other Cancer Research Results
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Scientific Papers found: Click to Expand⟱
*Risk↓, There is evidence that damage or dysfunction of the 5-HT system contributes to the development of AD, and different subtypes of 5-HT receptors are a potential target for the treatment of AD
*5HT↓, Serotonin is an antioxidant that inhibits the generation of ROS, malondialdehyde and carbonyls, prevents thiol oxidation, reduces the degradation of 2-deoxy-D-ribose, and prevents apoptosis
*ROS↓,
*MDA↓,
*Apoptosis↓,
*Mood↑, Serotonin deficiency may be responsible for the increase in aggressive behavior and depression often observed in patients with AD.
*other↑, Exercise and a Mediterranean diet increase 5-HT and BDNF levels, thereby improving mood and cognition.
*other↑, In particular, the evidence suggests that sulforaphane’s beneficial effects can be mainly ascribed to its peculiar ability to activate the Nrf2/ARE pathway [271].
*other↑, Low glycemic index foods seem to improve attention, memory and functional capacity, while those rich in simple sugars are associated with difficulty in concentration and attention.
*other↓, Low levels of serotonin have been linked to decreased learning, reasoning and memory.
*cognitive↑, It is advisable to consume diets with an adequate ratio (5:1) of omega-6: 3 fatty acids (Mediterranean diet) given that they are associated with better memory capacity and lower risk of cognitive deterioration.
*eff↑, Vitamins B1, B6, B12, B9 (folic acid) and D, choline, iron and iodine exert neuroprotective effects and improve intellectual performance.
*eff↑, In parallel, antioxidants (vitamins C, E, A, zinc, selenium, lutein and zeaxanthin) have a very important role in the defense against oxidative stress associated with mental deterioration and in the improvement of cognition.
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Review, |
AD, |
NA |
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Review, |
Park, |
NA |
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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.
Wound Healing↑, The notable antimicrobial properties of silver render it indispensable for wound healing, infection control, cancer therapy and tissue regeneration applications.
AntiCan↑,
other↑, Additionally, AgNPs hold great promise as versatile drug carriers for targeted therapies and as contrast agents for advanced medical imaging techniques
MPT↑, these nanoparticles exert their effects by disrupting cell membrane permeability, interfering with cellular respiration processes and instigating the production of free radicals.
ROS↑,
other↑, Additionally, it has been proposed that AgNPs may release silver ions, which can bind to thiol groups found in essential enzymes, rendering them inactive
DNAdam↑, DNA typically contains sulfur, and nanoparticles may interact with these bases, potentially causing damage to the DNA molecule, and thereby contributing to cell demise
*eff↑, Pongamia pinnata seed extracts loaded with nanogel formulations (AgNPs CUD NG) to improve the retention, accumulation, and the penetration of AgNPs into the epidermal layer of psoriasis.
*other↑, AgNPs CUD NG enhanced the retention of AgNPs on the psoriatic skin compared to normal skin
Apoptosis↑, According to our findings AgNPs are able to kill osteosarcoma cells independently from their actual p53 status and induce p53-independent cancer cell apoptosis.
other↑, AgNPs kill cells through a Trojan-horse type mechanism, suggesting that the intracellularly accumulated nanoparticles release toxic silver ions
ROS↑, Those ions induce the generation of reactive oxygen species (ROS)
eff↑, t has been reported that 5 nm AgNPs were more toxic compared to 20 nm and 50 nm particles in four different cell lines
P53↝, Nearly 50% of all human cancers have been characterised by impaired p53 function which attenuates therapeutic efficacy. The level of p53 protein increased markedly upon 20 μM of 5 nm and 85 μM of 35 nm sized AgNP treatments
Apoptosis↑, Induction of apoptosis was verified by immunostaining U2Os and Saos-2 cells with cleaved caspase 3 specific antibody after treatments with 20 μM of 5 nm and with 85 μM of 35 nm sized AgNPs for 24 h
cl‑Casp3↑,
survivin↓, as decreased survivin and elevated caspase 3 mRNA levels were measured
MMP↓, Decreased mitochondrial membrane potential was detected in 5 nm and 35 nm AgNPs treated U2Os (a) and Saos-2
Cyt‑c↑, Elevated levels of cytoplasmic cytochrome c was detected in 5 nm and 35 nm AgNP-treated U2Os and Saos-2 cells
eff↓, toxicity of AgNPs was prevented by use of the antioxidant N-acetylcysteine, and AgNP-induced DNA damage was also prevented by N-acetylcysteine.
ROS↑, AgNP cytotoxicity is primarily the result of oxidative stress and is independent of the toxicity of Ag+ ions.
other↑, Ag exposure is associated with specific clinical symptoms, such as argyria, which causes an irreversible gray coloration of the skin
*other↑, The Vitamin C (Ascorbic Acid) acts as a chemical reductant to successfully reduce silver ions into silver nanoparticles
*other↝, The optimized synthetic method utilizes higher pH conditions, sodium citrate as a silver ion stabilizer, hydrogen peroxide as an etching agent, and ascorbic acid as a reducing agent, allowing nanoscale-sized silver particles to be achieved even at t
other↑, high accumulation fn AuNP in tumor tissues
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in-vitro, |
BC, |
MCF-7 |
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in-vitro, |
Bladder, |
HTB-22 |
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Apoptosis↑,
P53↑, Up-regulation in the expression level of p53, iNOS and NF-kB genes as well as down-regulation of Bcl-2 and miRNA-125b genes were detected post treatment.
iNOS↑,
NF-kB↑,
Bcl-2↓,
ROS↑, the present study evaluated the levels of ROS as well as the antioxidant enzymes (SOD and CAT)
SOD↑,
TumCCA↑, S phase arrest and accumulation of cells in G2/M phase was observed following exposure to AgNPs and EMF, respectively.
