AntiAge Cancer Research Results
AntiAge, Anti-aging: Click to Expand ⟱
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Anti-aging strategies hold promise for improving overall health and potentially reducing cancer risk, the intricate interplay between the molecular mechanisms of aging and cancer requires careful consideration.
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Scientific Papers found: Click to Expand⟱
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*antiOx↑, Both of alpha lipoic acid and its reduced form have been shown to possess anti-oxidant, cardiovascular, cognitive, anti-ageing, detoxifying, anti-inflammatory, anti-cancer, and neuroprotective pharmacological properties
*cardioP↑,
*cognitive↑, Alpha lipoic acid has the ability to decrease cognitive impairment and may be a successful therapy for Alzheimer’s disease and any disease related dementias
*AntiAge↑,
*Inflam↓,
*AntiCan↑,
*neuroP↑, ALA has neuroprotective effects in experimental brain injury caused by trauma and subarachnoid hemorrhage
*IronCh↑, Also, the ability of ALA to chelate metals can produce an antioxidant effect
*ROS↑, DHLA can exert a pro-oxidant effect of donating its electrons for the reduction of iron, which can then break down peroxide to the prooxidant hydroxyl radical via the Fenton reaction [10]. So, ALA and its reduced form DHLA, can promote antioxidant pr
*Weight↓, α-lipoic acid supplementation at a dose of 300 mg/day might help to could help to promote weight loss and fat mass reduction in healthy overweight/obese women following an energy-restricted balanced diet
*Ach↑, Alpha lipoic acid increases the production of Acetylcholine (Ach) via activating choline acetyl transferase and increases glucose uptake, hence, supplying more acetyl-CoA for the production of Ach of each
*ROS↓, also scavenges
reactive oxygen species, thereby increasing the concentration levels
of reduced Glutathione (GSH).
*GSH↑,
*lipid-P↓, Alpha lipoic acid can scavenge lipid peroxidation products as hydroxynonenal and
acrolein.
*memory↑, learning and memory in the passive avoidance test partially
through its antioxidant activity.
*NRF2↑, α-LA treatment has been shown to increase Nrf2 nuclear localization
*ChAT↑, Alpha lipoic acid increases the production of Acetylcholine (Ach) via activating choline acetyl transferase and increases glucose uptake, hence, supplying more acetyl-CoA for the production of Ach of each
*GlucoseCon↑,
*Acetyl-CoA↑,
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*antiOx↑, antioxidant potential and free radical scavenging activity.
*ROS↓,
*IronCh↑, Lipoic acid acts as a chelating agent for metal ions, a quenching agent for reactive oxygen species, and a reducing agent for the oxidized form of glutathione and vitamins C and E.
*cognitive↑, α-Lipoic acid enantiomers and its reduced form have antioxidant, cognitive, cardiovascular, detoxifying, anti-aging, dietary supplement, anti-cancer, neuroprotective, antimicrobial, and anti-inflammatory properties.
*cardioP↓,
AntiCan↑,
*neuroP↑,
*Inflam↓, α-Lipoic acid can reduce inflammatory markers in patients with heart disease
*BioAv↓, bioavailability in its pure form is low (approximately 30%).
*AntiAge↑, As a dietary supplements α-lipoic acid has become a common ingredient in regular products like anti-aging supplements and multivitamin formulations
*Half-Life↓, it has a half-life (t1/2) of 30 min to 1 h.
*BioAv↝, It should be stored in a cool, dark, and dry environment, at 0 °C for short-term storage (few days to weeks) and at − 20 °C for long-term storage (few months to years).
other↝, Remarkably, neither α-lipoic acid nor dihydrolipoic acid can scavenge hydrogen peroxide, possibly the most abundant second messenger ROS, in the absence of enzymatic catalysis.
EGFR↓, α-Lipoic acid inhibits cell proliferation via the epidermal growth factor receptor (EGFR) and the protein kinase B (PKB), also known as the Akt signaling, and induces apoptosis in human breast cancer cells
Akt↓,
ROS↓, α-Lipoic acid tramps the ROS followed by arrest in the G1 phase of the cell cycle and activates p27 (kip1)-dependent cell cycle arrest via changing of the ratio of the apoptotic-related protein Bax/Bcl-2
TumCCA↑,
p27↑,
PDH↑, α-Lipoic acid drives pyruvate dehydrogenase by downregulating aerobic glycolysis and activation of apoptosis in breast cancer cells, lactate production
Glycolysis↓,
ROS↑, HT-29 human colon cancer cells; It was concluded that α-lipoic acid induces apoptosis by a pro-oxidant mechanism triggered by an escalated uptake of mitochondrial substrates in oxidizable form
*eff↑, Several studies have found that combining α-lipoic acid and omega-3 fatty acids has a synergistic effect in slowing functional and cognitive decline in Alzheimer’s disease
*memory↑, α-lipoic acid inhibits brain weight loss, downregulates oxidative tissue damage resulting in neuronal cell loss, repairs memory and motor function,
*motorD↑,
*GutMicro↑, modulates the gut microbiota without reducing the microbial diversity (
*antiOx↑, ALA is a low molecular weight antioxidant, readily absorbed from the diet or an oral dose, and crosses the blood brain barrier
*BBB↑,
*VitC↑, DHLA regenerates through redox cycling other antioxidants like vitamin C and E and raises levels of intracellular glutathione, an important thiol antioxidant
*VitE↑,
*GSH↑,
*IronCh↑, ALA al-
so chelates certain metals, forming stable complexes with copper,
manganese and zinc (Sigel 1978)
*neuroP↑, ALA would seem an ideal candidate as an antioxidant agent in neurodegenerative diseases.
*NO↓, ALA also modulates nitric oxide levels in brain and neural tissue, which may have effects in neurodegeneration, learning, cognition, and aging (Gross 1995)
*cognitive↑, elderly patients with dementia were given ALA. Findings suggested a stabilization of cognitive functions in the study group,
*AntiAge↑,
*memory↑, ALA has gained considerable attention following studies demonstrating partial reversal of memory loss in aged rats.
*ROS↓, scavenging hy-
droxyl or superoxide radicals (Suzuki 1991) and by scavenging per-
oxyl radicals (
*ROS↓, carnosine may be potentially beneficial in the treatment of AD because of its free-radical scavenger and metal chelating properties.
*IronCh↑, Carnosine chelates intracellular Zn2+
*Aβ↓, strong reduction in the hippocampal intraneuronal accumulation of Aβ
*AntiAge↑, Carnosine also exerts anti-aging activities by neutralizing injurious glycated proteins and aldehydic products of lipids peroxydation
*lipid-P↓,
*cognitive↑, We observed a positive trend toward a better cognitive performance as indicated by the decreased latency to find the platform
*memory∅, Carnosine supplementation was not able to completely rescue long-term memory deficits in treated 3xTg-AD mice.
