓, Lycopene suppressed Akt activation and non-phosphorylated β-Catenin,
PI3K↓, inhibited the proliferation of colon cancer HT-29 cells, which was associated with suppressing PI3K/Akt/mTOR signaling pathway
mTOR↓,
PDGF↓, Lycopene, however, could inhibit PDGF-BB-induced signaling and cell migration in both human cultured skin fibroblasts and melanoma-derived fibroblasts
NF-kB↓, anticancer properties of lycopene may occur to play its role through the inhibition of the NF-κB signaling pathway
eff↑, lycopene increased the sensitization of cervical cancer cells to cisplatin via the suppression of NF-κB-mediated inflammatory responses, and the modulation of Nrf2-mediated oxidative stress
*AntiDiabetic↑, Metformin is a drug commonly prescribed to treat patients with type 2 diabetes.
*AntiAge↑, Here we show that long-term treatment with metformin (0.1% w/w in diet) starting at middle age extends healthspan and lifespan in male mice
*toxicity⇅, while a higher dose (1% w/w) was toxic.
*CRM↑, The effects of metformin resembled to some extent the effects of caloric restriction, even though food intake was increased.
*Strength↑, Treatment with metformin mimics some of the benefits of calorie restriction, such as improved physical performance, increased insulin sensitivity, and reduced LDL and cholesterol levels without a decrease in caloric intake
*LDL↓,
*AMPK↑, metformin increases AMP-activated protein kinase activity and increases antioxidant protection, resulting in reductions in both oxidative damage accumulation and chronic inflammation
*TAC↑,
*ROS↓, consistent with decreased oxidative stress damage in the liver of metformin-treated mice
*Inflam↓, Metformin inhibits chronic inflammation
Risk↓, metformin treatment has been associated with reduced risk of cancer4 and cardiovascular disease
*cardioP↑,
*ALAT↓, Ala aminotransferase (U/L) 90 ± 58 64 ± 29
*NRF2↑, The increase in Nrf2/ARE reporter activity occurred with an ED50 of ~1.5 mM metformin without reduction in cell survival
*SOD2↑, 0.1% metformin contributed to an increase in the level of antioxidant and stress response proteins, including SOD2, TrxR1, NQO1 and NQO2
*TrxR1↑,
*NQO1↑,
*NQO2↑,
BioEnh↑, a natural bioenhancer and reported to enhance the bioavailability of drugs by inhibiting cytochrome P450 and P-glycoprotein (P-gp)
LDL↓, Animals received AST along with naringin (15 and 30 mg/kg) shown higher percent reduction in both cholesterol and triglycerides levels
P450↓,
P-gp↓,
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*ROS↓, sodium phenylbutyrate (NaPB), an FDA-approved therapy for reducing plasma ammonia and glutamine in urea cycle disorders, can suppress both proinflammatory molecules and reactive oxygen species (ROS) in activated glial cells
*Inflam↑,
*P21↓, Inhibition of both p21ras and p21rac activation by NaPB in microglial cells suggests that NaPB exerts anti-inflammatory and antioxidative effects via inhibition of these small G proteins
*antiOx↑,
*GSH↑, protected nigral reduced glutathione
*NF-kB↓, attenuated nigral activation of NF-κB
*neuroP↑, These results identify novel mode of action of NaPB and suggest that NaPB may be of therapeutic benefit for neurodegenerative disorders.
*HDAC↓, Because NaPB is a known inhibitor of histone deacetylase (HDAC)
*iNOS↓, Similar to the inhibition of iNOS, NaPB dose-dependently inhibited the production of TNF-α and IL-1β protein in activated microglia
*TNF-α↓,
*IL1β↓,
*LDL↓, NaPB reduced the level of cholesterol in serum of mice by about 30%; and this reduction was comparable to that (∼29%) by the so-called cholesterol-lowering drug pravastatin
ROS↓, NaPB strongly inhibited MPP+-induced production of intracellular ROS
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*Inflam↓, remarkable anti-inflammatory and antioxidant effects.
*antiOx↑,
*BioAv↑, high bioavailability and low toxicity in many species has contributed to its promising research prospects.