eff↑, Apoptosis induction was obvious following exposure to either ELF-EMF or AgNPs, however their apoptotic potential was intensified when applied in combination
Catalase↑, Catalase (CAT)
other↑, swollen cells, swollen nuclei with mixed euchromatin and heterochromatin, ruptured cell membranes
other↑, Mechanistically, oral Akkermansia massiliensis supplementation increased CAR T-cell infiltration into the bone marrow, inverted the CD4/CD8 CAR T-cell ratio
eff↑, Akkermansia spp. Supplementation Improves the Efficacy of CD19/CD28-ζ CAR T Cells against B-cell Lymphoma
AntiAg↑, This review suggests that garlic and its preparations have a beneficial effect against thrombosis and have an antiplatelet aggregation property.
other↑, Garlic been shown to inhibit platelet aggregation, both in vivo and in vitro
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Review, |
AD, |
NA |
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Review, |
Var, |
NA |
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Review, |
Park, |
NA |
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Review, |
Stroke, |
NA |
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*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB/CCNB1↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,
Inflam↓, , anti-inflammatory, anti-cancer, and immune-modulatory activities
AntiCan↑,
ROS↑, allicin treatment led to the accumulation of ROS
MAPK↑, activation of MAPK/JNK
JNK↑,
TumAuto↑, of autophagy in non small cell lung cancer (NSCLC) cells.
other↑, autophagy at a low dose of allicin is cytoprotective
Dose↝, whereas a high dose of allicin leads to autophagic cell death.
MALAT1↓, allicin could considerably induce oxidative stress and autophagy to suppress osteosarcoma growth via inactivating the MALAT1-miR-376a-Wnt/β-catenin axis,
Wnt↓,
β-catenin/ZEB1↓,
*BBB↑, alpha linolenic acid (ALA), the precursor of the majoritarian brain component docosahexaenoic acid (DHA), emerges as a potential novel brain savior, acting via BBB functional improvements,
*other↑, Apolipoprotein E4 (ApoE4) allele carriers are at increased risk to develop AD compared with those carrying the ApoE3 or E2 alleles
*other↑, Our emerging, yet unpublished results, suggest that ALA dietary enrichment in ApoE4 compared with ApoE3 mice brain, restores part of the decreased lipids, and in particular cholesterol and phospholipids, and leads to DHA enrichment in brain blood ve
*DHA↑, We propose that, by conversion to DHA, ALA– the natural substrate in the DHA metabolic pathway– may produce the DHA beneficial effects on BBB and brain health.
*neuroP↑, It has also been shown that DHA confers long-term protection against ischemic brain damage through multiple mechanisms, including suppression of inflammatory responses, decrease in oxidative stress and stimulation of angiogenesis and neurogenesis
*ROS↓,
*other?, while AD pathology follows a long preclinical course, with DHA decrease being a hallmark of brain deterioration with aging [67].
other↑, Serum carnitine level increased with ALC but remained stable with placebo
NP/CIPN↑, This is the first study to our knowledge showing that a nutritional supplement increased CIPN. Patients should be discouraged from using supplements without proven efficacy.
*Risk↑, The unequivocal neurotoxicity of aluminum must mean that when brain burdens of aluminum exceed toxic thresholds that it is inevitable that aluminum contributes toward disease.
*cognitive↓, EVIDENCE NOW POINTS TO ALUMINUM AS A CONTRIBUTORY FACTOR IN ALL FORMS OF ALZHEIMER’S DISEASE
*neuroP↓, We also know that the addition of aluminum to feed or water exacerbates the many symptoms of Alzheimer’s disease in these animal models
*other↑, Postmortem analyses of their brain tissues revealed very high levels of aluminum.
*other↝, physical exercise can increase the perspiration volume many times and so improve the excretion of aluminum from the body.
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vitro+vivo, |
CRC, |
SW480 |
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vitro+vivo, |
CRC, |
DLD1 |
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vitro+vivo, |
CRC, |
LS174T |
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MMP↓,
p‑Akt↓,
TumCP↓, Apigenin inhibits cell proliferation and invasion
TumCI↓,
NADH↓, down-regulated proteins by apigenin included NADH dehydrogenase [ubiquinone] iron-sulphur
protein 3, heat shock protein HSP 90-alpha, stress-70 protein and NADH dehydrogenase
HSP90↓,
other↑, whereas the up-regulated proteins include Transgelin, Ras-related protein Rab-3D and 28S ribosomal protein S22
talin?,
*cognitive↑, Aromatherapy may have some potential for improving cognitive function, especially in AD patients.
*other↑, Lavandula angustifolia Mill, Salvia rosmarinus and lemon citrus:potential for improving cognitive function, especially in AD patients.
*other↓, Rosmarinus officinalis: improving cognitive function by inhaled administration
*BioAv↑, There is no doubt that components from EOs are often absorbed through the skin, enter into the circulation then
cross the BBB.
*BBB?,
TumMeta↓, The included studies demonstrated that aspirin suppresses metastatic dissemination across multiple cancer types through coordinated platelet-dependent and tumor-intrinsic mechanisms.
COX1↓, Aspirin consistently inhibited platelet aggregation and COX-1-dependent TXA2 production, disrupting platelet–tumor cell interactions, intravascular metastatic niche formation, and platelet-mediated immune suppression.
TXA2↓,
AntiAg↑, Beyond platelet effects, aspirin suppressed EMT, migration, and invasion through modulation of EMT transcriptional regulators and inflammatory signaling pathways.
EMT↓,
TumCMig↓,
TumCI↓,
AMPK↑, Additional mechanisms included activation of AMPK, inhibition of c-MYC signaling, regulation of redox-responsive pathways and impairment of anoikis resistance.
cMyc↓,
PGE2↓, Importantly, oral aspirin (20 mg/kg/day; human-equivalent ≈ 150 mg/day), administered before tumor cell injection, prevented platelet-induced metastatic enhancement and suppressed TXA2 and PGE2 production.
Dose↑, medium and high doses of aspirin reduced pulmonary metastatic burden by more than 50%, whereas low-dose aspirin was ineffective.
RadioS↑, Wang et al. [45] demonstrated that low-dose aspirin suppresses radiotherapy-induced release of immunosuppressive exosomes in breast cancer, restoring NK-cell proliferation and enhancing antitumor immunity in vivo.