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*ROS↓, carnosine scavenges reactive oxygen species (ROS)
*IronCh↑, it can chelate divalent metal ions: heavy metal chelating activity
*AntiAge↑, can slow down aging.
*antiOx↑, natural antioxidant [4] and has anti-inflammatory and neuroprotective properties
*Inflam↓,
*neuroP↑,
*lipid-P↓, Carnosine reduces lipid peroxidation, but also inhibits oxidative modification of protein exposed to hydroxyl radicals
*toxicity↓, carnosine can be recommended as a natural cure that has no side effects but is highly efficient
*NOX4↓, human kidney tubular epithelial (HK2) cells indicated that carnosine decreased NADPH oxidase (Nox) 4 expression and increased total superoxide dismutase (T-SOD) activity, thus reducing the production of intracellular ROS,
*SOD↑,
*HNE↓, Rising data indicate that carnosine acts as a scavenger of reactive and cytotoxic carbonyl species including 4-hydroxynonenal (HNE)
*IL6↓, anserine and/or carnosine supplementation significantly decreased IL-6, TNF-α, and IL-1β in pre-treated mice with MPTP-induced PD,
*TNF-α↓,
*IL1β↓,
*Sepsis↓, carnosine has a beneficial effect on reducing acute kidney injury due to septic shock
*eff↑, carnosine on ischemic stroke, there was a 29.4% average reduction in infarct volume with a clear dose-dependent effect (38.1% reduction on 1000 mg/kg dose compared with 13.2% for doses less than 500 mg/kg)
*GABA↝, In addition to the carnosine-histidine-histamine pathway, carnosine can also have a direct impact on CA1 pyramidal neurons [212] or act as a precursor for the neurotransmitter GABA
*Aβ↓, Several studies have reported that carnosine supplementation reduced β-amyloid cumulation in the hippocampus of a transgenic mouse model of AD
Glycolysis↓, carnosine has the ability to inhibit glycolysis and thus achieve an antitumor effect
AntiTum↑,
p‑Akt↓, significant reduction of Akt phosphorylation in the U87 glioblastoma cell line
TumCCA↑, Carnosine has an effect in bladder cancer by stopping the G1 phase cell cycle by increasing p21WAF1 expression and decreasing cyclin/CDK complexes
angioG↓, inhibits angiogenesis by suppressing VEGFR-2
VEGFR2↓,
NF-kB↓, suppressing nuclear factor kB (NF-κB) signaling pathway activation in human colon cancer cells
*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↓,
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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
*OS↑, The permanent or periodic reduction of calorie intake without malnutrition (caloric restriction and fasting) is the only strategy that reliably extends healthspan in mammals including non-human primates.
*AntiAge↑, CRMs will become part of the pharmacological armamentarium against aging and age-related cardiovascular, neurodegenerative, and malignant diseases.
*cardioP↑,
*neuroP↑,
AntiCan↑,
*TNF-α↓, In healthy humans, CR also decreases the levels of circulating tumor necrosis factor-α
*Weight↓, In obese humans, CR promotes significant weight loss and improves general health
*BP↓, Figure 1
*Inflam↓,
*Insulin↓,
*ROS↓,
*AMPK↑,
*mTOR↓,
*SIRT1↑, Resveratrol and Other SIRT1 Activators
CRM↑, Figure2: HCA, Resveratrol, Spermidine, Aspirin, Berberine, EGCG, QC, etc
*CRM↓, AcCoA depleting agents (e.g., hydroxycitrate),
*Dose?, acetyltransferase inhibitors (e.g., anacardic acid, curcumin, epigallocatechin-3-gallate, garcinol, spermidine)
*AntiAge↑, Another common characteristic of these agents is their capacity to reduce aging-associated diseases and to confer protective responses against ischemia-induced organ damage.
*Acetyl-CoA↓, Altogether, these observations point to the idea that starvation causes autophagy because it results in the early depletion of AcCoA
*SIRT1↑, nduction of the deacetylase activity of sirtuins (as a result of changing NADH/NAD+ ratios and increased SIRT1 expression)
*AMPK↑, activation of AMPK activity (as a result of changing ATP/ADP ratios)
*mTORC1↓, inhibition of MTORC1 (as a result of amino acid depletion).
*AntiAge↑, CR or intermittent fasting are known for their wide life-span-extending
chemoP↑, fasting can reduce the subjective and objective toxicity of cytotoxic anticancer chemotherapies, both in humans and in mouse models, at the same time that it improves treatment outcome in mice
*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.
*antiOx↑, Curcumin is a dietary polyphenol and a bioactive phytochemical agent that possesses anti-inflammatory, antioxidant, anticancer, and chemopreventive properties.
*Inflam↓,
AntiCan↑,
chemoPv↑,
*AntiAge↑, antiaging, and neuroprotective as well as wound healing and regenerative effects of curcumin.
*neuroP↑,
*Wound Healing↑,
AntiAge↑, dietary restriction of methionine (MR), an essential amino acid, and the reduction of which has anti-aging and anti-obesogenic properties, influences cancer outcome through controlled and reproducible changes to one-carbon metabolism.
MethCyc↓, MR reduced the levels of methionine-related metabolites within two days, which were sustained throughout the intervention
TumCG↓, MR inhibited tumour growth in CRC119
ChemoSen↑, However, MR synergized with 5-FU treatment, leading to a marked inhibition on tumour growth
RadioS↑, Strikingly, MR with a focal dose of 20 Gy reduced tumour growth and extended the tumour tripling time by 52%
OS↑,
GSH↓, MR reduced NAC and glutathione in all subjects
IGF-1↓, Long-term CR is reported to reduce IGF-1 serum levels in rodents by ~30–40%, protecting them against several types of cancers
OS↑, effects of CR in retarding aging, by increasing lifespan by ~35%, reducing the incidence of kidney disorders, chronic pneumonia and tumors [
AntiAge↑,
glucose↓, underline mechanisms could be mediated by the decrease in blood glucose, IGF-1 and insulin levels
Insulin↓,
*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.
MMP↓, nsPEF bypasses plasma-membrane shielding to porate organelles, collapse mitochondrial potential, perturb ER calcium, and transiently open the nuclear envelope.
Ca+2↑,
eff↑, synergy with checkpoint blockade.
ER Stress↑, capacity to directly target organelles such as mitochondria, endoplasmic reticulum (ER),
selectivity↑, selectively ablate solid tumors, suppress metastatic spread, and prime systemic anti-tumor immunity while sparing adjacent normal tissue [7,9,10,11,12,13,14,15].