*toxicity↓,
*NADPH↓, Pterostilbene significantly down-regulates nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX),
*ROS↓, which is the key enzyme family that induces the release of reactive oxygen species (ROS)
*Catalase↑, pterostilbene treatment as it increases the expression levels of catalase (CAT), glutathione (GSH), superoxide dismutase (SOD), and other antioxidants in diabetic rats [
*GSH↑,
*SOD↑,
*TNF-α↓, (tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-4), matrix metalloproteinases (MMPs), and cyclooxygenase (COX)-2 are all suppressed by pterostilbene treatment.
*IL1β↓,
*IL4↓,
*MMPs↓,
*COX2↓,
*MAPK↝, anti-inflammatory action of pterostilbene has been proved to be associated with modulating mitogen-activated protein kinase (MAPK) and nuclear factor kappa B (NF-κB) pathways
*NF-kB↓,
*IL8↓, pterostilbene can successfully reverse the elevation of related pro-inflammatory cytokines (IL-8, monocyte chemoattractant protein (MCP)-1, and E-selectin)
*MCP1↓,
*E-sel↓,
*lipid-P↓, Pterostilbene has been demonstrated to reduce lipid peroxidation by regulating the expression of Nrf2, exhibiting anti-peroxidation and anti-hyperlipidemic effects
*NRF2↑,
*PPARα↑, Pterostilbene acts as a potent PPAR-α agonist
*LDL↓, pterostilbene could effectively reduce the plasma low-density lipoprotein (LDL) cholesterol levels of hamsters by 29% and increase the plasma high-density lipoprotein (HDL) cholesterol levels by almost 7%
other↓, Ability to Protect against Stroke
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*Inflam↓, known for its anti-inflammatory, antihypertensive, vasodilator effects, antiobesity, antihypercholesterolemic and antiatherosclerotic activities
*cardioP↑, beneficial effects include cardiovascular protection, anticancer, antitumor, anti-ulcer, anti-allergy, anti-viral, anti-inflammatory activity, anti-diabetic, gastroprotective effects, antihypertensive, immunomodulatory, and anti-infective.
AntiCan↑,
AntiTum↑,
*neuroP↑, The consumption of flavonoids rich food limits neurodegeneration and to reverse age-dependent loss in cognitive performance.
*cognitive↑,
*ROS↓, It is known to protect brain cells against the oxidative stress, which damages tissue leading to Alzheimer and other neurological conditions
*BP↓, Quercetin supplementation (150 mg/day) reduced systolic blood pressure and plasma oxidized LDL concentrations in overweight subjects
*LDL↓,
*neuroP↑, exerts neuroprotective and antioxidant properties
*antiOx↑,
*LDL↓, RSV decreases total cholesterol concentration in hypercholesterolemic rats
*ADAM10↑, RSV under experimental conditions in CHO (chinese hamster ovary) cells expressing human APP695 containing a Swedish mutation showed a significant increase in ADAM10 expression,
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AntiCan↑, anticancer, anti-inflammatory, antinociceptive, antioxidant
*Inflam↓,
*antiOx↑,
*cognitive↑, 60 drops/day of alcoholic extract for week 16 Improvement of cognitive functions
*memory↑, 167–1332 mg of ethanolic extract was administrated 1, 2.5, 4 and 6 h before assessment Improvement of memory and attention
*LDL↓, 300 mL of sage tea twice daily for 4 weeks Reduction of total cholesterol and LDL;
TumCG↓, inhibit growth of MCF-7 and HCT-116 tumor cells
MAPK↓, inhibition of Mitogen-Activated Protein Kinase/Extracellular Signal-regulated Kinase pathway, the suppression of reactive oxygen species (ROS) and nuclear transcription factor-kappa B, and the reduction of pro-inflammatory gene cyclooxygenase-2 expr
ROS↓,
NF-kB↓,
COX2↓,
angioG↓, inhibits several phases of angiogenesis (proliferation, migration, adhesion and tube formation) in endothelial cells
*AST↓, It could decrease the level of triglyceride, cholesterol, urea, uric acid, creatinine, aspartate amino transferase (AST), and alanine amino transferase (ALT) in streptozotocin-induced diabetic rats
*ALAT?,
*glucose↓, MO-SeNPs treatment significantly reduced blood glucose levels (p < 0.05) and restored insulin resistance, with lower dose demonstrating better glycaemic control than larger dose.
*antiOx↑, MO-SeNPs also increased hepatic antioxidant enzyme activity, including GSH-Px, CAT, and T-SOD, which neutralise oxidative stress
*GPx↑,
*Catalase↑,
*SOD↑,
*ROS↓,
*cardioP↑, MO-SeNPs also improves cardiovascular health by raising HDL and lowering LDL.