PD-L1↓, Similarly, Xiao et al. [46] showed that aspirin epigenetically downregulates PD-L1 expression by inhibiting KAT5-dependent histone acetylation, thereby restoring T-cell activation
E-cadherin↑, Aspirin restored E-cadherin expression and suppressed EMT regulators, including Slug, vimentin, Twist, MMP-2, and MMP-9.
EMT↓,
Slug↓,
Vim↓,
Twist↓,
MMP2↓,
MMP9↓,
other↑, definitive conclusions regarding clinical efficacy across cancer types cannot yet be drawn. Nevertheless, the consistency of mechanistic signals across experimental systems supports further investigation of aspirin as a low-cost adjunct in oncology
Risk↓, Meta-analyses of 118 observational studies of mortality in cancer patients give evidence consistent with reductions of about 20% in mortality associated with aspirin use.
*toxicity↓, Reasons against aspirin use include increased risk of a gastrointestinal bleed though there appears to be no valid evidence that aspirin is responsible for fatal gastrointestinal bleeding.
other↑, In conclusion, given the relative safety and the favourable effects of aspirin, its use in cancer seems justified, and ethical implications of this imply that cancer patients should be informed of the present evidence
*COX1↓, recent evidence highlights additional targets for aspirin in tackling cancer progression directly, irrespective of COX activity [3, 4]
TumCP↓, Such targets include energy metabolism involved in cancer proliferation, cancer associated inflammation [5] and platelet driven pro-carcinogenic activity [2].
DNArepair↑, beneficial effect of aspirin on colon cancer risk through an enhancement of DNA-repair mechanisms [2].
ChemoSen↑, ‘basic science’ basis to justify using aspirin as an adjunct to other pre-existing therapies (e.g., immunotherapy and cytotoxic chemotherapy) in the treatment of cancer progression and metastasis [2, 14].
other↓, Aspirin has been shown repeatedly to reduce thromboembolism, including in patients with cancer [15]
*COX1↓, Aspirin is the acetate ester of salicylic acid and acts by binding irreversibly to cyclooxygenase-1 and cyclooxygenases-2
*COX2↓,
*cardioP↑, Aspirin is consumed most often at low-doses for cardio-protection and at higher doses as an analgesic, antipyretic, and anti-inflammatory agents.
*BioAv↑, Orally ingested aspirin is absorbed rapidly and the peak concentration is reached in about 1 hour.
*BioAv↝, a rise in pH also increases the solubility of aspirin and thus the dissolution of the tablets and the presence of food delays absorption of aspirin.
*Half-Life↓, The elimination half-life of aspirin in plasma is about 20 min
Risk↓, Patients who received 100 mg daily of aspirin had reduced risks of colorectal cancer and gastric cancer and an increased risk of gastrointestinal bleeding [6].
*other↑, Low-dose of aspirin treatment significantly improves ovarian responsiveness, uterine and ovarian blood flow velocity, and pregnancy-rates in women undergoing in-vitro fertilization [19].
*AntiAg↑, antiplatelet effect of aspirin [13],
other↑, We found that the blood with AP emitted an ESR signal whose singlet shape, width, and location precisely correlate with the known characteristics of the ascorbyl radical in vitro.
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in-vivo, |
Melanoma, |
B16-F10 |
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Dose↝, we developed a dual drug delivery system to encapsulate ascorbyl palmitate (AP) and paclitaxel (PTX) for synergistic cancer therapy. 223 nm
TumCG↓, In vivo, AP/PTX-SLNs were revealed to be much more effective in suppressing tumor growth in B16F10-bearing mice and in eliminating cancer cells in the lungs
TumCP↓, AP has been found to inhibit the cell proliferation and DNA synthesis of various cancer cells, including breast, colon, glioblastoma, skin, and brain cancer cells (Naidu, 2003a).
BioAv↓, AP is limited due to its water insolubility, rapid degradation (accelerated by metal ions and/or light), and low bioavailability.
BioAv↑, Therefore, new technologies including nanoparticles that can enhance its delivery efficacy and reduce the dose of administration for Vc while not reducing its anti-cancer efficacy are highly desired.
other↑, These results conformed to the conclusion that only high doses of ascorbic acid have the ability to induce cancer cell death.
Apoptosis↑, Conclusively, the AP/PTX-SLNs exhibited a greater efficacy in inducing cell apoptosis by reducing the Bcl-2/Bax ratio accompanied by promoting tubulin polymerization
Bax:Bcl2↑,
EPR↑, such nanocarriers to permeate into tumor sites because of the enhanced permeation and retention (EPR) effect.
toxicity↝, AP/PTX synergistic combination-based SLN therapy did not induce toxicity and represents a promising strategy for paclitaxel/the vitamin C derivative in promoting anti-cancer effects.
HMG-CoA↓, Statins are drugs that have been utilized for years to treat hyperlipidemia through inhibition of the rate-limiting enzyme of the mevalonate (MVA) pathway, 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR)
AntiAg↑, Dipyridamole (DP), a commonly prescribed anti-platelet agent potentiated the anti-cancer effects of atorvastatin
eff↑, DP-statin combination was synergistic and capable of inducing apoptosis in a variety of acute myelogenous leukemia (AML), MM and breast cancer cell lines.
Apoptosis↑, DP-statin combination also induced apoptosis in primary AML patient samples, but was not toxic to normal PBSCs.
selectivity↑,
*toxicity↓,
TumCG↓, In an in vivo AML tumor model, the DP-statin combination was found to be effective at inhibiting tumor growth.
PDE4↓, DP is known to elicit numerous effects, amongst them, phosphodiesterase (PDE) inhibition
other↑, . As both statins and DP are pre-approved for use in humans, off-patent, and readily available, they have the potential to directly impact patient care.
eff↑, cytotoxicity of BCA and SFN was found to be around 24.5 µM and 27.2 µM respectively, while the combination of BCA and SFN had shown an inhibitory activity at about 20.1 µM.
ROS↑,
other↑, profound increase in apoptogenic activity of compounds when treated in combination at lower dose.