CSCs↓, Preclinical investigations have demonstrated that nsPEFs significantly reduce CSC-associated subpopulations, including CD44+/CD24− cells in breast cancer xenografts and CD133+ glioma stem-like cells
CD44↓,
CD133↓,
ROS↑, nsPEFs release Ca2+ from the ER, disrupt mitochondrial membrane potential, induce reactive oxygen species (ROS) generation, and perturb nuclear chromatin structure within nanoseconds
Imm↑, nsPEFs not only eliminate local tumor cells but also convert the tumor into an in situ vaccine, amplifying their therapeutic relevance in the era of immunotherapy
DNAdam↑, figure 2
MOMP↑, induce mitochondrial outer membrane permeabilization (MOMP)
Cyt‑c↑,
Casp9↑, Subsequent release of cytochrome c enables apoptosome assembly, caspase-9 activation, and downstream activation of caspases-3/7, culminating in cell death
Casp3↑,
Casp9↑,
TumCD↑,
Fas↑, In certain cell types, nsEP can also activate the extrinsic pathway, where Fas receptor clustering stimulates caspase-8.
UPR↑, This rapid surge triggers ER stress pathways, activates unfolded protein response (UPR) signaling, and promotes cross-talk with mitochondria through mitochondria-associated membranes (MAMs)
Dose↝, longer ns pulses (100–300 ns) generate sustained plasma membrane charging, resulting in robust Ca2+ influx, osmotic imbalance, and apoptotic priming.
Dose↝, A critical threshold of 10–20 kV/cm is generally required to initiate pore formation in malignant cells, with higher amplitudes (>30–40 kV/cm) producing more extensive permeabilization [100].
Dose↓, Low pulse counts (<100) frequently produce reversible stress responses, such as transient mitochondrial depolarization or ER Ca2+ release, without committing cells to apoptosis. I
Dose↑, In contrast, higher pulse counts (500–1000) lead to irreversible apoptosis, caspase activation, and release of DAMPs that initiate ICD [80,106].
HMGB1↓, ICD after nsPEF is characterized by surface exposure of calreticulin, extracellular ATP release, and HMGB1 emission
eff↑, The integration of nsPEFs with NP-based systems thus represents a synergistic platform where physical membrane poration and molecular targeting cooperate to maximize therapeutic efficacy.
EPR↑, demonstrates that PEF + AuNPs enhanced membrane permeabilization compared with PEF alone,
ChemoSen↑, The superior efficacy of delayed drug administration following nsPEF exposure can be attributed to transient biophysical and biochemical changes that persist after pulsing.
ETC↝, study demonstrated that nsPEFs dynamically alter trans-plasma membrane electron transport (tPMET) and mitochondrial electron transport chain activity, resulting in differential ROS generation in cancer versus non-cancer cells (Figure 9).
*AntiAge↑, Mechanistically, nsPEFs upregulated HIF-1α and SIRT1, mediators of mitochondrial retrograde signaling, thereby reversing hallmarks of aging
*Hif1a↑,
*SIRT1↑,
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*MMP↑, NsPEF treatment reverses d-galactose-induced endothelial senescence by restoring mitochondrial membrane potential. marked elevation in mitochondrial membrane potential
*Hif1a↑, NsPEF activates key MNRC markers HIF-1α and SIRT1, rescuing mitochondrial-nuclear communication.
*SIRT1↑,
*ROS↓, These effects were confirmed by concurrent reductions in SA-β-Gal activity and in ROS production, and increases in EdU-positive (DNA-synthesizing) cells.
*AntiAge↑, These findings suggest that nsPEF treatments rescue ECs from aging by restoring MNRC, highlighting its potential as a therapeutic strategy for age-related vascular diseases.
*Dose↝, mice received daily nsPEF treatment (3 kV/cm) for 14 consecutive days.
*angioG↑, The nsPEF treatments stimulate skin angiogenesis in different aged rodent models.
eff↑, Due to FIS’s poor solubility and high lipophilicity, it was encapsulated in D-limonene-modified phospholipid carriers, limosomes (LIMOs), co-formulated with Ascorbyl Palmitate (AP) and Hyaluronan (HYA) to improve FIS’s solubility, skin penetration, a
*antiOx↑, FIS-AP-HYA-LIMOs showed potent in vitro antioxidant activity, high biocompatibility, and remained stable for 6 months.
*MMP9↓, In vivo studies revealed the downregulation of MMP9, TNFα, and NF-κB, accompanied by increased SOD and CAT levels, indicating superior anti-ageing, anti-inflammatory, and antioxidant effects compared to FIS suspension
*TNF-α↓,
*NF-kB↓,
*SOD↑,
*Catalase↑,
*AntiAge↑,
*Inflam↓,
*JNK↓, AP-HYA-LIMOs decreased JNK expression, preserved the integrity of skin layers, and reduced collagen degradation.
*tau↓, fulvic acid, the main active principle, blocks tau self-aggregation, opening an avenue toward the study of Alzheimer's therapy.
*AntiAge↑, Shilajit has been known and used for centuries by the Ayurvedic medicine, as a rejuvenator and as antiaging compound
*Strength↑, two important characteristics of a rasayana compound in the ancient Indian Ayurvedic medicine: that is, to increase physical strength and to promote human health
*Dose↝, health benefits of shilajit have been shown to differ from region to region, depending on the place from which it was extracted [3, 4].
*BioAv↑, Fulvic acid is soluble in water under different pH conditions, and because of its low molecular weight (around 2 kDa), it is well absorbed in the intestinal tract and eliminated within hours from the body
*antiOx↑, fulvic acid is known by its strong antioxidant actions [9] and likely has systemic effects as complement activator
*memory↑, figure 1 memory enhancer
*Inflam↓, fulvic acid, is known by its properties such as antioxidant, anti-inflammatory, and memory enhancer
*cognitive↑, Our laboratory has found evidence on the high activity of the Andean form of shilajit in improving cognitive disorders and as a stimulant of cognitive activity in humans
*neuroP↑, neuroprotective agent against cognitive disorders
*toxicity↝, Studies indicate the shilajit consumption without preliminary purification may lead to risks of intoxication given the presence of mycotoxin, heavy metal ions, polymeric quinones (oxidant agents), and free radicals, among others
*toxicity↑, recent studies indicate that several ayurvedic products including shilajit and other Indian manufactured products commercialized by the Internet may contain detectable heavy metals levels as lead, mercury, and arsenic
*ROS↓, Magnolia officinalis (M. officinalis) extract significantly lowered the levels of ROS in senescent fibroblasts.
*antiOx↑, honokiol was demonstrated as a core ingredient of M. officinalis extract that exhibits antioxidant effects.
