Strength Cancer Research Results
Strength, physical strength: Click to Expand ⟱
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Physical strength
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Scientific Papers found: Click to Expand⟱
Strength↑, improved physical performance (total physical activity, mean movement velocity and total travelled distance).
*Casp3↓, Interestingly, l-carnitine treatment also decreases caspase-3 mRNA content therefore suggesting a modulation of apoptosis.
cachexia↓, concluded that l-carnitine supplementation may be a good approach for a multi-targeted therapy for the treatment of cancer-related cachexia.
*Dose↝, It is a natural compound free from toxicity up to 6 g/day in human subjects with cancer10 and up to 9 g/day i.v. in patients with acute cardiac infarction.
*cognitive↑, Cognition Promoting Effect
*Inflam↓, anti-inflammatory and anti-arthritic
*Strength↑, swimming time was approximately doubled after Withania somnifera (WS) treatment
*VitC↑, Withania somnifera treatment prevents, decrease of adrenal cortisol and ascorbic acid which occurs due to swimming stress.
*memory↑, It is useful for different types of diseases like Parkinson, dementia, memory loss, stress induced diseases, malignoma and others.
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*cachexia↑, suggesting that it could be an anti-cachectic agent in the settings of ovarian cancer.
*UPR↑, WFA treatment and our xenograft model differentially regulate the UPR pathways in skeletal muscle
Strength↑, promisingly, WFA treatment led to significant improvements in muscle grip strength
*neuroP↑, neuroprotective, sedative and adaptogenic effects and effects on sleep.
*Sleep↑,
*Inflam↓, anti-inflammatory, antimicrobial, cardioprotective and anti-diabetic properties
*cardioP↑,
*cognitive↑, Significant improvements in cognitive function were observed as a result of the inhibition of amyloid β-42, and a reduction in pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and MCP-1, nitric oxide, and lipid peroxidation was also observed.
*Aβ↓,
*TNF-α↓,
*IL1β↓,
*IL6↓,
*MCP1↓,
*lipid-P↓,
*tau↓, reducing β-amyloid aggregation and inhibiting τ protein accumulation.
*ROS↓, withaferin A is responsible for inhibiting oxidative and pro-inflammatory chemicals and regulating heat shock proteins (HSPs), the expression of which increases when cells are exposed to stressors.
*BBB↑, ability of withanolide A to penetrate the blood-brain barrier (BBB) was demonstrated.
*AChE↓, potentially inhibiting acetylcholinesterase activity, which may have benefits in the treatment of canine cognitive dysfunction and Alzheimer’s disease
*GSH↑, increased glutathione concentration, increased glutathione S-transferase, glutathione reductase, glutathione peroxidase, superoxide dismutase and catalase activities,
*GSTs↑,
*GSR↑,
*GPx↑,
*SOD↑,
*Catalase↑,
ChemoSen↑, combination of Ashwagandha extract and intermittent fasting has potential as an effective breast cancer treatment that may be used in conjunction with cisplatin
*Strength↑, combination of Ashwagandha extract and intermittent fasting has potential as an effective breast cancer treatment that may be used in conjunction with cisplatin
*Strength↑, All the patients of the exercise group had significantly better left upper body strength, higher aerobic endurance, and left and right balance maintenance time than those of the no-exercise group
*QoL↑, Moreover, the exercise group had significantly lesser unexpected hospitalization than the no-exercise group in the patients with mild dementia
*cognitive∅, However, in the mild and moderate dementia subgroups, age, sex, education years, and MMSE showed no significant differences between the groups
*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
*OS↑, mice treated with HC exhibited significant delays in spontaneous early mortality at 70%–90% mice survival in the longevity study
*toxicity↓, suggesting that chronic exposure to HC does not produce toxicity at the given dose
*AST∅, (AST) and ALT markers of liver damage were not altered
*ALAT∅,
*Strength↑, Remarkably, HC produced an increase in wire hang performance
*memory∅, HC did not produce remarkable effects in neurocognitive health and muscle strength in HFD‐fed mice
*other↑, HC promotes a rich energetic status in the liver
*other↑, HC potentiates muscle regeneration in vivo
*other↑, HC potentiates muscle regeneration in vivo
*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↑,
PleEff↓,
breath↑, decreased shortness of breath
Pain↓,
Appetite↑,
Strength↑,
BowelM↑, regular Bowel Movements
OS↑, ELF-MFs may prolong survival and improve general symptoms of advanced NSCLC patients. Median survival 6 mnts vs 4mnts. median survival of patients treated with ELF-MFs was longer than that of those receiving supportive care.