ERK↓,
Apoptosis↑,
*P-gp↓, In conclusion, SD formulation improved the in vivo effectiveness of biochanin A as a P-gp inhibitor
BioAv↑, In order to solubilize poorly water soluble drugs, formulation of solid dispersions (SD) with hydrophilic carriers has been demonstrated as a promising technique
other↝, P-gp inhibitiors should play an important role in relieving MDR in anticancer treatment and
also enhancing the bioavailability of various drugs acting as P-gp substrates.
other↑, SD formulation with the mixture of Solutol ® HS15 and HPMC 2910 should be effective to improve the solubility and dissolution of biochanin A.
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Review, |
Var, |
NA |
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Review, |
AMD, |
NA |
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Dose↝, Bevacizumab is a clear, colorless solution administered i.v. [2, 3] in combination with chemotherapy in doses of 5, 7.5, 10, or 15 mg/kg
other↑, promising results are being achieved in patients with chronic diffuse diabetic macular edema and age-related macular degeneration (AMD), for which bevacizumab is being injected intravitreally at a dose of 1.25 mg [
VEGF↓, Bevacizumab acts by selectively binding circulating VEGF, thereby inhibiting the binding of VEGF to its cell surface receptors.
eff↑, These effects also lower tissue interstitial pressure, increase vascular permeability, may increase delivery of chemotherapeutic agents, and favor apoptosis of tumor endothelial cells
Half-Life↑, estimated half-life was 19.9 days (range, 11–50 days) and the predicted time to reach steady-state was approximately 100 days
eff↑, oral administration of Bifidobacterium enhanced the anti-tumor efficacy of PD-L1 inhibitors by promoting dendritic cell (DC) maturation and increasing tumor-specific CD8 + T cell activity.
DCells↑,
CD8+↑,
eff↑, One study analyzing plasma samples from colorectal cancer (CRC) patients treated with ACT and chemotherapy found that responders had significantly higher blood levels of Bifidobacterium, Lactobacillus, and Enterococcus, indicating that the blood micr
AntiTum↑, Inosine, a purine metabolite produced by Akkermansia muciniphila and Bifidobacterium longum, enhances antitumor immunity by inhibiting UBA6 expression in tumor cells,
other↑, Likewise, vitamin B6, synthesized by Lactobacillus acidophilus and Bifidobacterium bifidum, boosts T lymphocyte proliferation and promotes antitumor immunity by stimulating T cell activity
selectivity↑, Additionally, Bifidobacterium preferentially accumulates in tumors . Bifidobacterium, for example, migrates to colonize and enrich CRC tumors198
GutMicro↑, Microbiome analysis revealed enrichment of beneficial bacteria (Bifidobacterium longum, Lachnospiraceae, Ruminococcaceae) and a decline in potentially detrimental species such as Bacteroides.
*cognitive∅, There was no difference between B. monnieri and the placebo or donepezil in the treatment of Alzheimer disease based on very low certainty evidence.
*other↑, All 5 studies were deemed to have a high risk of bias.
*BBB↑, A growing body of evidence confirms that the ‘orifice-opening’ effect of borneol is principally derived from opening the BBB. Borneol is therefore believed to be an effective adjuvant that can improve drug delivery to the brain
*other↑, Borneol also protects the structural integrity of the BBB against pathological damage.
*P-gp↓, Both in vitro and in vivo studies have shown that borneol inhibited the expression of P-gp and other ABC transporters,
*toxicity⇅, Natural borneol has been extensively used in aromatherapy and in natural and cosmetic products because of its low toxicity compared to synthetic borneol, which toxicity is relatively high as it degrades slowly during storage, and noxious camphor
*BioAv⇅, In mice, a single oral dose of borneol accumulates in organs in the order of liver > brain > kidney > heart > spleen > muscle > lung, which confirms its considerably higher bioavailability in the brain than in most other organs
*Dose↑, Intranasal drug delivery can avoid gastrointestinal destruction and hepatic first-pass metabolism, resulting in rapid onset of effect and high brain bioavailability.
*ABC↓, Both in vitro and in vivo studies have shown that borneol inhibited the expression of P-gp and other ABC transporters,
*MRP1↓, including multidrug resistance protein 1 (Mrp1), 1a (Mdr1a) and 1 b (Mdr1b),
*5HT↑, systemic borneol was found to increase the levels of histamine and serotonin in the hypothalamus
*GABA↑, and levels of l-aspartic acid, glutamate, glycine and γ-aminobutyric acid (GABA) in the corpus striatum of rats (Zhang et al., 2012).
*eff↑, Co-incubation with borneol increased the uptake of Huperzine A loaded aprotinin-modified nanoparticles by capillary endothelial cells
*toxicity↓, A comprehensive toxicological evaluation, including a 30-day rat study, demonstrated that borneol did not induce cytotoxicity, inflammation, or tissue damage at daily doses up to 270 mg/kg
*EPR↑, evaluate borneol as a permeation enhancer for improving the oral absorption of intact poly(lactic-co-glycolic acid) (PLGA) nanoparticles with different mean sizes (50-300 nm)
*other↑, Our findings establish borneol as a safe and effective oral permeation enhancer for intact nanocarriers, offering a viable strategy to enhance the oral bioavailability of therapeutics, particularly those encapsulated within small-sized NPs.