*AntiAge↑, new approaches to anti–aging treatments
*MMP↑, increases MMP
*ECAR↓, senescent fibroblasts treated with M. officinalis extract had lower ECAR values than those treated with DMSO, suggesting that M. officinalis treatment lowed glycolysis rate
*Glycolysis↓, honokiol, similar to M. officinalis, reduced the dependence of glycolysis as an energy source, indicating restoration of mitochondrial function by honokiol.
*PAR-2↓, downregulation of PAR–2 expression by M. officinalis may reduce skin pigmentation.
*CXCL12↑, upregulation of SDF–1 expression by M. officinalis may reduce skin pigmentation.
*BMAL1↑, activation of Bmal–1 expression by M. officinalis promote skin turnover.
*mt-ROS↓, compared to M. officinalis extract, honokiol at 1 and 10 μM was more effective in lowering mitochondrial ROS levels
*OXPHOS↓, Inhibition of oxidative phosphorylation and induction of a compensatory shift toward glycolysis resulted in lower compensatory glycolysis in honokiol–treated senescent fibroblasts
*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↑,
*AntiAge↑, RMF exposure prolonged the lifespan of C. elegans and slowed the aging of HUVECs
*AMPK↑, RMF treatment of HUVECs showed that activation of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) was associated with decreased mitochondrial membrane potential (MMP) due to increased intracellular Ca2+ concentrations induced by endo
*mPGES-1↓,
*Ca+2↑,
*ER Stress↑,
*OS↑, prolonged lifespan of C. elegans was associated with decreased levels of daf-16 which related to the insulin/insulin-like growth factor signaling pathway (IIS) activity and reactive oxygen species (ROS),
*ROS↓,
AntiCan↑, RMF can inhibit the growth of various types of cancer cells in vitro and in vivo and improve clinical symptoms of patients with advanced cancer.
breath↑, 0.4T, 7Hz RMF was applied to treat 13 advanced non-small cell lung cancer patients (2 h/day, 5 days per week, for 6–10 weeks)
Pain↓, Decreased pleural effusion (2 patients, 15.4%), remission of shortness of breath (5 patients, 38.5%), relief of cancer pain (5 patients, 38.5%), increased appetite (6 patients, 46.2%), improved physical strength (9 patients, 69.2%), regular bowel mov
Appetite↑,
Strength↑,
BowelM↑,
TumMeta↓, The same RMF (2 h/day, for 43 days) can also suppress the growth and metastasis of B16-F10 cells in vivo
TumCCA↑, The up-regulated transcription of miR-34a induced cell proliferation inhibition, cell cycle arrest, and cell senescence by targeting E2F1/E2F3, two members of E2F family which are major regulators of the cell cycle,
ETC↓, 2h exposure) effectively inhibited the growth of two types of cultured brain cancer cells, glioblastoma cells and diffuse intrinsic pontine glioma cells. They found that the mitochondrial electron transport chain was significantly disturbed by RMF,
MMP↓, which caused loss of mitochondrial integrity, decreased mitochondrial carbon flux in cancer cells, and eventual cancer cell death (Sharpe et al., 2021).
TumCD↑,
selectivity↑, same group further reported that the
same RMF can also selectively kill cultured human glioblastoma and
non-small cell lung cancer cells, and leave normal cells unharmed
ROS↑, Mechanistic studies revealed that RMF can increase the mitochondrial ROS level, which further activated the caspase-3 and disturbed the electron fflow in the respiratory chain pathway in cancer cells. (Helekar et al., 2021).
Casp3↑,
TumCG↓, 0.4T, 7.5Hz RMF (2 h/day, for 5 days) inhibited the growth of mouse melanoma cell line B16–F10 in vitro,
TumCCA↑, and its mechanism involved cell cycle arrest and decomposition of chromatins.
ChrMod↑,
TumMeta↓, (2 h/day, for 43 days) can also suppress the
growth and metastasis of B16–F10 cells in vivo,
Imm↑, benefiting from improved immune function, including decreased regulatory T cells, increased T cells, and dendritic cells
DCells↑,
Akt↓, inhibiting the activation of the AKT pathway (Tang et al., 2016). T
OS⇅, 51 women with advanced breast cancer underwent RMF treatment. The results showed that 27 patients among them achieved signicant therapeutic effects, and there were no side-effects
toxicity↓,
QoL↑, 13 advanced non-small cell lung cancer patients the quality of life was improved in different degrees. Median survival and 1-year survival rate was 50% and 100% longer
hepatoP↑, In addition, it seems that the RMF can also attenuate liver damage in mice bearing MCF7 and GIST-T1 cells (Zha et al., 2018)
Pain↓, The results showed that the RMF treatment reduced abdominal pain by 42.9% (9/21), nausea/vomiting by 19.0% (4/21), weight loss by 52.4% (11/21), ongoing blood loss by 9.5% (2/21), improved physical strength by 23.8% (5/21) and sleep quality by 19.0%
Weight↑,
Strength↑,
Sleep↑,
IL6↓, Furthermore, decreased levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and keratinocyte-derived chemokine (KC) were observed
CD4+↑, it was discovered that macrophages and dendritic cells were
activated, CD4+ T and CD8+ T lymphocytes increased, and the ratio of
Th17/Treg was balanced.
CD8+↑,
Ca+2↑, effects of RMF were strongly
associated with increased calcium tunnel activity and intracellular Ca2+
level in CNS
radioP↑, These results suggest that RMF may be helpful to alleviate the
damage of hematopoietic function caused by radiotherapy and chemotherapy
chemoP↑,
*BMD↑, 0.4T, 8Hz RMF treatment (30min/day, for 30 days) along with calcium supplement, synergistically improved bone density
*AntiAge↑, In 2019, Xu et al. reported that a 4h exposure to a 0.2T, 4Hz RMF
delayed the aging of human umbilical vein endothelial cells (HUVEC)
*AMPK↑, Mechanistic research revealed that RMF treatment increased the expression of AMPK while reducing the expression of p21, p53 and mTOR.
*P21↓,
*P53↓,
*mTOR↓,
*OS↑, They also discovered that the RMF (2 h/day, for 6, 10 or 14days) can prolong the
health status lifespan of Caenorhabditis elegans.
*β-Endo↑, 0.1–0.8T, 0.33Hz RMF treatment signicantly increased the β-endorphin level in the blood of rabbits and humans (23 times higher than before). Moreover, it decreased serotonin (5-HT) in brains, small intestine tissue and serum of mice.
*5HT↓,
*Dose↝, MSM is effective in reducing visual signs of skin ageing even at a low dose of 1 g/d.