*HDL↑,
*LDL↓,
*hepatoP↑, MO-SeNPs showed hepatoprotective benefits by lowering inflammatory markers such TNF-α, IL-6, IL-1β, iNOS, and AGEs, and reduced lipid peroxidation.
*TNF-α↓,
*IL6↓,
*IL1β↓,
*lipid-P↓,
*Inflam↓, The reduction in these indicators shows MO-SeNPs reduce liver inflammation and protect the liver.
*ALAT↓, The normalisation of liver enzyme levels (ALT, AST, ALP) showed improved liver function.
*AST↓,
*ALP↓,
*Dose↝, For the aqueous extract, 20 g of powdered leaves were homogenized in 800 mL of boiling distilled water, shaken at 150 rpm for 4 hours, centrifuged at 4000 rpm for 20 minutes, and filtered using Whatman filter paper No. 1 (Cat No. 1001 125) from GE H
*Dose↝, Selenium nanoparticles (MO-SeNPs) were synthesized by adding 5 mL of a 50 mM sodium selenite solution dropwise to 20 mL of Moringa oleifera extract under magnetic stirring, followed by incubation at 37 °C for 48 hours at pH 8 to facilitate the green
*antiOx↑, esame oil has been shown to have antioxidant and health-promoting benefits due to its high concentration of tocopherol, phytosterol, lignan, and other components
*LDL↓, sesame oil can reduce levels of low-density lipoprotein (LDL) and decrease the risk of atherosclerosis and cardiovascular diseases.
*Aβ↓, Alzheimer’s disease is linked to the deposition of toxic cellular amyloid proteins, and the prolonged consumption of sesamol may efficiently hinder this buildup
*TNF-α↓, Figure 2
*SOD↑,
*SIRT1↑,
*Catalase↑,
*GSH↑,
*MDA↓,
*GSTs↑,
*IL4↑,
*GPx↑,
*COX2↓,
*PGE2↓,
*NO↓,
CDK2↑,
COX2↑,
MMP9↑,
ICAM-1↓,
*BDNF↑, sesame oil increased brain-derived neurotrophic factor (BDNF) and peroxisome proliferator-activated receptor gamma (PPAR-γ) levels.
*PPARγ↑,
*AChE↓, figure 2
*Inflam↓, potent antioxidant properties, which may contribute to its anti-inflammatory effects.
*HO-1↑, activation of HO-1, leading to the inhibition of the IKKα/NFκB pathway, recognized for its involvement in inflammatory processes
*NF-kB↓,
*ROS↓, sesamin was found to decrease oxidative stress markers, including malondialdehyde (MDA) and reactive oxygen species (ROS), and increase the activity of antioxidant enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px).
*LDL↓, Plasma total cholesterol and low-density-lipoprotein cholesterol levels were significantly decreased in the TQRF- and TQ-treated rats compared to untreated rats.
*SOD1↑, TQRF and TQ caused the up-regulation of the superoxide dismutase 1 (SOD1), catalase, and glutathione peroxidase 2 (GPX) genes compared to untreated rats
*Catalase↑,
*GPx↑,
*antiOx↑, enhanced the expression of liver antioxidant genes of hypercholesterolemic rats.
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*antiOx↑, shown to possess various pharmacological properties including antioxidant, free radical scavenging, anti-inflammatory, analgesic, antispasmodic, antibacterial, antifungal, antiseptic and antitumor activities.
*ROS↓,
*Inflam↓,
*Bacteria↓,
AntiTum↑,
IronCh↑, chelation of metal ions
*HDL↑, antihyperlipidemic (via increasing the levels of high density lipoprotein cholesterol and decreasing the levels of low density lipoprotein cholesterol
*LDL↓,
*BioAv↝, videnced the presence of thymol in the stomach, intestine, and urine after its oral administration with sesame oil at a dose around 500 mg in rats and 1–3 g in rabbits.
