other Cancer Research Results
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Scientific Papers found: Click to Expand⟱
*cognitive↑, The odds of IADL impairment increased significantly with decreasing intake of vitamins B2, B6, and B12
*neuroP↑, possible long-term neuroprotective effect of dietary fibre, n-3 polyunsaturated fats, and B-group vitamins, and support dietary intervention to prevent cognitive decline.
*other↝, Recent cognitive decline was associated with lower intakes of poultry, fish, and animal fats, as well as higher intakes of dairy dessert and ice-cream.
*other⇅, IADL impairment was associated with lower intake of vegetables
Glycolysis↓, 2-DG inhibits glycolysis due to formation and intracellular accumulation of 2-deoxy-d-glucose-6-phosphate (2-DG6P), inhibiting the function of hexokinase and glucose-6-phosphate isomerase, and inducing cell death
HK2↓,
mt-ROS↑, 2-DG-mediated glucose deprivation stimulates reactive oxygen species (ROS) production in mitochondria, also leading to AMPK activation and autophagy stimulation.
AMPK↑,
PPP↓, 2-DG has been shown to block the pentose phosphate shunt
NADPH↓, Decreased levels of NADPH correlate with reduced glutathione levels, one of the major cellular antioxidants.
GSH↓,
Bax:Bcl2↑, Valera et al. also observed that in bladder cancer cells, 2-DG treatment modulates the Bcl-2/Bax protein ratio, driving apoptosis induction
Apoptosis↑,
RadioS↑, 2-DG radiosensitization results from its effect on thiol metabolism
eff↓, (NAC) treatment, downregulated glutamate cysteine ligase activity, or overexpression of ROS scavenging enzymes
Half-Life↓, its plasma half-life was only 48 min [117]) make 2-DG a rather poor drug candidate
other↝, Adverse effects of 2-DG administration in humans include fatigue, sweating, dizziness, and nausea, mimicking the symptoms of hypoglycemia
eff↓, Moreover, 2-DG has to be used at relatively high concentrations (≥5 mmol/L) in order to compete with blood glucose
other↝, Since the use of ALA-based drugs for tumor diagnosis or therapy depends on preferential PpIX tumor accumulation, we begin this review with an overview of PpIX biosynthesis from ALA and end with the prospect of combining the diagnostic and therapeutic
ROS↑, These components individually are not harmful but become cytotoxic when combined due to the generation of reactive oxygen species (ROS) via type I and II photochemical reactions.
other↝, ALA was known to cause endogenous PpIX accumulation in human lymphocytes in the 1970s [15].
mtDam↑, which causes direct mitochondrial structural damage and Ca2+ release [24].
Ca+2↑,
ER Stress↑, ALA-PDT is known to damage the endoplasmic reticulum (ER) and cause Ca2+ release, triggering apoptosis through ER-stress signaling [25].
Apoptosis↑,
TumAuto↑, Lastly, ALA-PDT is also known to induce autophagy, the degradation of cellular components by lysosomes.
other↝, ALA administration exhibits red fluorescence and photosensitizing activity upon light activation.
Dose↝, Although blue and red light-emitting diode (LED) illuminators are commonly used as the light source to activate ALA and MAL for PDT of AK lesions, natural daylight is emerging as an attractive and convenient alternative.
Imm↑, ALA-PDT not only directly kills tumor cells but also elicits potent immune responses with important implications in the long-term therapeutic outcome.
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AD, |
NA |
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Park, |
NA |
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*other↝, exact causes of neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS) are not fully understood, researchers believe that regulating the 5-HT system could help alleviate symptoms
*cognitive↑, 5-HT-related drugs may also improve the most prominent cognitive impairment issues in AD.
*memory↑, 5-HT6 receptor antagonists (such as idalopirdine) have the potential to improve memory and learning abilities in clinical trials.
*Ach↑, 5-HT4 receptor agonists can enhance acetylcholine release, which helps improve cognitive function and memory formation.
*Sleep↑, Finally, trp and various metabolites, including melatonin, are regulators of sleep, with disorders of sleep being an important risk factor for the development of AD.
*5HT↑, Figure 1. Conversion of tryptophan to serotonin.
*memory↑, Sleep has important roles in learning and memory consolidation. Not surprisingly, there are accumulating data suggesting that sleep disorders contribute to cognitive decline and the development of AD [23].
*other↝, People who sleep six hours or less per night are more likely to develop Alzheimer’s dementia later in life, an observation which suggests that inadequate sleep duration increases dementia risk
*other↝, In aging and AD, the brain's 5-HT system undergoes structural and functional changes that contribute to cognitive decline.
*cognitive↝, Theoretically, targeted therapies aimed at restoring the brain's 5-HT projection network or functions could potentially have cognitive-enhancing effects in AD. However, preclinical studies have shown inconsistent effects
*BioAv↝, intramuscularly administered gold is greater than 95% bioavailable, whereas only 20 to 30% of an orally administered dose of auranofin is absorbed.
*Dose↝, 50mg intramuscular injection of GST, serum gold concentrations rise sharply, peaking between 4 and 8 mg/L in approximately 2 hours and declining to an average of 3 mg/L by 7 days.
*Half-Life↑, Both compounds are retained within the body for prolonged periods.
*BioAv↝, In human subjects, parenterally administered gold is widely distributed among bodily tissues, showing a predilection for tissues of the reticuloendothelial system as well as the kidney and adrenal cortex.
*other↝, auranofin but animal studies have shown comparatively less affinity for the liver, kidney and spleen.