*AntiAge↑, (MSM) is an organosulfur compound with known benefits for joint health, sports nutrition, immune function, and anti-aging formulations and is gaining popularity as a nutritional supplement for the support of hair, skin and nails.
*AntiAge↑, Hericium erinaceus (He) has been demonstrated to display a variety of physiological effects, including anti-aging properties.
*other↑, H. erinaceus primordium (He2) extract contains a high amount of Ergothioneine (ERGO), the longevity vitamin.
*NOS2↓, This effect was accompanied by a significant decrease in some oxidative stress markers (NOS2, COX2) paralleled by an increase in P53,
*COX2↓,
*P53↑,
*neuroP↑, emonstrated the neuro-protective and preventive effects of He2 extract during aging,
*AntiAge↑, resveratrol shows significant promise in combating skin photoaging, pterostilbene is still in the early exploration phases.
*eff↑, Pterostilbene demonstrates potential to outperform resveratrol
*Inflam↓, well known for properties, such as anti-aging, anti-inflammatory, anti-melanogenesis, and anti-cancer
*AntiCan↑,
*ROS↓, Pterostilbene significantly prevented UVB-induced reduction in cell viability and increased reactive oxygen species (ROS) production
*Catalase↑, pterostilbene significantly increased gene expression of catalase (CAT)
*GSR↑, glutathione reductase (GSR), heme oxygenase-1 (HMOX-1) and NAD(P)H quinone dehydrogenase 1 (NQO1);
*HO-1↑,
*NAD↑,
*NQO1↑,
*SOD↑, while significantly increasing glutathione disulfide (GSSH), SOD, nuclear Nrf2,
*NRF2↑,
*AntiAge↑, Resveratrol produces changes associated with longer lifespan, including increased insulin sensitivity, reduced insulin-like growth factor-1 (IGF-I) levels, increased AMP-activated protein kinase (AMPK)
*IGF-1↓,
*AMPK↑,
*CRM↑, resveratrol opposed the effects of the high-calorie diet in 144 out of 153 significantly altered pathways.
*PGC-1α↑, activated receptor- γ coactivator 1α (PGC-1α) activity, increased mitochondrial number, and improved motor function.
*mtDam↓,
*motorD↑, Surprisingly, the resveratrol-fed HC mice steadily improved their motor skills as they aged
*hepatoP↑, At 18 months of age it was apparent that the high-calorie diet greatly increased the size and weight of livers and that resveratrol prevented these changes
*Dose↝, this study shows that an orally available small molecule at doses achievable in humans can safely reduce many of the negative consequences of excess caloric intake, with an overall improvement in health and survival.
*AntiAge↑, potentially slowing the aging process
*Dose↑, generally 5 g per day [23,45,54]. These doses demonstrate that a Cmax of approximately 4 µM is attainable in human plasma
*BioAv↑, combining various food and beverage consumption with resveratrol administration, with the notion that the combination of resveratrol with multiple polyphenols is ultimately responsible for the “French Paradox”
*BioAv↑, standard breakfast with 2000 mg resveratrol supplementation yielded a significantly greater Cmax and AUC than that obtained following a high fat breakfast.
*BioAv∅, no major differences in bioavailability parameters between fed and fasted conditions following 400 mg of resveratrol administration
*BioAv↑, SRT501, the patented formulation of resveratrol which is micronized with particle sizes < 5 µm and solubilized (fourfold increase)
*BioAv↑, For this reason, it has been suggested that combining resveratrol with other polyphenols which are targeted by these enzymes may increase bioavailability
*BioAv↑, Piperine, a polyphenol found in black pepper, has been shown to substantially increase serum Cmax and AUC of resveratrol in rats
*BioAv↑, Resveratrol loaded onto lipid-core nanocapsules improved tissue concentration in the brain, liver, and kidney of healthy rats compared to free resveratrol
*RenoP↑, Resveratrol improved renal function, proteinuria, histological changes and inflammation in aging mice
*Inflam↓,
*NRF2↑, expression of Nrf2-HO-1-NOQ-1 signaling and SIRT1-AMPK-PGC-1α signaling was increased in the RSV group
*HO-1↑,
*SIRT1↑,
*ROS↓, Activation of the Nrf2 and SIRT1 signaling pathways ameliorated oxidative stress and mitochondrial dysfunction.
AntiAge↑, Pharmacological targeting of Nrf2 signaling molecules may reduce the pathologic changes of aging in the kidney
*antiOx↑, Curcumin, epigallocatechin gallate (EGCG), thymoquinone, and resveratrol exhibit antioxidant, anti-inflammatory, and autophagy-enhancing effects that target core pathways involved in cellular senescence and tissue degeneration.
*Inflam↓,
*AntiAge↑, phytochemicals regulate key molecular players such as sirtuins, AMPK, NF-κB, and mTOR, offering promise in delaying age-associated pathologies and promoting longevity.
*SIRT1↑, Resveratrol (20 µM) ‘s contributions to mitochondrial function improvement are evident through its activation of the Sirt1/Sirt3-FoxO pathway
*SIRT3↑,
*FOXO↑,
*ROS↓, reduced intracellular ROS levels,
TumCP↓, including in tumor cell proliferation, apoptosis, metastasis, and inflammation
Apoptosis↑,
TumMeta↓,
Inflam↓,
*antiOx↑, RA is therefore considered to be the strongest antioxidant of all hydroxycinnamic acid derivatives
*AntiAge↑, , it also exerts powerful antimicrobial, anti-inflammatory, antioxidant and even antidepressant, anti-aging effects
*ROS↓, RA and its metabolites can directly neutralize reactive oxygen species (ROS) [10] and thereby reduce the formation of oxidative damage products.
BioAv↑, RA is water-soluble, and according to literature data, the efficacy of secretion of this compound in infusions is about 90%
Dose↝, Accordingly, it is possible to consume approximately 110 mg RA daily, i.e., approximately 1.6 mg/kg for adult men weighing 70 kg.