TumMeta↓, We focus on the updated works of improving therapeutic efficacy, reducing toxicity, inhibiting tumor metastasis, reversing multidrug resistance, and enhancing brain targeting
BBB↑,
EPR↑, Nanocarriers can increase the concentration of a drug at the tumor site via the enhanced permeability and retention (EPR) effect, which also reduces systemic toxicity
toxicity↓,
BioAv↑, Moreover, borneol can promote the transdermal absorption of other drugs and increase their blood concentration and bioavailability
ChemoSen↑, application of borneol in nanocarriers has great potential to improve the targeting and enhance the accumulation of chemotherapeutic drugs in tumors.
eff↑, Borneol enhanced the antidepressant effects of asiaticoside by promoting its penetration of the BBB, thus enhancing the anti-depressant effects with enhanced 5-HT and BDNF, and reduced TNF-α levels
other↑, Borneol enhanced the antidepressant effects of asiaticoside by promoting its penetration of the BBB, thus enhancing the anti-depressant effects with enhanced 5-HT and BDNF, and reduced TNF-α levels
P-gp↓, inhibition of the function and expression of P-gp
MDR1↓, borneol could significantly inhibit the activity of drug resistance proteins such as multidrug resistance mutation 1 (MDR1) and P-gp and accelerate the transportation of drugs
ROS↑, chemotherapeutic sensitizer works along with the chemotherapeutic drugs to promote anticancer effect by increasing the level of reactive oxygen species (ROS) (119), arresting cell cycle (120)
TumCCA↑,
other↝, volatility of borneol makes it extremely unstable during preparation and storage.
BioAv↓, the poor water solubility of NB is not conducive to blood circulation, which greatly limits the effective delivery to the treatment site and greatly reduces its therapeutic effect.
DNAdam↑, lead to the activation of signaling pathways, including those involved in ROS, DNA damage, and apoptosis
BioEnh↑,
*Half-Life↑, The half-life of boric acid in humans is on the order of 1 day. They also infused 600 mg of
boric acid into seven human subjects and calculated a mean half-life of 21 hr.
*other↑, Bone contained the highest level of boron of any tissue. After only 1 day on the
diet, the boron content of bone increased
20-fold.
other↑, Overall, current data demonstrate that water in Germany varies significantly in the content of boron and that only boron-rich mineral water improves the boron status in both flies and humans.
BioAv↑, Moreover, the consumption of HB mineral water led to an increase in serum boron concentrations up to 72 ± 5.8 µg L−1 and a subsequent decline over 24 h to final circulating boron levels that were again comparable to baseline values.
*GutMicro↑, Beneficial effects of the microbiota-derived metabolite butyrate at the colonic level are well established, particularly through its relevance in colorectal cancer (CRC) and inflammatory bowel disease (IBD)
*other↑, (2) stimulates growth and proliferation of normal intestinal epithelial cells;
*Inflam↓, (3) inhibits inflammation;
*ROS↓, (4) inhibits oxidative stress;
AntiCan↑, (8) inhibits colon carcinogenesis
HCAR2↑, three cell-surface G-protein-coupled receptors, GPR41, GPR43, and GPR109A, are targets for butyrate [1,2].
HDAC↓, butyrate also has intracellular actions (HDAC inhibition),
*Bacteria↓, Carvacrol, either alone or in combination with other compounds, has a strong antimicrobial effect on many different strains of bacteria and fungi that are dangerous to humans
*Inflam↓, Carvacrol also exerts strong anti-inflammatory properties by preventing the peroxidation of polyunsaturated fatty acids by inducing SOD, GPx, GR, and CAT, as well as reducing the level of pro-inflammatory cytokines in the body.
*SOD↑,
*GPx↑,
*GSR↑,
*Catalase↑,
*toxicity↓, Carvacrol is considered a safe compound despite the limited amount of data on its metabolism in humans.
*Pain↓, carvacrol has been used as a substitute for cretol and carbolic acid in the treatment of toothache, sensitive dentine, and alveolar abscess, and as an antiseptic in the pulp canals of the teeth
*other↑, because it has much greater activity as a mosquito repellent than the commercial preparation, N,N-diethyl-m-methylbenzamide
*cardioP↑, other biological activities, including cardio-, reno-, and neuroprotective [20]; immune response-modulating [21]; antioxidant; anti-inflammatory [22];
*RenoP↑,
*neuroP↑,
*antiOx↑,
*AntiDiabetic↑, antidiabetic; hepatoprotective [28]; and anti-obesity properties
*hepatoP↑,
*Obesity↓,
*AntiAg↑, figure 1
*BioAv↓, challenges surrounding the wider use of carvacrol in food or feed are its unpleasant and pungent taste at higher doses; low bioavailability;
BioAv↝, sensitivity to the surrounding environment, such as in processing conditions (e.g., heat or other ingredients); and the acidic environment in the digestive tract.
*OS↑, pneumonia. Administration of carvacrol to mice (10, 25, 50 mg/kg) was associated with increased survival and significantly reduced bacterial load
MMP↓, carvacrol was found to cause greater membrane depolarization and increased oxidative stress in E. coli cells;
ROS↑,
*MDA↓, In studies conducted in guinea pigs, carvacrol concentrations of 120 and 240 μg/mL have been shown to reduce malondialdehyde levels compared to the control group
*lipid-P↓, Carvacrol prevents lipid peroxidation by inducing SOD, GPx, GR, and CAT [85,86].
*COX2↓, A decrease in COX-2 gene expression was found at carvacrol concentrations of 0.008% and 0.016%
*Dose↝, Phase I clinical trial, carvacrol was administered to healthy subjects at 1 and 2 mg/kg/day for 1 month, and no critical adverse reactions
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*Inflam↓, anti-inflammatory, antioxidant, and AChEI properties
*antiOx↑,
*AChE↓,
*BBB↑, Carvacrol is able to cross the blood brain barrier easily, notably improving its therapeutic efficacy in neurodegenerative disorders
*cardioP↑, prevention of many chronic diseases, such as cancer as well as infectious, cardiovascular and neurodegenerative diseases
*neuroP↑, Extensive researches have revealed carvacrol neuroprotective properties
*memory↑, memory-enhancing activities
*TAC↑, Carvacrol has antioxidant activity and was shown to act as a dietary phyto-additive to boost animal antioxidant status (sharifi-Rad et al., 2018
*ROS↓, carvacrol could protect neuronal injuries against Aluminum-induced oxidative stress leading to lipid peroxidation
*lipid-P↓,
*MDA↓, carvacrol has been indicated to reduce malondialdehyde (MDA) and neuronal cell necrosis, and increase superoxide dismutase (SOD) and catalase (CAT) activity levels in the hippocampus (
*SOD↑,
*Catalase↑,
*NRF2↑, carvacrol activated nuclear factor-erythroid 2-related factor 2 (Nrf2) as an endogenous antioxidant
*cognitive↑, Carvacrol administration (25, 50, and 100 mg/kg) during 21 days attenuated memory impairments and enhanced cognition compared to the control group.