TrxR↓, mechanism of action of auranofin was correlated with thioredoxin reductase inhibition,
other↝, but other modes of action such as interference with mitochondrial protein import and NADH kinase were also described and discussed
IL6↑, Conversely, auranofin stimulated IL-6 and IL-8 secretion in monocytes,
IL8↑,
NK cell⇅, NK activation was only observed at low doses of auranofin, while high doses inhibited NK activity
COX2↓, suppression of pro-inflammatory factors such as COX-2 (cyclooxygenase-2), NOS (nitric oxide synthase), NF-κB (nuclear factor-κB), and TrxR, as well as on the activation of peroxyredoxin-1 and Nrf2 (nuclear factor erythroid 2-related factor 2) [19].
NOS2↓,
NRF2↑,
Prx↑,
Half-Life↑, plasma half-lives of 15–25 days [24]
Dose↝, To avoid frequently occurring diarrhea, oral doses of 3–6 mg per day, or below, should also be considered when repurposing auranofin for the treatment of other human diseases.
ROS↑, Imbalances in this system lead to the accumulation of cytotoxic ROS.
NF-kB↓, Auranofin can bind to IKK, which ultimately leads to NF-κB inhibition
chemoP↑, Our study concluded PG2 combined with adjuvant chemotherapy can reduce CIF, insomnia, the negative effect on future perspectives, and improve global health status, especially for premenopausal patients with breast cancer.
other↝, n this study, the primary endpoint, encompassing changes in FGS and fatigue intensity, was similar in both treatment groups.
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BC, |
MCF-7 |
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Nor, |
MCF10 |
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
BC, |
BT549 |
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in-vivo, |
BC, |
MDA-MB-231 |
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ROS↑, AgNPs is known to cause dose-dependent toxicities, including induction of oxidative stress and DNA damage, which can lead to cell death.
DNAdam↑,
selectivity↑, We show that AgNPs are highly cytotoxic toward TNBC cells at doses that have little effect on nontumorigenic breast cells or cells derived from liver, kidney, and monocyte lineages.
TumCG↓, reduce TNBC growth and improve radiation therapy.
RadioS↑,
Dose↝, s 23±14 nm: particles were diluted to 40 μg/mL. 25 μg/mL AgNP dilution for 24 hours. zeta potential of AgNPs in water at pH 7 was approximately −36 mV, indicating good colloidal stability.
selectivity↑, Depending on AgNP dose, all three TNBC cell lines were 5- to 10-fold more sensitive to AgNP exposure than the nontumorigenic breast cells.
other↝, this study demonstrate that the cytotoxicity was dependent on exposure of cells to intact AgNPs and not due to Ag+ ions
eff↓, toxicity of AgNPs was significantly reduced in MDA-MB-231, MCF-7, and MCF-10A cells following pretreatment with GSH
eff↑, Selective depletion of GSH by BSO resulted in increased AgNP toxicity in all cell lines.
γH2AX↑, AgNPs significantly increased γH2AX in these cells compared to radiation alone.
Dose↓, Strikingly, an AgNP dose of as little as 1 μg/mL resulted in a dose enhancement of IR treatment (approximately 2-fold at the 2 Gy dose) f
eff↑, Moreover, intratumoral injection of AgNPs with or without radiation treatment can inhibit the growth of TNBC xenografts in mice
selectivity↑, IC50: ≤4.25 μg/ml for normal and ≤32.5 μg/ml cerival cancer cells
eff↝, in vitro cytotoxicity assessment of the AgNPs has significant correlation with the total protein concentration in treated cells.
other↝, In the present study, silver nanoparticles were biologically synthesized using pure enzyme α-amylase and the other one by using soluble proteins of neem leaf extracts.
IL1α↓, berry extracts in silver nanoparticles instead to obtain a particle size ranging from 20 to 80 nm and a significantly reduced production of IL-1 α compared to the control cells
other↝, hyperproliferation of keratinocytes as the psoriatic skin cell lifetime is more than six times shorter than that of normal skin cells, this is thought to be due to hyperactivity of growth factors
*other↝, Silver therapy, in principle, has many benefits, such as (1) a multilevel antibacterial effect on cells, which considerably reduces the organism's chances of developing resistance; (2) effectiveness against multi-drug-resistant organisms;
*toxicity↓, (3) low systemic toxicity.
*eff↑, Decreasing the dimension of nanoparticles has a pronounced effect on their physical properties, which significantly differ from those of the bulk material
*eff↑, Bacterial resistance to elemental silver is extremely rare
*Inflam↓, Anti-inflammatory properties of silver nanoparticles also promote wound healing by reducing cytokine release,56 decreasing lymphocyte and mast cell infiltration.
*IL6↓, Levels of IL-6 mRNA in the wound areas treated with silver nanoparticles were maintained at statistically significantly lower levels throughout the healing process,
*TGF-β↑, mRNA levels of TGF-β1 were higher during the initial period of healing in the site treated with silver nanoparticles
*MMP9↓, Nanocrystalline silver dressings significantly reduced MMP-9 levels in a porcine mode
*eff↑, Wounds treated with silver nanoparticles completely healed in 25.2 ± 0.72 days after injury, whereas those treated with antibiotics required 28.6 ± 1.02 days (P < .01).
*Bacteria↓, broad-spectrum antimicrobial efficacy, silver nanoparticles have opened new horizons towards novel approaches in the control of infections in wound healing.
*eff↑, It is accepted that Ag nanoparticles with small diameter have a superior antimicrobial effect than those with a larger diameter, and their antibacterial activity is higher than their bulk equivalents
*other↝, Today, due to their broad-spectrum antibacterial capability, silver-based creams and ointments, as well as AgNPs-based biomedical products, such as wound dressings, are commercially available for different medical applications
*toxicity↓, In low concentrations, silver has been indicated as non-toxic material to humans, and it has been assessed as a promising material in pharmaceutical and biomedical fields
*other↝, after 1 month of washing them up with distilled water, 75% and 80% of the silver was eliminated from the liver and the blood, respectively, and just 5% of the silver was eliminated from the brain
*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
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CRC, |
HCT116 |
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in-vitro, |
Nor, |
HEK293 |
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NRF2↑, Nanosilver increased Nrf2 protein expression and disrupted the cell cycle at the G1 and G2/M phases.