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↓,
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OS↑, 8months compared to 3-5 normally
Pain↓, low-frequency rotary MFs improved abdominal pain in 9/21 (42.9%), nausea/vomiting in 4/21 (19.0%), weight loss in 11/21 (52.4%), ongoing blood loss in 2/21 (9.5%), physical strength in 5/21 (23.8%), and sleep quality in 4/21 (19.0%) patients.
ChemoSideEff↓,
Weight↑,
Strength↑,
Sleep↑,
*Dose↑, Clinical efficacy expressed by blood NAD concentration and physical performance reaches highest at a dose of 600 mg daily oral intake
*Strength↑, Participants in the 600 mg NMN-treated group had a statistically longer walking distance compared to the 300 mg NMN-treated group at days 30 and 60
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AD, |
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Park, |
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*neuroP↑, Silymarin can be used as a neuroprotective therapy against AD, PD and CI
*ROS↓, Silymarin prohibit oxidative stress, pathologic protein aggregation.
*Inflam↓, Silymarin inhibit neuroinflammation, apoptosis, and estrogenic receptor modulation.
*Apoptosis↓,
*BBB?, Silymarin, as a polyphenolic complex, can cross the blood-brain barrier (BBB)
*tau↓, inhibitory action of Silibinin on tau protein phosphorylation in the hippocampus and cortical region of the brain could describe an important neuro-protective effect against AD progression
*NF-kB↓, inhibiting the NF-κB pathway leading to attenuating the activity of NF-κB (
*IL1β↓, inhibition of inflammatory responses such as IL-1β and TNF-α mRNA gene
*TNF-α↓,
*IL4↓, enhance the production of IL-4 in the hippocampal region
*MAPK↓, down-regulation of MAPK activation
*memory↑, Silibinin exhibited its beneficial effect on
improvement of memory impairment in rats
*cognitive↑, Silymarin was able to alleviated the impairment in cognitive, learning and memory ability caused by Aβ aggravation through making a reduction in oxidative stress in the hippocampal region
*Aβ↓,
*ROS↓,
*lipid-P↓, eduction in lipid peroxidation, controlling the GSH levels and then cellular anti-oxidant status improvement,
*GSH↑,
*MDA↓, Silymarin could reduce MDA content and significantly increased the reduced activity level of antioxidant enzyme, including SOD, CAT and GSH in the brain tissue induced by aluminum
*SOD↑,
*Catalase↑,
*AChE↓, Silibinin/ Silymarin, as a strong suppressor of AChE and BChE activity, exerted a positive effect against AD symptoms via increasing the ACh level in the brain
*BChE↓,
*p‑ERK↓, Silibinin could inhibit increased level of phosphorylated ERK, JNK and p38 (p-ERK, p-JNK and p-p38, respectively
*p‑JNK↓,
*p‑p38↓,
*GutMicro↑, demonstrated in APP/PS1 transgenic mice model of AD which was associated with controlling of the gut microbiota by both Silymarin and Silibinin
*COX2↓, Inhibition of the NF-κB pathway/ expression, Inhibition of IL-1β, TNF-α, COX_2 and iNOS level/ expression
*iNOS↓,
*TLR4↓, suppress TLR4 pathways and then subsequently diminished elevated level of TNF-α and up-regulated percentage of NF-κB mRNA expression
*neuroP↑, neuro-protective mechanisms on cerebral ischemia (CI)
*Strength↑, Silymarin decreased the loss of grip strength in the experimental rats
*AMPK↑, In SH-SY5Y cells, Silibinin blocked OGD/re-oxygenation- induced neuronal degeneration via AMPK activation as well as suppression in both ROS production and MMP reduction and even reduced neuronal apoptosis and necrosis.
*MMP↑,
*necrosis↓,
*NRF2↑, Silymarin up-regulated Nrf-2/HO-1 signaling (Yuan et al., 2017
*HO-1↑,
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TumCG↓,
Glycolysis↓,
cMyc↓,
STAT3↓,
TumCP↓,
Weight∅, prevents the loss of body weight and muscle.