*IL1β↓, Carvacrol administration diminished the expression of interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), and tumor necrosis factor-α (TNF-α).
*COX2↓,
*TNF-α↓,
*TLR4↓, carvacrol could significantly decrease Toll-like receptor 4 (TLR4) and increase brain-derived neurotrophic factor (BDNF) expression.
*BDNF↑,
*PKCδ↑, carvacrol and thymol might have protective ability on cognitive function in AD by activation of PKC pathway
*5LO↓, Carvacrol inhibited AChE and lipoxygenase activity that supports its anti-inflammation and anti-Alzheimer effects
*TRPM7↓, Reduced caspase-3 levels, and TRPM7 channels inhibitor
*GSH↑, Antioxidant activity, Increased glutathione
*other↑, revealed a remarkable neuroprotective action of carvacrol in cerebral ischemia in animal models
*Ferroptosis↓, via ferroptosis inhibition by elevating GPx4 expression
*GPx4↑,
*cognitive↑, The number of patients clinically diagnosed as AD at follow-up in placebo group was 4, but 0 in active group
*other↑, Oral ACS may protect against the onset of AD in Patients with Mild Cognitive Impairment, especially patients with the APOE4 allele.
PSA↓, A decrease in serum prostate specific antigen (PSA) was observed on the PolyE arm
other↑, A significant increase in plasma EGCG concentration was achieved in the treatment arm at 6 and 12 months
Risk↝, was well tolerated but did not reduce the likelihood of a subsequent PCa diagnosis in men with baseline HGPIN or ASAP.
*other↑, Our results showed that CBD exerted a differentiating and protective effect on SCCs. somatic stem cells
CSCs↓, n addition, this molecule demonstrated an antiproliferative effect on some CSCs
SOX2↓, CBD decreased the expression levels of Id‐1 and SOX2 in the neurospheres formed.
other↝, On the other hand, CBD sensitivity was inversely correlated with ROS expression in GSCs both in vitro and in vivo,
Fenton↑, Fenton- and Fenton-like reaction-based chemodynamic therapy (CDT) are new strategies to enhance anticancer efficacy due to their capacity to generate reactive oxygen species (ROS) and oxygen (O2).
ROS↑,
RadioS↑, the generated O2 can relieve the hypoxic condition in the tumor microenvironment (TME) which hinders efficient photodynamic therapy, radiotherapy, etc.
other↑, due to their high catalytic efficiency and excellent biocompatibility; these include iron-based nanomaterials, other metal-based nanomaterials (including Mn2+, Cu2+, and Mo3+, etc.),
GSH↓, In ferroptosis, the activity of system xc- (SLC7A11) is inhibited, resulting in decreased import of cysteine, GSH depletion, inactivation of the glutathione peroxidase 4 (GPX4), and finally ferroptosis
GPx4↓,
ChemoSen↑, increasingly been recognized as a promising strategy for tumor therapy and have been explored in combination with chemotherapy, PDT, PTT, gas therapy, sonodynamic therapy, radiotherapy, immunotherapy, and magnetic hyperthermia therapy (MHT)
sonoS↑, SDT has many advantages, including deep tissue penetration, controllability, and good patient compliance; however, its therapeutic effect is limited in the hypoxic TME and where there is low ROS release and low sensitivity
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*other↝, The most abundant and promising bioactive compound derived from the root of this plant is celastrol, also called tripterine, which possess a broad range of biological activities
*other↝, TW is generally used in the treatment of Crohn’s disease (CD) in China.
*CRP↓, Inflammatory parameters, including c-reactive protein (CRP), also decreased
*eff↝, Etanercept plus TW had an equivalent therapeutic effect to that of Etanercept plus MTX and were both well tolerated
*other↑, TW in human kidney transplantation (26). Rejection occurred in 4.1% of patients treated with TW versus 24.5% of control patients, showing efficacy in the prevention of renal allograph rejection
*CXCR4↓, celastrol decreases hypoxia-induced FLS invasion by inhibiting HIF-1α-mediated CXCR4 transcription
*IL1β↓, Authors have shown that it decreases the production of IL-1β, IL-6, IL-17, IL-18, and TNF by SIC cells harvested from arthritic rats
*IL6↓,
*IL17↓,
*IL18↓,
*TNF-α↓,
*MMP9↓, celastrol reduces MMP-9 production, which limits bone damage
*PGE2↓, celastrol suppresses LPS-induced expression of PEG2 via the downregulation of COX-1 and COX-2 activation
*COX1↓,
*COX2↓,
*PI3K↓, associated with a decrease in PI3K/Akt pathway
*Akt↓,
*other↑, Remarkably, this bone-protective property of celastrol in arthritic models is further supported by studies performed in cancer models
TumCCA↑, celastrol induces cell cycle arrest, apoptosis, and autophagy by the activation of reactive oxygen species (ROS)/c-Jun N-terminal kinases (JNK) signaling pathway
Apoptosis↑,
ROS↑,
JNK↑,
TumAuto↑, celastrol is still able to induce autophagy through HIF/BNIP3 activation
Hif1a↓, The inhibitory effect of celastrol on angiogenesis is mediated by the suppression of HIF-1α,
BNIP3↝,
HSP90↓, The inhibition of HSP90 by celastrol
Fas↑, activation of Fas/Fas ligand pathway in non-small-cell lung cancer
FasL↑,
ETC↓, inhibition of mitochondrial respiratory chain (MRC) complex I
VEGF↓, This inhibition of HIF-1α leads to the decrease of its target genes, such as the VEGF
angioG↓, Angiogenesis Inhibition
RadioS↑, celastrol can overcome tumor resistance to radiotherapy in prostate (129) and lung cancer cells
*neuroP↑, celastrol is a promising neuroprotective agent in animal models of neurodegenerative diseases, such as Parkinson disease (149), Huntington disease (149–151), Alzheimer disease
*HSP70/HSPA5↑, his induction of HSP70 by celastrol explains its beneficial effects not only in neurodegenerative disorders but also in inflammatory diseases.