TumCCA↑, AgNPs interact with DNA to stop
the cell cycle and lead to apoptosis
ROS↑, Nanosilver induced significant mitochondrial oxidative stress in HCT116, whereas it did not in the non-cancer HIEC-6 and nanosilver/sodium ascorbate co-treatment was preferentially lethal to HCT116 cells,
selectivity↑,
*AntiViral↑, AgNPs are effective antiviral agents against various viruses such as human
immunodeficiency virus, hepatitis B virus, and monkey pox virus through interaction with
surface glycoproteins on the virus
*toxicity↝, Citrate and PVP-coated AgNPs have been found to be less toxic than non-coated AgNPs
ETC↓, AgNPs affects mitochondrial function through the disruption of the electron transport
chain2,24,26,33,39–41
MMP↓, Studies have shown that exposure to AgNPs resulted in a decrease of mitochondrial membrane potential (MMP) in various in vitro and in vivo experiments
DNAdam↑, AgNPs has also been shown to interact with and induce damage to DNA, DNA strand breaks, DNA damage
Apoptosis↑, apoptosis induced by AgNPs were through membrane lipid peroxidation, ROS, and oxidative stress
lipid-P↑,
other↝, Several studies have showed AgNPs interact with various proteins such as haemoglobin, serum albumin, metallothioneins, copper transporters, glyceraldehyde 3-phosphate dehydrogenase (GAPDH), malate dehydrogenase (MDH), and bacterial proteins.
UPR↑, Studies have shown exposure to AgNPs induces activation of the UPR
*GRP78/BiP↑, AgNPs induced increased levels of GRP78, phosphorylated PERK, phosphorylated eIF2-α, and
phosphorylated IRE1α, spliced XBP1, cleaved ATF-6, CHOP, JNK and caspase 12
*p‑PERK↑,
*cl‑eIF2α↑,
*CHOP↑,
*JNK↑,
Hif1a↓, One study showed AgNPs inhibits HIF-1 accumulation and suppresses expression of HIF-1 target genes in breast cancer cells (MCF-7) and also found the protein
levels of HIF-1α and HIF-1β decreased
AntiCan↑, Many studies have shown that ascorbic acid, on its own, has anti-cancer effects
*toxicity↓, However, when the rats were treated with both ascorbic acid
and AgNPs, a decrease in toxic effects was observed in non-cancer parotid glands in rats
eff↑, Studies have shown both AgNPs and ascorbic acid have greater effects and toxicity in
cancer cells relative to non-cancer cells
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Diabetic, |
NA |
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ROS↑, action mechanisms of AgNPs, which mainly involve the release of silver ions (Ag+), generation of reactive oxygen species (ROS), destruction of membrane structure.
eff↑, briefly introduce a new type of Ag particles smaller than AgNPs, silver Ångstrom (Å, 1 Å = 0.1 nm) particles (AgÅPs), which exhibit better biological activity and lower toxicity compared with AgNPs.
other↝, This method involves reducing silver ions to silver atoms 9, and the process can be divided into two steps, nucleation and growth
DNAdam↑, antimicrobial mechanisms of AgNPs includes destructing bacterial cell walls, producing reactive oxygen species (ROS) and damaging DNA structure
EPR↑, Due to the enhanced permeability and retention (EPR) effect, tumor cells preferentially absorb NPs-sized bodies than normal tissues
eff↑, Large surface area may lead to increased silver ions (Ag+) released from AgNPs, which may enhance the toxicity of nanoparticles.
eff↑, Our team prepared Ångstrom silver particles, capped with fructose as stabilizer, can be stable for a long time
TumMeta↓, AgNPs can induce tumor cell apoptosis through inactivating proteins and regulating signaling pathways, or blocking tumor cell metastasis by inhibiting angiogenesis
angioG↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
*Bacteria↓, Rather than Gram-positive bacteria, AgNPs show a stronger effect on the Gram-negative ones. This may be due to the different thickness of cell wall between two kinds of bacteria
*eff↑, In general, as particle size decreases, the antibacterial effect of AgNPs increases significantly
*AntiViral↑, AgNPs with less than 10 nm size exhibit good antiviral activity 185, 186, which may be due to their large reaction area and strong adhesion to the virus surface.
*AntiFungal↑, Some studies confirm that AgNPs exhibit good antifungal properties against Colletotrichum coccodes, Monilinia sp. 178, Candida spp.
eff↑, The greater cytotoxicity and more ROS production are observed in tumor cells exposed to high positive charged AgNPs
eff↑, Nanoparticles exposed to a protein-containing medium are covered with a layer of mixed protein called protein corona. formation of protein coronas around AgNPs can be a prerequisite for their cytotoxicity
TumCP↓, Numerous experiments in vitro and in vivo have proved that AgNPs can decrease the proliferation and viability of cancer cells.
tumCV↓,
P53↝, gNPs can promote apoptosis by up- or down-regulating expression of key genes, such as p53 242, and regulating essential signaling pathways, such as hypoxia-inducible factor (HIF) pathway
HIF-1↓, Yang et al. found that AgNPs could disrupt the HIF signaling pathway by attenuating HIF-1 protein accumulation and downstream target genes expression
TumCCA↑, Cancer cells treated with AgNPs may also show cell cycle arrest 160, 244
lipid-P↑, Ag+ released by AgNPs induces oxidation of glutathione, and increases lipid peroxidation in cellular membranes, resulting in cytoplasmic constituents leaking from damaged cells
ATP↓, mitochondrial function can be inhibited by AgNPs via disrupting mitochondrial respiratory chain, suppressing ATP production
Cyt‑c↑, and the release of Cyt c, destroy the electron transport chain, and impair mitochondrial function
MMPs↓, AgNPs can also inhibit the progression of tumors by inhibiting MMPs activity.