Strength↑,
DNAdam↑,
Casp3↑,
Casp9↑,
GLUT1↓,
HK2↓,
LDHA↓,
GlucoseCon↓, silibinin inhibits glucose uptake and lactate release
lactateProd↓,
PPP↓, significant reduction in pentose phosphate pathway (PPP) metabolites, including 6-phosphogluconate (~50%), erythrose-4-phosphate (~40%), sedoheptulose-7-phosphate and sedoheptulose bis-phosphate (~ 70%)
Ki-67↓, reduced Ki67-positive cells
p‑STAT3↓,
cachexia↓,
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*MitoP↑, key biological effects of UA, including its promotion of mitophagy and mitochondrial homeostasis, as well as its anti-inflammatory, antioxidant, anti-senescence, and anti-apoptotic properties
*Inflam↓,
*antiOx↑,
*Risk↓, UA’s therapeutic potential in CNS disorders, such as Alzheimer’s disease, Parkinson’s disease, and stroke.
*Aβ↓, UA enhances microglial phagocytosis of Aβ plaques, suppresses neuroinflammation, and reduces tau hyperphosphorylation by restoring mitophagy to eliminate abnormal mitochondria
*p‑tau↓,
*p62↓, In doxorubicin-induced cardiomyopathy mice, UA upregulates p62, LC3-II, PINK1, and Parkin expression, restoring impaired mitophagy, mitigating membrane potential loss and ROS accumulation,
*PARK2↑,
*MMP↑,
*ROS↓,
*Strength↑, Randomized controlled trials in healthy middle-aged and older adults show that oral supplementation with 500–1000 mg of UA significantly improves skeletal muscle endurance and mitochondrial efficiency, reduces plasma inflammatory markers (such as C-r
*CRP↓,
*IL1β↓, UA activates sirtuin 1 (SIRT1)-mediated deacetylation of NF-κB p65, suppressing glial cell activation and the production of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α)
*IL6↓,
*TNF-α↓,
*AMPK↑, UA enhances brain adenosine 5′-monophosphate-activated protein kinase (AMPK) activation, attenuating NF-κB and MAPK activity, mitigating neuroinflammation, and supporting synaptic recovery
*NF-kB↓,
*MAPK↓,
*p62↑, In a renal ischemia-reperfusion injury model, UA activates the p62—kelch-like ECH-associated protein 1 (Keap1)—nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, boosting superoxide dismutase and catalase activity while lowering ROS levels
*NRF2↑,
*SOD↑,
*Catalase↑,
*HO-1↑, UA upregulates the Keap1-Nrf2/heme oxygenase 1 (HO-1) pathway to inhibit ferroptosis and reduce lipid peroxide accumulation in lung tissue
*Ferroptosis↓,
*lipid-P↓,
*Cartilage↑, reducing cartilage degradation and synovial inflammation
*PI3K↓, UA suppresses the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) and Akt/IκB kinase (IKK)/NF-κB signaling pathways, reducing neuronal apoptosis while enhancing BBB integrity and neurological outcomes
*Akt↓,
*mTOR↓,
*Apoptosis↓,
*neuroP↑,
*Bcl-2↓, cerebral artery occlusion model, UA treatment lowers Bcl-2 expression and elevates Bcl-2 associated X protein (Bax) and caspase-3 levels
*BAX↑,
*Casp3↑,
*ATP↑, UA restores mitochondrial membrane potential and ATP production in cardiomyocytes, balancing carnitine palmitoyltransferase1-dependent fatty acid oxidation to reduce apoptosis
*eff↑, in humanized homozygous amyloid beta knockin mice modeling late-onset AD, UA combined with green tea extract (Epigallocatechin gallate) more effectively reduces brain Aβ40 and Aβ42 levels compared to UA alone [106].
*motorD↑, UA administration elevated striatal dopamine levels and enhanced motor coordination, accompanied by suppression of NLRP3 inflammasome activation
*NLRP3↓,
*radioP↑, In a radiation-induced primary astrocyte model, UA activated the PINK1/Parkin-mediated mitophagy pathway, significantly reducing ROS levels in both cells and mitochondria,
*BBB↑, preclinical studies showing that UA primarily crosses the mouse BBB
*neuroP↑, urolithin A is discussed, focusing on its neuroprotective properties and its potential to induce mitophagy.