*Half-Life↝, Oral administration of a single dose of thymol (50 mg/kg) was rapidly absorbed and slowly eliminated approximately within 24 h.The maximum concentration (Tmax) was reached after 30 min, while approximately 0.3 h was needed for the half-life
*BioAv↑, The rapid absorption of thymol indicates that it’s mainly absorbed in the upper component of the gut
*SOD↑, scavenging of free radicals by increasing the activities of several endogenous antioxidant enzymes levels viz. superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione-S-transferase (GST)
*GPx↑,
*GSTs↑,
*eff↑, Thymol (0.02–0.20%) showed better antioxidant capacity than its isomer carvacrol in lipid systems due to its greater steric hindrance
radioP↑, Owing to its potent antioxidant potential, thymol showed radioprotective and anticlastogenic potential in gamma radiation induced Swiss albino mice
*MDA↓, Thymol supplementation increased the antioxidant status and decreased malondialdehyde (MDA) levels in broiler chickens
*other↑, Dietary supplementation with the combination of carvacrol–thymol (1:1) (100 mg/kg) reduced the occurrence of oxidative stress and the impairment of the intestinal barrier in weaning piglets by its potent antioxidant property
*COX1↓, by inhibiting both isoforms of cyclooxygenase (COX), with the most active being against COX-1 with an IC50 value of 0.2 μM.
*COX2↓,
*AntiAg↑, Thymol (1.1 μg/ml) exhibited inhibitory effects against arachidonic-acid-induced blood coagulation and platelet aggregation in vitro
*RNS↓, Thymol inhibited ROS (IC50= 3 μg/ml), reactive nitrogen species (RNS) (IC50= 4.7) and significantly reduced generation of NO and H2O2 as well as activities of nitric oxide synthase (NOS) and nicotinamide adenine dinucleotide reduced oxidase (NADH oxi
*NO↓,
*H2O2↓,
*NOS2↓,
*NADH↓,
*Imm↑, Thymol (25–200 mg/kg) was shown to modulate the immune system in cyclosporine-A treated Swiss albino mice by enhancing the expressions of cluster of differentiation 4 (CD4),
Apoptosis↑, anticancer actions of thymol include induction of apoptosis, anti-proliferation, inhibition of angiogenesis and migration
TumCP↓,
angioG↓,
TumCMig↓,
Ca+2↑, Intracellular Ca2+ overload
TumCCA↑, Cytotoxicity by stimulating cell cycle arrest in G0/G1 phase
DNAdam↑, DNA fragmentation, Bax protein expression, activation of caspase -9, -8 and -3 & concomitant PARP cleavage, AIF translocation
BAX↑,
Casp9↑,
Casp8↑,
Casp3↑,
cl‑PARP↑,
AIF↑,
i-ROS↑, intracellular ROS, depolarizing MMP, cytochrome-c release, cleavage of caspases, DNA fragmentation, activation of apaf-1,
MMP↓,
Cyt‑c↑,
APAF1↑,
Ca+2↑, In human glioblastoma cells, thymol (200–600 μM) produced a rise in (Ca2+)i levels
MMP9↓, diminished matrix metallopeptidase-9 (MMP9) and matrix metallopeptidase-2 (MMP2) production as well as protein kinase Cα (PKCα) and extracellular signal-regulated kinases (ERK1/2) phosphorylation
MMP2↓,
PKCδ↓,
ERK↓,
H2O2↑, Thymol increased the production of ROS and mitochondrial H2O2 thereby depolarizing mitochondrial membrane potential.
BAX↑, up-regulating Bcl-2 associated X protein (Bax) expression and down-regulating B-cell lymphoma (Bcl-2)
Bcl-2↓,
DNAdam↑, Thymol (IC50= 497 and 266 mM) was shown to induce DNA damage by increasing the levels of lipid peroxidation products;
lipid-P↑,
ChemoSen↑, This study recommended the combination of thymol with various chemotherapeutic agents to minimize its toxicity on normal cells and to improve the effectiveness of cancer treatment
chemoP↑,
*cardioP↑, significant increase in the activities of heart mitochondrial antioxidants (SOD, catalase, GPx, GSH)
*SOD↑,
*Catalase↑,
*GPx↑,
*GSH↑,
*BP↓, Thymol (1, 3, and 10 mg/kg) administration decreased the blood pressure and heart rate of Wistar rats whereas thymol (5 mg/kg) attenuated blood pressure in rabbits
*AntiDiabetic↑, protective effects of thymol in metabolic disorders such as diabetes mellitus and obesity
*Obesity↓,
RenoP↑, Thymol (20 mg/kg) was shown to inhibit cisplatin-induced renal injury by attenuating oxidative stress, inflammation and apoptosis in male adult Swiss Albino rats
*GastroP↑, This gastroprotective effect of thymol is believed to be due to increased mucus secretion
hepatoP↑, Thymol (150 mg/kg) showed to inhibit paracetamol induced hepatotoxicity in mice by preventing the alterations in the activities of hepatic marker enzymes
*AChE↓, Thymol (EC50= 0.74 mg/mL) was shown to possess acetylcholine esterase inhibitory activity but much less than its isomer carvacrol
*cognitive↑, Thymol (0.5–2 mg/kg) has been shown to inhibit cognitive impairments caused by increased Aβ levels or cholinergic hypofunction in Aβ
*BChE↓, whereas thymol (100 and 1000 μg/ml) also inhibited both AChE and butyrylcholinesterase (BChE) in a dose dependent manner
*other↓, Thymol (100 mg/kg) was shown to inhibit collagen induced arthritis by decreasing lipid peroxidation mediated oxidative stress by increasing the status of antioxidants in male Wistar rats
*BioAv↑, The encapsulation of thymol into methylcellulose microspheres by spray drying remarkably increases the bioavailability compared to free thymol
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*ROS↓, Urolithins have been shown to protect cells from oxidative stress, reduce inflammation, and inhibit tumor growth.