PI3K↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
Akt↓,
*Wound Healing↑, AgNPs exhibit good properties in promoting wound repair and bone healing, as well as inhibition of inflammation.
*Inflam↓,
*Bone Healing↑,
*glucose↓, blood glucose level of diabetic rats decreased when treated with AgNPs for 14 days and 21 days without significant acute toxicity.
*AntiDiabetic↑,
*BBB↑, The small-sized AgNPs are easy to penetrate the body and cross biological barriers like the blood-brain barrier and the blood-testis barrier
*other↝, The synthesis of AgNPs was primarily identified by the appearance of yellow colour and confirmed by showing λmax =409 nm in UV-visible spectroscopy.
*other↝, In this study, the bottom-up strategy was used to synthesize AgNPs using ascorbic
acid as a reductive agent and citric acid as a potent complex stabilizer, effectively.
*eff↑, It clearly explained that the reaction mixture having a pH at 10
is most appropriate to reduce Ag+ ions into AgNPs and stable over a month.
*eff↑, The FTIR results indicate that the citric acid is directly involved in the stabilization and capping of AgNPs, whereas ascorbic acid reduces Ag+ ions to Ag0.
*Half-Life↝, Fecal silver began to decline at 12 h for all the AgNPs and was at baseline levels by 48 h.
*toxicity↓, Acute ingestion of AgNP is well-tolerated at high doses, irrespective of size or coating
*Dose↑, The doses utilized in this study (0.1, 1 and 10 mg/kg bw/d) were equivalent to, respectively, 20×, 200× and 2000× the EPA oral reference dose (RfD, 0.005 mg/kg bw/d) for silver
*other↝, Previous estimates of colloidal silver doses associated with clinically evident argyria range between 40× and 700× the oral RfD, although these typically represent repeated exposures
*eff↝, Acute ingestion of AgNP is well-tolerated with concurrent antibiotic administration
*BioAv↓, Oral bioavailability was previously determined as low (4.2%) for a single 10 mg/kg bw dose of 7.9 nm AgNP-citrate in rats
*other↝, point-of-need detection of divalent mercuric (Hg2+) ions within several minutes. An intense red TE signal will be created in the colloidal AgNP solution under the irradiation of a portable laser pointer pen (635 nm).
*other↝, Upon introduction of Hg2+ sample, the degradation of AgNPs takes place because of the specific redox reactions between the analyte ions and the nanoprobes, leading to a significant decrease or even disappearance of the TE in the final reaction mixtur
*other↝, On the other hand, upon the addition of 5 μM creatinine into the Cit-AgNP solution, the color of the resulting mixture changed from yellow to pink
OS↑, remission
Dose↓, Electron microscopy of AgNP solution revealed bimodal nanoparticle size
distribution: 3 and 12 nm.
BioAv↝, basal **silver ion** concentrations of 32 ng/g, rising to 46 ng/g 1 hour after ingesting 60 mL of AgNP solution.
toxicity↓, no toxicities were observed and he had complete radiographic resolution of his cancer
Remission↑,
other↝, patient serum was analyzed and intact nanoparticles were not identified. Thus, we could not isolate the circulating AgNP form
other↝, Analysis of urine showed no AgNP or detectable nanoparticle fragments
other↝, AgNP solution was also exposed to simulated gastric fluid, in which they aggregated into larger nanoparticles according to UV-Vis absorption.
Dose↝, GDH: based on repeat setup, estimated PPM is 20PPM assuming 67% effecient. 1.2mg/60mL (he took 160mL/day
BioAv↝, GDH: chatAI computed the estimated bioavailability at 7%
*VEGF↓,
*IL1↓, IL-1β-induced permeability
toxicity↝, Since low concentrations of Ag-NP were found to be non-toxic
other↝, Our results indicate that Ag-NP have a therapeutic benefit in vascular permeability.
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Cerv, |
HeLa |
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BC, |
MDA-MB-231 |
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Vim↑, Surprisingly, and apparently contradictory to the role that vimentin plays in metastasis, a time-dependent increase in total vimentin protein was observed
TumCI↓, Ajoene inhibits invasion and migration
TumCMig↓,
TumMeta↓, offer protection against metastatic cancer, mediated through binding to the vimentin target.
Vim↓, our vimentin finding is therefore the second example in the literature, where ajoene has been found to target and inhibit a protein, with a simultaneous increase in its expression.
other↝, We argue that ajoenes increased vimentin expression may be a response to restore the malfunctioning vimentin network.
AntiCan↑, Allicin not only protects against tumors but also alleviates the adverse effects of anticancer treatment and enhances the chemotherapeutic response under certain conditions.
ChemoSen↑,
angioG↓, DATS works against tumors by blocking the cell cycle, inhibiting tumor cell proliferation, and inhibiting angiogenesis
chemoP↑,
*GutMicro↑, In addition to against bacteria, allicin has also been shown to modulate the composition of gut microbiota (GM) and increase the diversity of beneficial bacteria in animal models
*antiOx↑, allicin was confirmed to have strong antioxidant properties
other↝, Allicin is a reactive sulfur species (RSS) and a potent thiol-trapping reagent, rapidly reacting with glutathione (GSH) to yield S-allylmercaptoglutathione (GSSA)
GSH↓, Thus, allicin depletes the intracellular GSH pool and reacts with cysteine thiols available in proteins through S-thioallylation
Thiols↓, This reaction is the key to the biological activity of allicin, and the reversible oxidation and reduction of protein-thiols is the core of many processes in cells
*ROS↓, In a hypertrophic heart mouse model, the clearance of intracellular ROS by allicin was measured, and has been shown to reduce the production of ROS and block ROS-dependent ERK1/2, JNK1/2, AKT, NF-κB and Smad signaling, which leads to the inhibition o
*hepatoP↑, Moreover, allicin has been proven to play a hepatoprotective role against acetaminophen (APAP)-induced liver injury by reducing oxidative stress
*Inflam↓, OSCs in garlic has been shown to inhibit the tumor-mediated pro-inflammatory activity by modulating the cytokine pattern in a way that leads to an overall inhibition of NF-κB
*NF-kB↓,
ChemoSideEff↓,
other↝, protection from cancer advancement
*cognitive↑, led to a stabilization of cognitive functions in the study group
*other↝, In patients with mild dementia (ADAScog < 15), the disease progressed extremely slowly (ADAScog: +1.2 points/year, MMSE: -0.6 points/year), in patients with moderate dementia at approximately twice the rate.