*Half-Life↝, Urolithins appear in the human circulation within a few hours of consumption of ET-containing foods, reaching maximum concentrations after 24–48 h and complete excretion in urine/faeces within 72 h.
*BBB↑, urolithins can permeate the blood–brain barrier (BBB)
*toxicity↓, Urolithins are relatively non-toxic, as shown by studies in rats. The lethal dose 50 (LD50) has been found to be greater than 5 g/kg body weight in rat
*Inflam↓, In a study of Fisher rats [185], urolithin A was found to be the most effective anti-inflammatory compound derived from pomegranate consumption.
*Strength↑, Another clinical trial has shown that UA at doses of 500 mg and 1,000 mg for 4 weeks modulated plasma acylcarnitines and skeletal muscle mitochondrial gene expression in elders [
*BACE↓, There is evidence suggesting that these molecules inhibit BACE1 activity, leading to reduced Aβ production.
*Aβ↓,
*MitoP↑, Urolithin A May Trigger Mitophagy
*SIRT1↑, Activation of SIRT1/3, AMPK, PGC1-α and Inhibition of mTOR1
*SIRT3↑,
*AMPK↑,
*PGC-1α↑,
*mTOR↓,
*PARK2↑, urolithin A (1000 mg) has been shown to transcriptionally increase Parkin and BECN1 levels after 28 days of treatment in humans
*Beclin-1↑,
*ROS↓, by their actions to reduce BACE1 activity, Aβ fibrillation, ROS damage, inflammation
*GutMicro↑, impact on the microbiome may be an additional contribution to reducing AD risk
*Risk↓,
*memory↑, Long‐term UA treatment significantly improved learning, memory, and olfactory function in different AD transgenic mice.
*Aβ↓, UA also reduced amyloid beta (Aβ) and tau pathologies and enhanced long‐term potentiation
*toxicity↓, A phase I clinical study confirmed that UA was safe in healthy, sedentary older adults, and that activation of mitochondrial biomarkers in muscle and plasma was observed
*BBB↑, may play a therapeutic role in the brain as it crosses the blood–brain barrier.
*p‑tau↓, UA decreased Aβ accumulation and tau phosphorylation in AD mice
*eff↓, and that the effects disappeared if UA treatment was suspended for 1 month.
*IL1α↓, several proinflammatory cytokines were increased in AD mice and decreased after UA treatment, including Interleukin 1 alpha (IL‐1α), monocyte chemoattractant protein‐1 (MCP‐1)
*MCP1↓,
*MIP‑1α↓, macrophage inflammatory protein‐1 alpha (MIP‐1α), tumor necrosis factor (TNFα), Interleukin 2 (IL‐2)
*TNF-α↓,
*IL2↓,
*SIRT1↓, UA induced sirtuin expression, mitophagy, and decreased DNA damage
*DNAdam↓,
*Dose↝, UA at doses from 250 to 2000 mg in humans 25 and 1–450 mg/kg in mice 80 has been reported to be safe.
*Strength↑, UA increased muscle strength and physical performance in a 6‐min walk test in elderly humans after 4 months of supplementation.
*motorD↑, Other studies reported that UA improved motor activity in the rotarod test and increased total distance traveled and average speed in the open field test in young C57BL/6J mice 82 and 3xTg AD mice
*CTSZ↓, Ctsz was highly expressed in multiple AD transgenic mouse models, and its expression was normalized by UA treatment
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*MitoP↓, Experimental models consistently show that UA increases mitophagy and mitochondrial function and blunts excessive inflammatory responses.
*Strength↑, UA is a promising strategy to target health and disease conditions of aging, especially those linked to mitochondrial and muscle dysfunction.
*PINK1↑, UA can activate. PTEN-induced kinase 1 (PINK1)/Parkin-dependent mitophagy starts with the stabilization of the kinase PINK1,
*PARK2↑, which recruits and phosphorylates the ubiquitin-conjugating protein Parkin.