*Inflam↓, Urolithins, particularly Urolithin A, have shown potent anti-inflammatory effects, which are crucial in managing chronic inflammatory diseases
TumCG↓,
*neuroP↑, They also have neuroprotective effects, potentially mitigating neurodegenerative diseases like Alzheimer's and Parkinson's.
*cardioP↑, Additionally, urolithins may contribute to cardiovascular health by reducing cholesterol levels and improving endothelial function.
*LDL↓,
*BioAv↝, bioavailability and production of urolithins can vary significantly among individuals due to differences in gut microbiota composition.
*BioAv↓, Due to poor water solubility and susceptibility to enzymatic degradation, urolithin bioavailability remains a challenge.
*BioAv↑, Compared to non-encapsulated UA, liposomal formulations resulted in significantly higher intestinal absorption and plasma concentrations. PEGylated liposomes further prolonged circulation time and enhanced therapeutic efficacy
*SIRT1↑, In neurodegenerative diseases caused by aging, Uro-A prevents brain aging by activating the SIRT1/mTOR signaling pathway in experimental animals
*mTOR↑,
*BDNF↑, UA administration was associated with increased Brain-Derived Neurotrophic Factor (BDNF) levels, reduced neuroinflammation, and improved cognitive performance
*cognitive↑,
*LDL↓, revealed consistent and statistically significant reductions of all atherogenic lipid fractions (total cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B) with parallel increases of high-density lipoprotein cholesterol and apolipo
*HDL↑,
*LDL↓, pantethine supplementation for 16 weeks (600 mg/d for weeks 1-8 then 900 mg/d for weeks 9-16) is safe and significantly lowers TC and LDL-C over and above the effect of TLC diet alone.
*BBB↝, BBB: not penetrant, but cysteamine (metabolite) is penetrant
*LDL↓, Pantethine has reduced total and LDL cholesterol though effects have been modest.
*lipid-P↓, Therapeutic Lifestyle Change (TLC) diet alone did
not significantly affect lipid profiles but when combined with pantethine supplementation, significantly
decreased lipid levels.
*AST↓, significantly reduced levels of liver enzymes (AST reduced from 66 to 33 IU/L, and ALT
reduced from 113 to 51 IU/L, or by 58%)
*ALAT↓,
*TGF-β↓, mean serum TGF-β level was significantly decreased
*adiP↑, while the mean serum level of high molecular adiponectin was increased.
*Inflam↓, inflammation was improved,
TumCG↓, mouse model of ovarian tumor, pantethine treatment (750 mg/kg/day, i.p.) for 4 weeks resulted in slower tumor progression,
FASN↓, Pantethine inhibits fatty acid synthase (FAS). Inhibition of FAS activity has been shown to be cytotoxic to human cancer cells in vitro and in
vivo [17].