*neuroP↑, alpha-lipoic acid might be a successful 'neuroprotective' therapy option for AD
*IronCh↑, a-Lipoic acid chelates redox-active transition metals, thus inhibiting the formation of hydroxyl radicals and also scavenges reactive oxygen species (ROS), thereby increasing the levels of reduced glutathione
*ROS↓,
*GSH↑,
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NA |
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AD, |
NA |
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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 (
*Inflam↓, LA and ALA attenuate neuroinflammation by modulating inflammatory signaling.
*other↝, ratio of LA to ALA in typical Western diets is reportedly 8–10:1 or higher, which is rather higher than the ideal ratio of LA to ALA (1–2:1) required to reach the maximal conversion of ALA to its longer chain PUFAs
*other↝, LA and ALA are essential PUFAs that must be obtained from dietary intake because they cannot be synthesized de novo
*neuroP↑, several studies have also suggested that lower dietary intake of LA influences AA metabolism in brain and subsequently causes progressive neurodegenerative disorders
*BioAv↝, LA cannot be synthesized in the human body
*adiP↑, study suggested that LA-rich oil consumption leads to the high levels of adiponectin in the blood [114], which could stimulate mitochondrial function in the liver and skeletal muscles for energy thermogenesis
*BBB↑, Although LA can penetrate the BBB, most of the LA that enters the brain cannot be changed into AA [48,49], and 59 % of the LA that enters the brain is broken down by fatty acid β-oxidation
*Casp6↓, In neurons, LA and ALA attenuate the activation of cleaved caspase-3/-9, p-NF-Kb and the production of TNF-a, IL-6, IL-1b, and ROS by binding GPR40 and GPR120.
*Casp9↓,
*TNF-α↓,
*IL6↓,
*IL1β↓,
*ROS↓,
*NO↓, LA reduces NO production and inducible nitric oxide synthases (iNOS) protein expression in BV-2 microglia
*iNOS↓,
*COX2↓, ALA increases antioxidant enzyme activities in the brain [182] and inhibits the activation of COX-2 in AD models
*JNK↓, ALA has also been shown to suppress the activation of c-Jun N-terminal kinases (JNKs) and p-NF-kB p65 (Ser536), which is involved in inflammatory signaling
*p‑NF-kB↓,
*Aβ↓, and to inhibit Aβ aggregation and neuronal cell necrosis
*BP↓, LA also improves blood pressure, blood triglyceride and cholesterol levels, and vascular inflammation
*memory↑, One study suggested that long-term intake of ALA enhances memory function by increasing hippocampal neuronal function through activation of cAMP response element-binding protein (CREB) [192], extracellular signal-regulated kinase (ERK), and Akt signa
*cAMP↑,
*ERK↑,
*Akt↑,
cognitive?, Furthermore, ALA administration inhibits Aβ induced neuroinflammation in the cortex and hippocampus and enhances cognitive function
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BC, |
SkBr3 |
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neuroblastoma, |
SK-N-SH |
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Review, |
AD, |
NA |
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PDH↑, ALA is capable of activating pyruvate dehydrogenase in tumor cells.
TumCG↓, ALA also significantly inhibited tumor growth in mouse xenograft model using BCPAP and FTC-133 cells
ROS↑, ALA is able to generate ROS, which promote ALA-dependent cell death in lung cancer [75], breast cancer [76] and colon cancer
AMPK↑,
EGR4↓,
Half-Life↓, Data suggests that ALA has a short half-life and bioavailability (about 30%)
BioAv↝,
*GSH↑, Moreover, it is able to increase the glutathione levels inside the cells, that chelate and excrete a wide variety of toxins, especially toxic metals from the body
*IronCh↑, The existence of thiol groups in ALA is responsible for its metal chelating abilities [14,35].
*ROS↓, ALA exerts a direct impact in oxidative stress reduction
*antiOx↑, ALA is being referred as the universal antioxidant
*neuroP↑, ALA has neuroprotective effects on Aβ-mediated cytotoxicity
*Ach↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*lipid-P↓, ALA has multiple and complex effects in this way, namely scavenging ROS, transition metal ions, increasing the levels of reduced glutathione [59,63], scavenging of lipid peroxidation products
*IL1β↓, ALA downregulated the levels of the inflammatory cytokines IL-1B and IL-6 in SK-N-BE human neuroblastoma cells
*IL6↓,
TumCP↓, ALA inhibited cell proliferation, [18F]-FDG uptake and lactate formation and increased apoptosis in neuroblastoma cell lines Kelly, SK-N-SH, Neuro-2a and in the breast cancer cell line SkBr3.
FDG↓,
Apoptosis↑,
AMPK↑, ALA suppressed thyroid cancer cell proliferation and growth through activation of AMPK and subsequent down-regulation of mTOR-S6 signaling pathway in BCPAP, HTH-83, CAL-62 and FTC-133 cells lines.
mTOR↓,
EGFR↓, ALA inhibited cell proliferation through Grb2-mediated EGFR down-regulation
TumCI↓, ALA inhibited metastatic breast cancer cells migration and invasion, partly through ERK1/2 and AKT signaling
TumCMig↓,
*memory↑, Alzheimer’s Disease: ALA led to a marked improvement in learning and memory retention
*BioAv↑, Since ALA is poorly soluble, lecithin has been used as an amphiphilic matrix to enhance its bioavailability.