*Inflam↓, anti-inflammatory effect of UA was reported for the first time as a decrease in mRNA and protein levels of the inflammatory marker cyclooxygenase 2 (COX2)
*COX2↓,
*IL1β↓, In neuronal tissues, UA treatment reduced levels of IL-1β, IL-6, and TNFα in the brains of the amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of AD
*IL6↓,
*TNF-α↓,
*OS↑, impact on worm longevity showed that UA extends lifespan by 45%,
*cardioP↑, reduction in IRI markers, such as circulating creatine kinase and lactate dehydrogenase levels, and by fewer apoptotic cells in the heart
*memory↑, Increased learning, memory retention, neuronal survival, and neurogenesis in the hippocampus was achieved with UA administration in the APP/PS1 mouse model of AD
*neuroG↑,
*neuroP↑, UA was shown to have neuroprotective effects in the EAE mouse model of multiple sclerosis (MS)
*Cartilage↑, In a model of osteoarthritis, an age-related and disabling joint disease caused by a slow degeneration of cartilage,
*Inflam↓, UA has protective effects against a chronic DSS-induced model of IBD, leading to reduced levels of colon inflammation markers and to better mucosal integrity.
*RenoP↑, UA consistently reduced tubular damage induced by cisplatin, as shown by histopathology and by a reduction in circulating markers of kidney damage
*eff↑, When administered as nanoparticles to increase its bioavailability, UA even improved the survival of mice that received a lethal dose of cisplatin
*Dose↝, UA showed a favorable safety profile, with no observed side effects following either single oral administration of UA up to 2000 mg or multiple oral dosing (28 days) of UA up to 1000 mg daily.
*Half-Life↑, It showed a relatively long-half life (t1/2 = 17–22 hours),
*NRF2↑, Other mechanisms of action have been proposed for UA, such as the activation of the Ahr/Nrf2 pathway and its downstream antioxidative stress response
*GutMicro↑, A recent report also showed an impact of direct UA supplementation on gut microflora in obese rats
Pain↓, The WBV group (mean age: 51.73 ± 10.73 years; body mass index (BMI): 25.56 ± 5.17 kg/m2) showed a statistically significant pain reduction
Strength↑, Concurrently, muscle strength, physical performance, and quality of life significantly improved in both groups, without significant differences between groups
QoL↑,
Dose∅, with a frequency of 30 Hz, peak-to-peak amplitude of 1.15 mm. in squatting position (110° knee flexion)
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MDA-MB-231 |
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BMD↑, Low-magnitude (≤1 g) high-frequency (≥30 Hz) (LMHF) vibration has been shown to enhance bone mineral density
YAP/TEAD↑, Combined treatment on osteocytes showed beneficial effects, including increasing the nuclear translocation of Yes-associated protein (YAP) in osteocytes
TumCG↓, The ability of carefully controlled high-magnitude mechanical loads to suppress breast cancer growth and maintain bone integrity has been shown using various models in vivo
Strength↑, Studies have shown the anabolic benefits of LMHF vibration (LMHFV) on the musculoskeletal system, including increased bone density [7], reduced marrow fat [8], and improved muscle and glucose metabolism
TumCI↓, Application of LMHF vibration on MDA-MB-231 cells does not affect their migration [25], cell viability, and apoptosis but suppresses their invasion and upregulates FAS, a membrane death receptor
Fas↑,