NRF2↑, liver cancer cell line, HepG2, transfected with plasmid containing ARE-luciferin gene, RA predominantly enhances ARE-luciferin activity and promotes nuclear factor E2-related factor-2 (Nrf2) translocation from cytoplasm to the nucleus
P-gp↑, and also increases MRP2 and P-gp efflux activity along with intercellular ATP level
ATP↑,
MMPs↓, RA concurrently induced necrosis and apoptosis and stimulated MMP dysfunction activated PARP-cleavage and caspase-independent apoptosis.
cl‑PARP↓,
Hif1a↓, inhibits transcription factor hypoxia-inducible factor-1α (HIF-1α) expression
GlucoseCon↓, it also suppressed glucose consumption and lactate production in colorectal cells
lactateProd↓,
Warburg↓, may suppress the Warburg effects through an inflammatory pathway involving activator of transcription-3 (STAT3) and signal transducer of interleukin (IL)-6
TNF-α↓, RA supplementation also reduced tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2) and IL-6 levels, and modulated p65 expression [
COX2↓,
IL6↓,
HDAC2↓, RA induced the cell cycle arrest and apoptosis in prostate cancer cell lines (PCa, PC-3, and DU145) [31]. These effects were mediated through modulation of histone deacetylases expression (HDACs), specifically HDAC2;
GSH↑, RA can also inhibit adhesion, invasion, and migration of Ls 174-T human colon carcinoma cells through enhancing GSH levels and decreasing ROS levels
ROS↓,
ChemoSen↑, RA also enhances chemosensitivity of human resistant gastric carcinoma SGC7901 cells
*BG↓, RA significantly increased insulin index sensitivity and reduced blood glucose, advanced glycation end-products, HbA1c, IL-1β, TNFα, IL-6, p-JNK, P38 mitogen-activated protein kinase (MAPK), and NF-κB levels
*IL1β↓,
*TNF-α↓,
*IL6↓,
*p‑JNK↓,
*p38↓,
*Catalase↑, The reduced activities of CAT, SOD, glutathione S-transferases (GST), and glutathione peroxidase (GPx) and the reduced levels of vitamins C and E, ceruloplasmin, and GSH in plasma of diabetic rats were also significantly recovered by RA application
*SOD↑,
*GSTs↑,
*VitC↑,
*VitE↑,
*GSH↑,
*GutMicro↑, protective effects of RA (30 mg/kg) against hypoglycemia, hyperlipidemia, oxidative stress, and an imbalanced gut microbiota architecture was studied in diabetic rats.
*cardioP↑, Cardioprotective Activity: RA also reduced fasting serum levels of vascular cell adhesion molecule 1 (VCAM-1), inter-cellular adhesion molecule 1 (ICAM-1), plasminogen-activator-inhibitor-1 (PAI-1), and increased GPX and SOD levels
*ROS↓, Finally, in H9c2 cardiac muscle cells, RA inhibited apoptosis by decreasing intracellular ROS generation and recovering mitochondria membrane potential
*MMP↓,
*lipid-P↓, At once, RA suppresses lipid peroxidation (LPO) and ROS generation, whereas in HSC-T6 cells it increases cellular GSH.
*NRF2↑, Additionally, it significantly increases Nrf2 translocation
*hepatoP↑, Hepatoprotective Activity
*neuroP↑, Nephroprotective Activity
*P450↑, RA also reduced CP-produced oxidative stress and amplified cytochrome P450 2E1 (CYP2E1), HO-1, and renal-4-hydroxynonenal expression.
*HO-1↑,
*AntiAge↑, Anti-Aging Activity
*motorD↓, A significantly delays motor neuron dysfunction in paw grip endurance tests,
*antiOx↑, antioxidant and anti-inflammatory responses by inducing Nrf2 pathway and inhibiting NF-κB
*Inflam↓,
*NRF2↑, increased Nrf2 expression and nuclear localization after SFN treatment
*NF-kB↓,
*HDAC↓, inhibiting HDAC and DNA methyltransferases a
*DNMTs↓,
*neuroP↑, prevent neurodegeneration.
*AntiAge↑, “miraculous” drug to prevent aging and neurodegeneration.
*DNMT1↓, decrease the expression of DNA methyltransferases (DNMTs), especially DNMT1 and DNMT3b.
*DNMT3A↓,
*memory↑, SFN prevented the memory impairment induced by OKA in rats.
*HO-1↑, restored Nrf2 and antioxidant protein (GCLC, HO-1) expression
*ROS↓, diminished the oxidative stress by attenuating ROS and NO levels, and increased GSH concentration.
*NO↓,
*GSH↑,
*NF-kB↓, reducing NF-κB and TNF-α, and by rising IL-10
*TNF-α↓,
*IL10↑,
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TumCCA↑, Spermidine specifically interferes with the tumour cell cycle, resulting in the inhibition of tumor cell proliferation and suppression of tumor growth.
TumCP↓,
TumCG↓,
*Inflam↓, health improving effects, that includes remarkable anti-inflammatory effects
*antiOx↑, It is also a potent antioxidant, and reportedly improves the respiratory function
*neuroP↑, Dietary intake of spermidine reduces the risk of neurodegeneration, metabolic diseases, heart ailments, and cancer.
*cognitive↑, spermidine-induced autophagy slows the rate of cognitive decline due to its ability to clear amyloid-beta plaques in the brain
*Aβ↓,
*mitResp↑, Spermidine supplementation also enhances mitochondrial metabolism, and translational activity.
AntiCan↑, anticancer properties of spermidine are of particular interest as it is known to reduce the cancer-related mortality in humans
TumCD↑, in addition to impacting their discourse with the immune effectors that result in expediting the identification of tumor-associated antigens and eventually cancer cell death
TumAuto↑, Inhibition of acetyltransferase EP300 by spermidine is known to induce autophagy, which is one of the desirable approaches in the treatment of cancer.
*AntiAge↑, Lifelong oral spermidine administration is reported to extend the lifespan in mice by 25%, as evidenced by genetic investigations.
LC3B-II↑, Western blotting experiments have showed a surge in the levels of LC3 II/LC3 I, Atg5, and Beclin 1 proteins in spermidine administered HeLa cells.
ATG5↑,
Beclin-1↑,
mt-ROS↑, Spermidine induces mitochondrial reactive oxygen species (mtROS) mediated M2-polarization by producing a surge in the levels of H2O2 and mitochondrial peroxide in the presence of spermidine.
H2O2↑,
Apoptosis↑, Spermine is known to induce apoptosis in primary human cells as well as the malignant tumor cells by producing a surge in the intracellular level of reactive oxygen species (ROS)
*ROS↑,
ChemoSen↑, A combination of 5-fluorouracil and spermine analogues N 1 , N 11 -diethylnorspermine (DENSPM) (6, Figure 5) at concentrations 1.25, 2.5, 5, and 10 μM or α-difluoromethylornithine (DFMO) led to a synergistic killing of HCT116 colon carcinoma cells
MMP↓, and loss of membrane potential of mitochondria followed by a subsequent release of cytochrome c
Cyt‑c↑,
*EP300↓, potent autophagy inducers including spermidine de facto act as EP300 inhibitors.
*mTORC1↓, simultaneously inhibit mTORC1.