*BioAv↝, ALA were found to be considerably higher in adults with mean age greater than 75 years as compared to young adults between the ages of 18 and 45 years.
*other↓, ALA treatment has been recently studied by some clinical trials to explain its efficacy in preventing miscarriage
*other↝, 1800 mg of ALA or placebo were administrated orally every day, except during the period 2 days before to 4 days after administration of each dose of platinum to avoid potential interference with platinum’s antitumor effects
*Half-Life↓, Data shows a short half-life and bioavailability of about 30% of ALA due to mechanisms involving hepatic degradation, reduced ALA solubility as well as instability in the stomach.
*BioAv↑, ALA bioavailability is greatly reduced after food intake and it has been recommended that ALA should be admitted at least 2 h after eating or if taken before; meal should be taken at least 30 min after ALA administration
*ChAT↑, ALA show anti-dementia or anti-AD properties by increasing acetylcholine (ACh) production through activation of choline acetyltransferase, which increases glucose absorption
*GlucoseCon↑,
*other↝, evening primrose (Oenothera biennis) (EPO) :nutrients of interest in this oil are linoleic acid (LA, 70-74%) and γ-linolenic acid (GLA, 8-10%), which are polyunsaturated fatty acids (PUFA) that account for EPO's popularity as a dietary supplement.
*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.
ChemoSen↓, In this review, the use of antioxidant supplements can benefit cancer cells in the same way as they do for normal cells during cancer treatment.
other↝, Therefore, oncologists should advise not to take antioxidant supplements during chemotherapy and/or radiotherapy.
other↝, Note possible bias in this review, as many of the selenium mega reviews he quotes state there is an improvement, but author rejects as "lack consistent findings"?
eff↓, Taking antioxidants in supplement form (again, remember that antioxidants in food are fine) may actually “protect” cancer cells during treatment.
ChemoSen↓, In other words, antioxidants in pill form have the potential to counteract the effects of chemotherapy or radiation therapy.
RadioS↓,
other↝, Common antioxidant supplements taken by patients include vitamins A, C, and E, carotenoids (such as beta-carotene and lycopene) as well as selenium and Coenzyme Q10.
*other↝, In the present study, the anti-diabetic effect of apigenin on pancreatic β-cell insulin secretion, apoptosis, and the mechanism underlying its anti-diabetic effects, were investigated in the INS-ID β-cell line
*Insulin↑, The results showed that apigenin concentration-dependently facilitated 11.1-mM glucose-induced insulin secretion, which peaked at 30 µM
ER Stress↓, Apigenin also concentration-dependently inhibited the expression of endoplasmic reticulum (ER) stress signaling proteins
*CHOP↓, CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP) and cleaved caspase-3
*cl‑Casp3↓,
*ROS↓, In contrast, the cytoprotective effect of apigenin against oxidative stress, inflammation, apoptosis, and oxidative and ER stresses has been demonstrated in various cell types
*Inflam↓,
*TXNIP↓, expression of TXNIP, which was increased by the thapsigargin treatment, was downregulated in INS-1D cells in response to apigenin.
| - |
in-vitro, |
AML, |
K562 |
|
|
|
- |
in-vitro, |
Liver, |
HepG2 |
|
|
|
Glycolysis↓, DHA prevented cell proliferation in K562 cells through inhibiting aerobic glycolysis.
GlucoseCon↓, Lactate product and glucose uptake were inhibited after DHA treatment.
lactateProd↓,
GLUT1↓, DHA modulates glucose uptake through downregulating glucose transporter 1 (GLUT1) in both gene and protein levels.
PKM2↓, DHA treatment, decreased expression of PKM2 was confirmed in situ.
ECAR↓, ECAR parameters including the glycolytic activity and capacity decreased in a concentration-dependent manner in K562 cells following DHA administration
LDHA↓, DHA treatment downregulated the relative expression of GLUT1, PKM2, LDH-A and c-Myc
cMyc↓,
other↝, The relative changes of PDK1, P53, HIF-1α, HK2, and PFK1 expression were modest, with most genes being altered by less than 2-fold
eff↓, Compared to control, ascorbate and H 2 O 2 both caused a significant decrease in cell count both at 24-h (p<0.05 and p<0.0001 for ascorbate and H 2 O 2 , respectively)
other↝, Vitamin C, a common supplement, has been shown to act as both a ROS generator in the presence of iron and copper (15) and as an antioxidant
ROS↑, From our results, we can postulate that ROS generation is causing cell death independently and in combination with DHA
eff↓, Ascorbate can convert ferric iron into ferrous iron (18), the active form that reacts with artemisinin, generating short lived free radicals.
eff↓, If this happens in the stomach of a person who is consuming artemisinin along with ascorbate, ascorbate will convert ferric iron in foods to the ferrous form, which may react with artemisinin locally, making the therapy less effective
Risk↓, The estimated 3-year cumulative incidence of recurrence was 7.7% with aspirin and 14.1% with placebo (hazard ratio, 0.49; 95% confidence interval [CI], 0.24 to 0.98; P = 0.04) among patients with group A alterations and 7.7% and 16.8%
other↝, Aspirin led to a significantly lower incidence of colorectal cancer recurrence than placebo among patients with PIK3CA hotspot mutations in exon 9 or 20 and appeared to have a similar benefit among those with other somatic alterations in PI3K pathway
*cardioP↑, Low dose aspirin reduces the secondary incidence of myocardial infarction and stroke.