Ca+2↑, concentration of intracellular calcium in MLO-Y4 was shown to significantly increase after 90 Hz of vibration for 1 h
Showing Research Papers: 1 to 20 of 20
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 20
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
ROS↑, 1,
Mitochondria & Bioenergetics ⓘ
ETC↓, 1, MMP↓, 1, PleEff↓, 1,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 1, GlucoseCon↓, 1, Glycolysis↓, 1, HK2↓, 1, lactateProd↓, 1, LDHA↓, 1, PPP↓, 1,
Cell Death ⓘ
Akt↓, 1, Casp3↑, 2, Casp9↑, 1, Fas↑, 1, TumCD↑, 1, YAP/TEAD↑, 1,
Transcription & Epigenetics ⓘ
BowelM↑, 2, ChrMod↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 1,
Cell Cycle & Senescence ⓘ
TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
STAT3↓, 1, p‑STAT3↓, 1, TumCG↓, 3,
Migration ⓘ
Ca+2↑, 2, Ki-67↓, 1, TumCI↓, 1, TumCP↓, 1, TumMeta↓, 2,
Barriers & Transport ⓘ
GLUT1↓, 1,
Immune & Inflammatory Signaling ⓘ
CD4+↑, 1, DCells↑, 1, IL6↓, 1, Imm↑, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 1, Dose∅, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
BMD↑, 1, IL6↓, 1, Ki-67↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, Appetite↑, 2, breath↑, 2, cachexia↓, 2, chemoP↑, 1, ChemoSideEff↓, 1, hepatoP↑, 1, OS↑, 2, OS⇅, 1, Pain↓, 5, QoL↑, 2, radioP↑, 1, Risk↓, 1, Sleep↑, 2, Strength↑, 9, toxicity↓, 1, Weight↑, 2, Weight∅, 1,
Infection & Microbiome ⓘ
CD8+↑, 1,
Total Targets: 59
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 2, Catalase↑, 3, Ferroptosis↓, 1, GPx↑, 1, GSH↑, 2, GSR↑, 1, GSTs↑, 1, HO-1↑, 2, lipid-P↓, 3, MDA↓, 1, NQO1↑, 1, NRF2↑, 4, PARK2↑, 3, ROS↓, 6, SIRT3↑, 1, SOD↑, 3, SOD2↑, 1, TAC↑, 1, TrxR1↑, 1, VitC↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↑, 1, MMP↑, 2, PGC-1α↑, 1, PINK1↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, ALAT∅, 1, AMPK↑, 5, CRM↑, 1, LDL↓, 1, SIRT1↓, 1, SIRT1↑, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↓, 2, BAX↑, 1, Bcl-2↓, 1, Casp3↓, 1, Casp3↑, 1, Ferroptosis↓, 1, iNOS↓, 1, p‑JNK↓, 1, MAPK↓, 2, necrosis↓, 1, p‑p38↓, 1,
Transcription & Epigenetics ⓘ
other↑, 3,
Protein Folding & ER Stress ⓘ
NQO2↑, 1, UPR↑, 1,
Autophagy & Lysosomes ⓘ
Beclin-1↑, 1, MitoP↓, 1, MitoP↑, 2, p62↓, 1, p62↑, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1, P53↓, 1,
Cell Cycle & Senescence ⓘ
P21↓, 1,
Proliferation, Differentiation & Cell State ⓘ
p‑ERK↓, 1, mTOR↓, 3, neuroG↑, 1, PI3K↓, 1,
Migration ⓘ
Cartilage↑, 2, β-Endo↑, 1,
Barriers & Transport ⓘ
BBB?, 1, BBB↑, 4,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, CRP↓, 1, CTSZ↓, 1, IL1α↓, 1, IL1β↓, 4, IL2↓, 1, IL4↓, 1, IL6↓, 3, Inflam↓, 9, MCP1↓, 2, MIP‑1α↓, 1, NF-kB↓, 2, TLR4↓, 1, TNF-α↓, 5,
Synaptic & Neurotransmission ⓘ
5HT↓, 1, AChE↓, 2, BChE↓, 1, tau↓, 3, p‑tau↓, 2,
Protein Aggregation ⓘ
Aβ↓, 5, BACE↓, 1, NLRP3↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, Dose↑, 1, Dose↝, 4, eff↓, 1, eff↑, 2, Half-Life↑, 1, Half-Life↝, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, ALAT∅, 1, AST∅, 1, BMD↑, 1, CRP↓, 1, GutMicro↑, 3, IL6↓, 3,
Functional Outcomes ⓘ
AntiAge↑, 3, AntiDiabetic↑, 1, cachexia↑, 1, cardioP↑, 3, cognitive↑, 4, cognitive∅, 1, memory↑, 5, memory∅, 1, motorD↑, 2, neuroP↑, 7, OS↑, 3, QoL↑, 1, radioP↑, 1, RenoP↑, 1, Risk↓, 2, Sleep↑, 1, Strength↑, 12, toxicity↓, 3, toxicity↑, 1, toxicity⇅, 1, toxicity↝, 1,
Total Targets: 119
Scientific Paper Hit Count for: Strength, physical strength
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#:578 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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