*CRM↑, caloric restriction or intermediate fasting,7 continuous or intermittent medication of rapamycin,8, 9, 10 administration of the sirtuin 1-activator resveratrol,11, 12 external supply of the polyamine spermidine,
*HATs↓, Spermidine turned out to be an efficient inhibitor of histone acetyltransferases in vitro
*p62↓, Moreover, all the mentioned acetyltransferase inhibitors induced a significant reduction of p62/SQSTM1 levels,
*AntiAge↑, Spermidine retards the manifestation of several major age-associated diseases including arterial aging,36 colon cancer37 and neurodegenerative processes in mice
AntiCan↑,
cardioP↑, Our results suggest a new and feasible strategy for the protection from cardiovascular disease.
eff↓, Spermidine feeding failed to provide cardioprotection in mice that lack the autophagy-related protein Atg5 in cardiomyocytes.
AntiAge↑, Spermidine extends the lifespan of wild-type C57BL/6 mice. prolonged median lifespan by ~10%
BioAv↑, permidine-fed animals displayed increased circulating spermidine levels, confirming its systemic bioavailability
CRM↝, mass composition were similar in spermidine-fed and control groups (Supplementary Fig. 2), excluding the possibility that polyamine supplementation extends lifespan by inducing a calorically-restricted state13.
*AntiCan↑, antimicrobial, antifungal, antiviral, anticancer, anti-inflammatory, immunomodulatory, anthelmintic, antidiabetic, antidepressant, antifertility, antioxidant, anti-agiing, analgesic, hepatoprotector, cardioprotector, neuroprotector and others.
*Inflam↓,
*antiOx↑,
*AntiAge↑,
*hepatoP↑,
*cardioP↑,
*neuroP↑,
*eff↑, Nano-delivery system in the formulation of the black cumin seed (Nigella sativa L.) essential oil
nanoemulsion as a whole shows that there is an increase in the stability of the preparation and the effectiveness
of the active substance
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BioAv↝, Urolithin A (UA), a metabolite derived from ellagic acid through gut microbiota metabolism, has emerged as a compelling anticancer agent.
TumAuto↝, UA has multiple mechanisms of action, including the regulation of autophagy, enhancement of mitochondrial function, and inhibition of tumor progression and metastatic pathways.
TumCG↓,
TumMeta↓,
ChemoSen↑, Additionally, its chemo-, immuno-, and radio-sensitization properties further increase its therapeutic advantages
Imm↑,
RadioS↑,
BioAv↑, Nanotechnology-driven approaches, such as nanoparticle formulations, lipids, and powder formulations, have successfully increased the solubility, stability, bioavailability, precise targeted delivery to cancer tissues
other↝, While sparingly soluble in water, UA shows better solubility in organic solvents, such as ethanol and dimethyl sulfoxide.
eff↓, prone to degradation at extreme pH values or high temperatures.
*antiOx↓, UA has gained increasing attention for its pharmacological properties, including anti-oxidant, anti-inflammatory, and anti-cancer activities.
*Inflam↓,
AntiCan↓,
AntiAge↑, UA has potential as a key component in antiaging interventions.
chemoP↑, UA can counteract age-related muscle wasting and enhance physical performance, making it a valuable therapeutic for improving muscle health and combating sarcopenia
*neuroP↑, UA has neuroprotective properties because of its ability to reduce neuroinflammation, improve mitochondrial function, and mitigate oxidative stress,
*ROS↓,
*cognitive↑, suggesting its potential application in neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and other age-related cognitive disorders)
*lipid-P↓, UA to reduce lipid peroxidation, combat oxidative stress, and improve endothelial function, promoting its role in cardiovascular health
*cardioP↑,
*TNF-α↓, exerts anti-inflammatory effects by suppressing the production of proinflammatory cytokines, such as TNF-α and IL-6, which can be employed for the management of chronic inflammatory conditions (such as rheumatoid arthritis and inflammatory bowel dise
*IL6↓,
GutMicro↑, Given that UA formation and bioactivity are influenced by the gut microbiota, its supplementation could promote a healthier gut microbiome, with potential therapeutic benefits for a wide range of conditions, including irritable bowel syndrome.
TumCCA↑, UA has potent anticancer effects through cell cycle arrest, apoptosis induction, and the modulation of oncogenic signaling pathways.
Apoptosis↑,
angioG↓, regulate the tumor microenvironment by inhibiting angiogenesis and inflammation
NF-kB↓, UA inhibited key signaling pathways, such as the NF-κB and PI3K/AKT pathways, which are critical for tumor progression
PI3K↓,
Akt↓,
Casp↑, UA also promoted apoptosis via the activation of caspases and the downregulation of survival proteins such as Survivin
survivin↓,
TumCP↓, inhibited MCF-7 cell proliferation in vitro and significantly reduced 27-HC-induced tumor growth in vivo.
cycD1/CCND1↓, UA induced cell cycle arrest by downregulating cyclin D1 and c-MYC and promoted apoptosis by increasing the expression of proapoptotic proteins such as Bax while reducing antiapoptotic BCL2 levels.
cMyc↑,
BAX↑,
Bcl-2↓,
COX2↓, UA, a metabolite of pomegranate mesocarp, synergistically reduced COX-2 expression by ~70% and increased cleaved caspase-3 levels
P53↑, UA induces the expression of tumor suppressor proteins such as p53 and p38-MAPK
p38↑,
*ROS↓, UA demonstrates significant antioxidant activity by reducing reactive oxygen species levels and enhancing the activities of key antioxidant enzymes, such as superoxide dismutase and glutathione peroxidase.
*SOD↑,
*GPx↑,
SIRT1↑, UA induced cell cycle arrest and apoptosis while enhancing the expression of key tumor suppressors, including Sirtuin 1 (Sirt1) and Forkhead box protein O1 (FOXO1)
FOXO1↑,
eff↑, UA preferentially accumulates in prostate and intestinal tissues, suggesting its targeted bioactivity.
ChemoSen↑, UA has emerged as a potent chemosensitizing agent that enhances the efficacy of conventional cancer therapies.