*other↝, Pseudoresistance, reflecting delayed and reduced drug absorption, complicates enteric coated but not immediate release aspirin administration.
*COX1↓, irreversible acetylation of Ser530 in the enzyme prostaglandin G/H synthase-1 (commonly termed cyclooxygenase [COX]-1) and the consequent suppression of thromboxane (Tx) A2 (TxA2) formation.
*TXA2↓,
Risk↝, aspirin was associated with an increased risk of incident cancer that had metastasized
Risk↑, These findings suggest that in older persons, aspirin may accelerate the progression of cancer and, thus, suggest caution with its use in this age group.
Risk∅, There was no association of aspirin with the overall incidence of solid tumors (HR = 1.05, 95% CI = 0.95 to 1.15) or with the incidence of cancers that were diagnosed at stages 1, 2, or 3.
Risk↑, By contrast, aspirin was associated with an increase in the incidence of cancers presenting at stage 4 (HR = 1.22, 95% CI = 1.02 to 1.45).
other↝, Prostate, colorectal, breast, melanoma, and lung were the most common incident cancers, accounting for 80% of all solid tumor cancers.
Risk↓, Current use of aspirin vs never use was associated with lower CRC risk (hazard ratio [HR] 0.87, 95% confidence interval
other↝, However, some large cohorts found no association between aspirin use and CRC risk when aspirin was initiated after 70 years of age (9) and when aspirin was used for less than 10 years (10) or 20 years (11).
Dose↝, Use of 160 mg tablets was associated with a greater CRC risk reduction than the use of 75 mg tablets.
Risk↓, We found a 13% lower CRC risk associated with current low-dose aspirin use vs never use,
other↓, In 2020, a large meta-analysis of 15 cohort, 11 nested case-control, and 19 case-control studies reported a 27% reduced CRC risk in regular users of aspirin (7)
other↝, It was argued later that the limited follow-up time of participants without history of aspirin use before the trial enrollment could partly explain the negative results in the ASPREE trial (9,36).
KRAS↓, A mechanism supporting the hypothesis that aspirin has a protective effect against CRC risk is that aspirin blocks the mutated APC (adenomatous polyposis coli) gene, leading to the inhibition of the KRAS pathway and the adenomatous polyp formation (3
other↓, By assuming a protective effect of aspirin against CRC, we estimated that 1,073 cases with CRC were prevented by aspirin use, equating to 2.7% lower CRC incidence.
other↓, In conclusion, our study provided novel and strong evidence that low-dose aspirin use is associated with a lower CRC risk.
*BioAv↝, The oral bioavailability was determined to be 32.4 ± 4.8% based on intravenous (5 mg/kg) and oral (10 mg/kg) administrations of WA in male rats.
*other↝, he in vitro results showed that WA could be easily transported across Caco-2 cells and WA did not show as a substrate for P-glycoprotein.
*Half-Life↓, and in liver microsomes (rapid depletion, with a half-life of 5.6 min). WA was further verified by rat intestine-liver in situ perfusion, revealing that WA rapidly decreased and 27.1% remained within 1 h,
OS↑, Statin use before diagnosis was associated with improved overall survival compared with no treatment (hazard ratio [HR], 0.85; 95% CI, 0.80 to 0.91) and specifically in patients with leukemia, lung, or renal cancers.
eff↑, This study suggests that the combination of statins with drugs that affect isoprenylation, such as bisphosphonates, improves survival in patients with cancer.
other↝, However, patients younger than age 65 years in the comparison of statin users versus nonusers had improved survival, whereas those older than age 65 years did not.
*BioAv↝, Baicalin and wogonoside in Scutellariae-Paeoniae couple extract had shown better absorption than which in pure baicalin and Radix Scutellariae extract
*other↝, The present result suggested that baicalin might convert to wogonoside in the rat body.
| - |
in-vitro, |
Colon, |
HT29 |
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|
|
- |
in-vivo, |
NA, |
NA |
|
|
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TumCG↓, BBR reduced the growth of colon cancer cells to a certain extent in vitro and in vivo,
GutMicro↑, BBR significantly mediated the abundance, composition and metabolic functions of the intestinal microbial flora in mice with colon cancer
other↝, The effect of BBR on inflammatory cytokines, including IL-6, FGF, and PDGF, was not obvious
IL10↓, BBR significantly downregulated IL-10 levels (P < 0.05) and reduced c-Myc, DNMT1, and DNMT3B
cMyc↓,
DNMT1↓,
DNMTs↓,
*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.
ACLY↓, the well-known Bempedoic acid (BA, Fig. 2), a prodrug of ACLY inhibitor developed by Esperion company
other↝, Overexpression of ACLY is related to poor survival in various types of breast cancer cells, such as MDA-MB-231, T47D and MCF-7 cells [32], [33].
CSCs↓, the knockdown of ACLY significantly suppressed the cell stemness [53].
ACLY↓, Bempedoic acid competitively inhibits ACLY activity and allosterically activates AMP-activated protein kinase-β1 (AMPKβ1)-
AMPK↑,
eff↑, unlike bempedoic acid30, EVT0185-CoA inhibited rather than activated AMPKβ1-containing complexes (Extended Data Fig. 5d), and also inhibited ACC1, ACC2 and ACSS2
other↝, Given the role of AMPK in pro-survival signalling38 and the compensatory upregulation of ACSS2 upon ACLY inhibition8,9,12, these findings highlight key mechanistic differences between EVT0185 and bempedoic acid
eff↝, EVT0185 reduced tumour burden, whereas bempedoic acid had limited efficacy
*cognitive↑, vitamin A supplementation has been to be effective in lowering cognitive decline and AD pathology
*cognitive↑, Studies that involved B12 supplementation have shown beneficial effects on cognition and inflammatory status.