Showing Research Papers: 1 to 50 of 51
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 51
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 1, GSH↓, 1, H2O2↑, 1, HO-1↓, 1, lipid-P↓, 1, lipid-P↑, 2, NRF2↓, 1, NRF2↑, 1, OXPHOS↑, 1, RNS↓, 1, ROS↓, 3, ROS↑, 6, i-ROS↑, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics ⓘ
AIF↑, 1, Insulin↓, 1, MMP↓, 3, MMP↑, 2, mtDam↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
ACLY↓, 3, ALAT↓, 1, AMPK↑, 2, FASN↓, 1, glucose↓, 1, GLUT2↓, 1, HK2↓, 1, HMG-CoA↓, 2, lactateProd↓, 1, LDH↓, 1, LDL↓, 11, PDK1↓, 1, PPARα↓, 1, PPARγ↑, 1, Warburg↓, 1,
Cell Death ⓘ
Akt↓, 2, p‑Akt↓, 1, APAF1↑, 1, Apoptosis↑, 7, BAD↑, 1, Bak↑, 1, BAX↑, 4, Bcl-2↓, 3, Bcl-xL↓, 1, BIM↑, 1, Casp↑, 1, Casp3↑, 3, Casp8↓, 1, Casp8↑, 2, Casp9↑, 1, Cyt‑c↑, 3, Fas↑, 1, hTERT/TERT↓, 1, iNOS↓, 1, MAPK↓, 1, Mcl-1↓, 1, Myc↓, 1, p27↑, 1,
Transcription & Epigenetics ⓘ
other↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, p‑eIF2α↑, 1, ER Stress↑, 2, GRP78/BiP↑, 2, UPR↑, 2, XBP-1↓, 1,
Autophagy & Lysosomes ⓘ
ATG5↑, 1, Beclin-1↑, 1, LC3B↑, 1, LC3II↑, 1, TumAuto↓, 1, TumAuto↑, 2,
DNA Damage & Repair ⓘ
DNAdam↑, 4, P53↑, 1, PARP↑, 2, cl‑PARP↑, 2, TP53↓, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK2↑, 1, CDK4↓, 1, cycD1/CCND1↓, 2, CycD3↓, 1, cycE/CCNE↓, 1, P21↑, 2, TumCCA↓, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, ERK↓, 2, HDAC↓, 2, HMGCR↓, 2, IGF-1↓, 2, IGF-1R↑, 1, mTOR↓, 3, mTORC1↓, 1, NOTCH1↑, 1, NOTCH3↓, 1, PI3K↓, 1, PTEN↑, 1, RAS↓, 1, STAT↓, 1, STAT3↓, 1, TOP1↓, 1, TumCG↓, 6, Wnt↓, 1, Wnt↑, 1,
Migration ⓘ
Ca+2↑, 3, CLDN1↓, 1, E-cadherin↑, 1, Fibronectin↓, 1, MMP-10↓, 1, MMP2↓, 2, MMP9↓, 2, MMP9↑, 1, PDGF↓, 1, PKCδ↓, 1, Rho↓, 1, Slug↓, 1, Snail↓, 1, TET1↑, 1, TumCI↓, 2, TumCMig↓, 2, TumCP↓, 4, TumMeta↓, 2, Twist↓, 1, Vim↓, 1, Zeb1↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 6, ATF4↑, 1, EGFR↓, 1, Hif1a↓, 2, VEGF↓, 3,
Barriers & Transport ⓘ
GLUT1↓, 1, P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, COX2↑, 2, ICAM-1↓, 1, IL10↓, 1, IL1β↓, 1, IL6↓, 1, Imm↑, 1, Inflam↓, 1, JAK1↓, 1, NF-kB↓, 2, NK cell↑, 1, PD-L1↑, 1, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 1,
Cellular Microenvironment ⓘ
cGAS–STING↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 2, BioEnh↑, 1, ChemoSen↑, 5, Dose↝, 2, eff↑, 12, Half-Life↝, 1, P450↓, 1, RadioS↑, 2, selectivity↑, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, ALP↓, 1, BP↓, 2, EGFR↓, 1, GutMicro↝, 1, hTERT/TERT↓, 1, IL6↓, 1, LDH↓, 1, Myc↓, 1, PD-L1↑, 1, TP53↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 3, AntiTum↑, 3, cardioP↑, 3, chemoP↑, 2, ChemoSideEff↓, 1, cognitive↑, 1, hepatoP↑, 1, memory↑, 2, neuroP↑, 2, OS↑, 1, QoL↑, 2, radioP↑, 1, Remission↑, 1, RenoP↑, 2, Risk↓, 4, toxicity↓, 3,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 187