Showing Research Papers: 1 to 36 of 36
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 36
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GSH↓, 1, GSH↑, 1, H2O2↑, 1, NRF2↑, 1, ROS↓, 2, ROS↑, 3, mt-ROS↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↑, 1, ETC↓, 1, ETC↝, 1, Insulin↓, 1, MMP↓, 3,
Core Metabolism/Glycolysis ⓘ
cMyc↑, 1, CRM↑, 1, CRM↝, 1, glucose↓, 1, GlucoseCon↓, 1, Glycolysis↓, 2, lactateProd↓, 1, MethCyc↓, 1, PDH↑, 1, SIRT1↑, 1, Warburg↓, 1,
Cell Death ⓘ
Akt↓, 3, p‑Akt↓, 1, Apoptosis↑, 3, BAX↑, 1, Bcl-2↓, 1, Casp↑, 1, Casp3↑, 2, Casp9↑, 2, Cyt‑c↑, 2, Fas↑, 1, MOMP↑, 1, p27↑, 1, p38↑, 1, survivin↓, 1, TumCD↑, 3,
Transcription & Epigenetics ⓘ
BowelM↑, 1, ChrMod↑, 1, other↝, 2,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1, UPR↑, 1,
Autophagy & Lysosomes ⓘ
ATG5↑, 1, Beclin-1↑, 1, LC3B-II↑, 1, TumAuto↑, 1, TumAuto↝, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 1, P53↑, 1, cl‑PARP↓, 1,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 1, TumCCA↑, 6,
Proliferation, Differentiation & Cell State ⓘ
CD133↓, 1, CD44↓, 1, CSCs↓, 1, FOXO1↑, 1, HDAC2↓, 1, IGF-1↓, 1, PI3K↓, 1, TumCG↓, 4,
Migration ⓘ
Ca+2↑, 2, MMPs↓, 1, TumCP↓, 3, TumMeta↓, 4,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EGFR↓, 1, EPR↑, 1, Hif1a↓, 1, VEGFR2↓, 1,
Barriers & Transport ⓘ
P-gp↑, 1,
Immune & Inflammatory Signaling ⓘ
CD4+↑, 1, COX2↓, 2, DCells↑, 1, HMGB1↓, 1, IL6↓, 2, Imm↑, 3, Inflam↓, 1, NF-kB↓, 2, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 3, BioAv↝, 1, ChemoSen↑, 6, Dose↓, 1, Dose↑, 1, Dose↝, 3, eff↓, 2, eff↑, 4, RadioS↑, 2, selectivity↑, 2,
Clinical Biomarkers ⓘ
EGFR↓, 1, GutMicro↑, 1, IL6↓, 2,
Functional Outcomes ⓘ
AntiAge↑, 5, AntiCan↓, 1, AntiCan↑, 6, AntiTum↑, 1, Appetite↑, 1, breath↑, 1, cardioP↑, 1, chemoP↑, 3, chemoPv↑, 1, hepatoP↑, 1, OS↑, 2, OS⇅, 1, Pain↓, 2, QoL↑, 1, radioP↑, 1, Risk↓, 1, Sleep↑, 1, Strength↑, 2, toxicity↓, 1, Weight↑, 1,
Infection & Microbiome ⓘ
CD8+↑, 1,
Total Targets: 114
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 16, Catalase↑, 3, GPx↑, 1, GSH↑, 5, GSR↑, 1, GSTs↑, 1, HDL↑, 1, HNE↓, 1, HO-1↑, 5, lipid-P↓, 7, MPO↓, 1, NOX4↓, 1, NQO1↑, 3, NRF2↑, 7, OXPHOS↓, 1, ROS↓, 20, ROS↑, 2, mt-ROS↓, 1, SIRT3↑, 1, SOD↑, 7, SOD2↑, 1, TAC↑, 1, TrxR1↑, 1, VitC↑, 2, VitE↑, 2,
Metal & Cofactor Biology ⓘ
IronCh↑, 5,
Mitochondria & Bioenergetics ⓘ
Insulin↓, 1, mitResp↑, 1, MMP↓, 1, MMP↑, 2, mtDam↓, 1, PGC-1α↑, 1,
Core Metabolism/Glycolysis ⓘ
Acetyl-CoA↓, 1, Acetyl-CoA↑, 1, ALAT↓, 1, AMPK↑, 7, BMAL1↑, 1, CRM↓, 1, CRM↑, 3, ECAR↓, 1, GlucoseCon↑, 1, Glycolysis↓, 1, LDL↓, 4, NAD↑, 1, NADPH↓, 1, SIRT1↑, 7,
Cell Death ⓘ
Apoptosis↓, 1, JNK↓, 1, p‑JNK↓, 1, p38↓, 1,
Kinase & Signal Transduction ⓘ
AMPKα↑, 1,
Transcription & Epigenetics ⓘ
Ach↑, 1, HATs↓, 1, other↑, 2, other↝, 2, other∅, 1,
Protein Folding & ER Stress ⓘ
ER Stress↓, 1, ER Stress↑, 1, NQO2↑, 1,
Autophagy & Lysosomes ⓘ
p62↓, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1, DNMT1↓, 1, DNMT3A↓, 1, DNMTs↓, 1, P53↓, 1, P53↑, 1,
Cell Cycle & Senescence ⓘ
P21↓, 1,
Proliferation, Differentiation & Cell State ⓘ
EP300↓, 1, FOXO↑, 1, GSK‐3β↓, 1, HDAC↓, 1, IGF-1↓, 1, IGF-1↑, 1, IGFBP1↑, 1, mTOR↓, 3, mTORC1↓, 2,
Migration ⓘ
Ca+2↑, 1, CDK5↓, 1, CXCL12↑, 1, MMP9↓, 1, TXNIP↓, 1, β-Endo↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↑, 1, Hif1a↑, 2, NO↓, 2,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, IL10↑, 2, IL17↓, 1, IL1β↓, 3, IL23↓, 1, IL6↓, 4, Inflam↓, 19, MCP1↓, 1, mPGES-1↓, 1, NF-kB↓, 4, PAR-2↓, 1, TNF-α↓, 8,
Synaptic & Neurotransmission ⓘ
5HT↓, 1, AChE↓, 1, BDNF↑, 1, ChAT↑, 1, GABA↝, 1, tau↓, 1, p‑tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 4, BACE↓, 1, NLRP3↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 8, BioAv↝, 1, BioAv∅, 1, Dose?, 1, Dose↑, 1, Dose↝, 5, eff↑, 6, Half-Life↓, 1, P450↑, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, BG↓, 1, BMD↑, 1, BP↓, 2, GutMicro↑, 2, IL6↓, 4, NOS2↓, 1,
Functional Outcomes ⓘ
AntiAge↑, 33, AntiCan↑, 3, AntiDiabetic↑, 1, cardioP↓, 1, cardioP↑, 7, cognitive↑, 8, hepatoP↑, 3, memory↑, 6, memory∅, 1, motorD↓, 1, motorD↑, 2, neuroP↑, 15, OS↑, 5, QoL↑, 1, RenoP↑, 2, Strength↑, 2, toxicity↓, 1, toxicity↑, 1, toxicity⇅, 1, toxicity↝, 1, Weight↓, 2, Weight∅, 1, Wound Healing↑, 1,
Infection & Microbiome ⓘ
Sepsis↓, 1,
Total Targets: 150
Scientific Paper Hit Count for: AntiAge, Anti-aging
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#:1245 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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