*Inflam↓,
*homoC↓, decreased serum homocysteine and TNF-α
*TNF-α↓,
*other↝, treatment with a high dose of B vitamins consisting of folic acid, B12, and B6 for 24 months was able to slow down the shrinkage of the whole brain volum
*memory↑, In line with the improved cognitive function, NAD+ treatment significantly alleviated neuroinflammation, impaired synaptic plasticity, DNA damage, and hippocampal neuronal loss in these mice.
Showing Research Papers: 1 to 50 of 190
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 190
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GSH↓, 2, lipid-P↑, 2, NRF2↑, 2, Prx↑, 1, ROS↓, 1, ROS↑, 8, mt-ROS↑, 1, Thiols↓, 1, TrxR↓, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, ETC↓, 1, MMP↓, 1, mtDam↑, 1,
Core Metabolism/Glycolysis ⓘ
ACLY↓, 2, AMPK↑, 4, cMyc↓, 2, ECAR↓, 1, FDG↓, 1, GlucoseCon↓, 1, Glycolysis↓, 3, HK2↓, 1, lactateProd↓, 1, LDHA↓, 1, NADPH↓, 1, PDH↑, 2, PKM2↓, 1, PPP↓, 1,
Cell Death ⓘ
Akt↓, 2, Apoptosis↑, 4, Bax:Bcl2↑, 1, Cyt‑c↑, 1, p27↑, 1,
Transcription & Epigenetics ⓘ
other↓, 3, other↑, 1, other↝, 33, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
ER Stress↓, 1, ER Stress↑, 1, UPR↑, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 3, DNMT1↓, 1, DNMTs↓, 1, P53↝, 1, γH2AX↑, 1,
Cell Cycle & Senescence ⓘ
TumCCA↑, 3,
Proliferation, Differentiation & Cell State ⓘ
CSCs↓, 1, mTOR↓, 1, PI3K↓, 1, TumCG↓, 3,
Migration ⓘ
Ca+2↑, 1, KRAS↓, 1, MMPs↓, 1, TumCI↓, 2, TumCMig↓, 2, TumCP↓, 2, TumMeta↓, 2, Vim↓, 1, Vim↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EGFR↓, 2, EGR4↓, 1, EPR↑, 1, HIF-1↓, 1, Hif1a↓, 1,
Barriers & Transport ⓘ
GLUT1↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL10↓, 1, IL1α↓, 1, IL6↑, 1, IL8↑, 1, Imm↑, 1, NF-kB↓, 1, NK cell⇅, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, BioAv↝, 3, ChemoSen↓, 2, ChemoSen↑, 1, Dose↓, 2, Dose↝, 5, eff↓, 7, eff↑, 10, eff↝, 2, Half-Life↓, 2, Half-Life↑, 1, RadioS↓, 1, RadioS↑, 2, selectivity↑, 4,
Clinical Biomarkers ⓘ
EGFR↓, 2, GutMicro↑, 1, IL6↑, 1, KRAS↓, 1, NOS2↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 3, chemoP↑, 2, ChemoSideEff↓, 1, cognitive?, 1, OS↑, 2, Remission↑, 1, Risk↓, 3, Risk↑, 2, Risk↝, 1, Risk∅, 1, toxicity↓, 1, toxicity↝, 1,
Total Targets: 105
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 3, GSH↑, 2, lipid-P↓, 1, ROS↓, 6,
Metal & Cofactor Biology ⓘ
IronCh↑, 3,
Mitochondria & Bioenergetics ⓘ
Insulin↑, 1,
Core Metabolism/Glycolysis ⓘ
adiP↑, 1, cAMP↑, 1, glucose↓, 1, GlucoseCon↑, 1, homoC↓, 1,
Cell Death ⓘ
Akt↑, 1, cl‑Casp3↓, 1, Casp6↓, 1, Casp9↓, 1, iNOS↓, 1, JNK↓, 1, JNK↑, 1,
Transcription & Epigenetics ⓘ
Ach↑, 2, other↓, 1, other↑, 2, other⇅, 1, other↝, 26,
Protein Folding & ER Stress ⓘ
CHOP↓, 1, CHOP↑, 1, cl‑eIF2α↑, 1, GRP78/BiP↑, 1, p‑PERK↑, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↑, 1,
Migration ⓘ
MMP9↓, 1, TGF-β↑, 1, TXNIP↓, 1,
Angiogenesis & Vasculature ⓘ
NO↓, 1, TXA2↓, 1, VEGF↓, 1,
Barriers & Transport ⓘ
BBB↑, 2, P-gp↓, 1,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, COX2↓, 1, IL1↓, 1, IL1β↓, 2, IL6↓, 3, Inflam↓, 7, NF-kB↓, 1, p‑NF-kB↓, 1, TNF-α↓, 2,
Synaptic & Neurotransmission ⓘ
5HT↑, 1, ChAT↑, 1,
Protein Aggregation ⓘ
Aβ↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, BioAv↑, 2, BioAv↝, 7, Dose↑, 1, Dose↝, 1, eff↑, 8, eff↝, 1, Half-Life↓, 3, Half-Life↑, 1, Half-Life↝, 1,
Clinical Biomarkers ⓘ
BP↓, 1, GutMicro↑, 2, IL6↓, 3,
Functional Outcomes ⓘ
AntiAge↑, 1, AntiDiabetic↑, 1, Bone Healing↑, 1, cardioP↓, 1, cardioP↑, 1, cognitive↓, 1, cognitive↑, 6, cognitive↝, 1, hepatoP↑, 1, memory↑, 6, motorD↑, 1, neuroP↓, 1, neuroP↑, 5, Risk↑, 1, Sleep↑, 1, toxicity↓, 4, toxicity↝, 1, Wound Healing↑, 1,
Infection & Microbiome ⓘ
AntiFungal↑, 1, AntiViral↑, 2, Bacteria↓, 2,
Total Targets: 83
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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