*ROS↓, celastrol protects human dopaminergic cells from injury and apoptosis and prevents ROS generation and mitochondrial membrane potential loss
*MMP↑,
*Cyt‑c↓, It inhibits cytochrome c release, Bax/Bcl-2 alterations, caspase-9/3 activation, and p38 MAPK activation
*Casp3↓,
*Casp9↓,
*MAPK↓,
*Dose⇅, Authors discuss that it seems to have a narrow therapeutic window, and suggest that it may have a biphasic effect with protective properties at low concentrations and toxic effects at higher concentrations.
*HSPs↑, induces a set of HSPs (HSP27, 32, and 70) in rat cerebral cortical cultures, which are selectively impacted during the progression of this disease
BioAv↓, Due to this poor water solubility, celastrol has low bioavailability. oral administration of celastrol in rats results in ineffective absorption into the systemic circulation, with an absolute bioavailability of 17.06%
Dose↝, narrow therapeutic window of dose together with the occurrence of adverse effects. Our own data showed in vivo that the doses of 2.5 and 5 μg/g/day are effective and non-toxic in the treatment of arthritis in rats;
other↑, Nanoscale systems based on natural polymers like chitosan have garnered significant attention as promising platforms for cancer diagnosis and therapy owing to chitosan's inherent biocompatibility, biodegradability, nontoxicity, and ease of functional
Imm↑, The immunomodulatory effects of chitosan and its role in impacting the tumor microenvironment are analyzed.
DDS↑,
DDS↑, Chitosan nanoparticles (CSNPs) have prospects as a revolutionary delivery system capable of enhancing anticancer drug activity and reducing negative impacts on normal cells.
BioAv↑, delivering materials to improve the bioactivity of NPs and to understand the intricacies of breast cancer has garnered significant interest.
EPR↑, Enhancement of the therapeutic efficacy of therapy, especially in tumor therapy, through passive targeting or enhanced permeation and retention (EPR) effects
TumCP↓, Inhibitory effects on tumor cell proliferation, tumor-associated angiogenesis, and metastasis, thus exhibiting good anticancer activity
angioG↓,
TumMeta↓,
other↑, The primary goal of modifying CS is to enhance its solubility, which may lead to a wider range of potential applications
other↑, Almost every tumor cell type investigated showed increased levels of tCho metabolites compared to non-malignant counterparts
other↝, the inhibition of choline transporters in cancer cells results in lower levels of intracellular choline accompanied by cell death induction
other↝, needed to define what orchestrates the different combinations of choline transporters and how they lead to enhanced choline transport in cancer cells to drive the discovery of potential cancer targets.
other↝, Meisamy et al. (78) reported a reduction in PCho levels as early as 24 h after the first treatment in locally advanced breast cancer patients who responded to doxorubicin chemotherapy, while it remained the same or increase in non-responders
other↝, Considering that PCho concentration correlates strongly with cell proliferation (104), one hypothesis is that a decrease in choline metabolites after therapy may reflect cell cycle arrest.
Risk↓, Among women, but not men, high choline concentration was associated with decreased CRC risk
other↑, Individuals with high plasma concentrations of methionine, choline, and betaine may be at reduced risk of CRC.
BioAv↑, Choline can either be derived from the food we consume or be synthesized within our bodies
other↑, Recent research has shown that choline metabolism undergoes significant changes in cancer, resulting in a heightened demand for choline and its metabolites (9).
other↑, PET imaging using radio-tagged choline has proven to be successful in identifying a range of cancers, such as liver and prostate cancer
other↝, Overexpression of GDPD5 has been linked to enhanced choline uptake and utilization, contributing to the dysregulation of choline metabolism in cancer
*other↑, [1], the components of eggs providing beneficial effects against disease [2,3,4,5,6],
*other↑, the relationship between egg intake and healthy eating index [7]
*Inflam↓, the protective effects of eggs against inflammation [8] and oxidative stress [9].
*ROS↓,
*antiOx↑, antioxidant and anti-inflammatory properties
*Iron↑, egg white protein was very useful for the recovery of iron-deficiency anemia
*cardioP∅, clear that heart disease does not increase by egg intake
Dose?, At low concentration, citrate increased both histone H4 acetylation and lipid deposition; at high concentration, citrate inhibited both
ac‑H4↓,
lipidDe↓,
ACLY↓, Considering the strong demand for acetyl-CoA but not for OAA in tumor cells, the exogenous citrate would behave like a trojan horse that carries OAA inside the cells and reduces ACLY expression and cellular metabolism.
selectivity↑, in non-tumor cells, changes of acetylated histone level do not correspond to a change of ACLY expression, as instead shown by HepG2 cells.
*ACLY∅, In contrast, ACLY expression in IHH (normal)cells was not modified after citrate exposure, suggesting that, in this case, ACLY expression was not regulated by histone H4 acetylation
Glycolysis↓, strong inhibition of glycolysis, which leads to a decrease in NADH necessary for OAA reduction
NADH↓,
OAA↑, exogenous citrate would behave like a trojan horse that releases OAA in the cells, where it could exert its therapeutic effect also on hepatoma cells.