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 24, Catalase↑, 8, GPx↑, 6, GPx1↑, 1, GSH↑, 8, GSTs↑, 2, H2O2↓, 1, HDL↑, 7, HDL∅, 1, HO-1↑, 4, HO-2↓, 1, lipid-P↓, 6, MDA↓, 4, MPO↓, 2, NADH↓, 1, NQO1↑, 2, NRF2↑, 5, RNS↓, 2, ROS↓, 17, ROS⇅, 1, mt-ROS↓, 1, SIRT3↑, 1, SOD↑, 10, SOD1↑, 1, SOD2↑, 1, TAC↑, 1, TrxR1↑, 1, VitC↑, 1,
Metal & Cofactor Biology ⓘ
Ferritin↑, 1, IronCh↑, 1,
Mitochondria & Bioenergetics ⓘ
mtDam↓, 1,
Core Metabolism/Glycolysis ⓘ
ACLY↓, 1, adiP↓, 1, adiP↑, 1, ALAT?, 1, ALAT↓, 3, AMPK↑, 2, CRM↑, 1, glucose↓, 3, LDL↓, 39, NADPH↓, 3, PPARα↑, 2, PPARγ↑, 1, SIRT1↑, 4,
Cell Death ⓘ
Akt↓, 1, Akt↑, 1, BAX↓, 1, Bcl-2↑, 1, Cyt‑c↓, 1, iNOS↓, 2, MAPK↝, 1,
Kinase & Signal Transduction ⓘ
AMPKα↑, 1, TRPV3↑, 1,
Transcription & Epigenetics ⓘ
Ach↑, 1, other↓, 3, other↑, 3, other↝, 1, other∅, 1,
Protein Folding & ER Stress ⓘ
ER Stress↓, 1, NQO2↑, 1,
Cell Cycle & Senescence ⓘ
P21↓, 1,
Proliferation, Differentiation & Cell State ⓘ
FOXO3↑, 1, GSK‐3β↓, 1, HDAC↓, 1, IGF-1↑, 1, IGFBP1↑, 1, mTOR↓, 2, mTOR↑, 1, PI3K↑, 1, PTEN↓, 1,
Migration ⓘ
AntiAg↑, 6, AntiAg∅, 1, Ca+2?, 1, CDK5↓, 1, E-sel↓, 1, MMPs↓, 2, RAGE↓, 1, TGF-β↓, 1, TXNIP↓, 1,
Angiogenesis & Vasculature ⓘ
NO↓, 6,
Barriers & Transport ⓘ
BBB↑, 3, BBB↝, 1, GastroP↑, 1,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, COX2↓, 8, CRP↓, 2, IL10↑, 1, IL17↓, 1, IL1β↓, 7, IL23↓, 1, IL4↓, 1, IL4↑, 1, IL6↓, 3, IL8↓, 1, Imm↑, 2, Inflam↓, 21, Inflam↑, 1, MCP1↓, 2, NF-kB↓, 7, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 8,
Synaptic & Neurotransmission ⓘ
AChE↓, 8, ADAM10↑, 1, BChE↓, 3, BDNF↑, 4, ChAT↑, 1, MAOA↓, 1, tau↓, 2, p‑tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 6, BACE↓, 2, MAOB↓, 1, NLRP3↓, 2,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 7, BioAv↝, 4, BioEnh↑, 2, Dose↝, 8, eff↓, 4, eff↑, 9, eff↝, 1, Half-Life↑, 2, Half-Life↝, 1,
Clinical Biomarkers ⓘ
ALAT?, 1, ALAT↓, 3, ALP↓, 1, AST↓, 4, BP↓, 6, CRP↓, 2, Ferritin↑, 1, GutMicro↑, 1, IL6↓, 3, NOS2↓, 1, RAGE↓, 1,
Functional Outcomes ⓘ
AntiAge↑, 4, AntiDiabetic↑, 5, BOLD↑, 1, cardioP↑, 16, cognitive↑, 11, hepatoP↑, 1, memory↑, 9, motorD↑, 1, MusCon↓, 1, neuroP↑, 12, Obesity↓, 2, OS↑, 3, QoL↑, 2, RenoP↑, 3, Risk↓, 4, Strength↑, 1, toxicity↓, 4, toxicity⇅, 1, toxicity∅, 1, Weight↓, 1, Weight↝, 1, Weight∅, 1,
Infection & Microbiome ⓘ
Bacteria↓, 1, Sepsis↓, 1,
Total Targets: 160
Scientific Paper Hit Count for: LDL, LDL-cholesterol
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#:71 State#:% Dir#:1
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