other↑, most important discovery is undoubtedly the demonstration that high concentrations of citrate decrease the availability of acetyl-CoA, a key molecule both in the metabolism of sugars and lipids
Showing Research Papers: 1 to 50 of 160
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 160
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Catalase↑, 1, Fenton↑, 1, GPx4↓, 1, GSH↓, 2, lipidDe↓, 1, NADH↓, 2, ROS↑, 11, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
ETC↓, 1, MMP↓, 3, MPT↑, 1,
Core Metabolism/Glycolysis ⓘ
ACLY↓, 1, AMPK↑, 1, cMyc↓, 1, Glycolysis↓, 1, HMG-CoA↓, 1, OAA↑, 1,
Cell Death ⓘ
p‑Akt↓, 1, Apoptosis↑, 7, Bax:Bcl2↑, 1, Bcl-2↓, 2, Casp12↑, 1, Casp3↑, 1, cl‑Casp3↑, 1, Casp8↑, 1, Casp9↑, 1, Cyt‑c↑, 2, Fas↑, 2, FasL↑, 1, iNOS↑, 1, JNK↑, 2, MAPK↑, 1, p38↑, 1, survivin↓, 1,
Kinase & Signal Transduction ⓘ
HCAR2↑, 1,
Transcription & Epigenetics ⓘ
ac‑H4↓, 1, other↓, 1, other↑, 31, other↝, 8, sonoS↑, 1,
Protein Folding & ER Stress ⓘ
HSP90↓, 2,
Autophagy & Lysosomes ⓘ
BNIP3↝, 1, TumAuto↑, 2,
DNA Damage & Repair ⓘ
CHK1↓, 1, DNAdam↑, 2, DNArepair↑, 1, P53↑, 2, P53↝, 1,
Cell Cycle & Senescence ⓘ
CycB/CCNB1↓, 1, P21↑, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State ⓘ
CSCs↓, 1, EMT↓, 2, ERK↓, 1, HDAC↓, 1, SOX2↓, 1, STAT3↓, 1, TumCG↓, 2, Wnt↓, 1,
Migration ⓘ
AntiAg↑, 3, E-cadherin↑, 1, p‑FAK↓, 1, MALAT1↓, 1, MMP2↓, 1, MMP9↓, 1, Slug↓, 1, talin?, 1, TumCI↓, 2, TumCMig↓, 2, TumCP↓, 4, TumMeta↓, 3, Twist↓, 1, Vim↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EPR↑, 3, Hif1a↓, 2, TXA2↓, 1, VEGF↓, 3, VEGFR2↓, 1,
Barriers & Transport ⓘ
BBB↑, 1, P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, DCells↑, 1, HCAR2↑, 1, IL8↓, 1, Imm↑, 1, Inflam↓, 1, NF-kB↑, 1, PD-L1↓, 1, PGE2↓, 1, PSA↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 3, BioAv↑, 6, BioAv↝, 1, BioEnh↑, 1, ChemoSen↑, 3, DDS↑, 2, Dose?, 1, Dose↑, 1, Dose↝, 4, eff↓, 1, eff↑, 9, Half-Life↑, 1, MDR1↓, 1, RadioS↑, 3, selectivity↑, 3,
Clinical Biomarkers ⓘ
GutMicro↑, 1, PD-L1↓, 1, PSA↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 4, AntiTum↑, 1, chemoP↑, 1, NP/CIPN↑, 1, PDE4↓, 1, Risk↓, 3, Risk↝, 1, toxicity↓, 1, toxicity↝, 1, Wound Healing↑, 1,
Infection & Microbiome ⓘ
CD8+↑, 1,
Total Targets: 121
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 5, Catalase↑, 2, Ferroptosis↓, 1, GPx↑, 2, GPx4↑, 1, GSH↑, 3, GSR↑, 1, GSTs↑, 1, HDL↑, 1, Iron↑, 1, Keap1↓, 1, lipid-P↓, 3, MDA↓, 5, MPO↓, 1, NRF2↑, 2, ROS↓, 8, SOD↑, 4, TAC↑, 1, TBARS↓, 1, VitC↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
ACLY∅, 1, adiP↓, 1, ALAT↓, 1, DHA↑, 1, H2S↑, 1, LDH↓, 2, LDL↓, 1,
Cell Death ⓘ
Akt↓, 2, Apoptosis↓, 1, Casp3↓, 1, Casp9↓, 1, Cyt‑c↓, 1, Ferroptosis↓, 1, iNOS↓, 1, MAPK↓, 1,
Transcription & Epigenetics ⓘ
other?, 1, other↓, 2, other↑, 25, other↝, 4,
Protein Folding & ER Stress ⓘ
HSP70/HSPA5↑, 1, HSPs↑, 1,
Proliferation, Differentiation & Cell State ⓘ
PI3K↓, 2, TRPM7↓, 1,
Migration ⓘ
5LO↓, 1, AntiAg↑, 2, MMP9↓, 1, PKCδ↑, 1,
Angiogenesis & Vasculature ⓘ
EPR↑, 1, NO↓, 2,
Barriers & Transport ⓘ
BBB?, 1, BBB↑, 4, P-gp↓, 2,
Immune & Inflammatory Signaling ⓘ
COX1↓, 3, COX2↓, 5, CRP↓, 2, CXCR4↓, 1, IL17↓, 1, IL18↓, 1, IL1β↓, 3, IL6↓, 2, Inflam↓, 6, NF-kB↓, 1, PGE2↓, 2, TLR4↓, 1, TNF-α↓, 3,
Synaptic & Neurotransmission ⓘ
5HT↓, 1, 5HT↑, 1, AChE↓, 1, BDNF↑, 1, GABA↑, 1,
Drug Metabolism & Resistance ⓘ
ABC↓, 1, BioAv↓, 1, BioAv↑, 2, BioAv⇅, 1, BioAv↝, 1, Dose↑, 1, Dose⇅, 1, Dose↝, 1, eff↓, 3, eff↑, 5, eff↝, 2, Half-Life↓, 1, Half-Life↑, 2, Half-Life↝, 1, MRP1↓, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 1, BP↓, 1, creat↓, 1, CRP↓, 2, GutMicro↑, 3, IL6↓, 2, LDH↓, 2,
Functional Outcomes ⓘ
AntiDiabetic↑, 1, BOLD↑, 1, cardioP↑, 5, cardioP∅, 1, cognitive↓, 1, cognitive↑, 6, cognitive∅, 1, hepatoP↑, 2, memory↑, 3, Mood↑, 1, neuroP↓, 1, neuroP↑, 7, Obesity↓, 1, OS↑, 1, Pain↓, 1, RenoP↑, 1, Risk↓, 4, Risk↑, 1, toxicity↓, 4, toxicity⇅, 1,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 116
Scientific Paper Hit Count for: other, other
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
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