BG Cancer Research Results
BG, Blood Glucose: Click to Expand ⟱
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Blood Glucose
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Scientific Papers found: Click to Expand⟱
*antiOx↑, α-LA has been widely used as an antioxidant compound in many multivitamin formulations, food supplements, anti-aging formulas, and even in human and pet food recipes
*IronCh↑, potential role in the chelation of metals and in restoring normal levels
of intracellular glutathione (GSH) after depletion caused by toxicants,
*GSH↑,
*BBB↑, ALA, which can pass through the blood-brain barrier (BBB
Apoptosis↑, increased level of apoptosis, mitochondrial membrane depolarization, ROS production, lipid peroxidation, poly-(ADP)-ribose polymerase 1 (PARP1), caspase 3 and 9 expression levels in simultaneous ALA (0.05 mM) and cisplatin(0.025 mM)-treated MCF7
MMP↓,
ROS↑,
lipid-P↑,
PARP1↑,
Casp3↑,
Casp9↑,
*NRF2↑, ALA's ability to activate Nfr2 in GSH production
*GSH↑,
*ROS↓, administration of ALA has been shown to reduce oxidative stress
RenoP↑, ALA also reduced lipid peroxidation in the kidneys caused by the anticancer drug cisplatin,
ChemoSen↑, ALA enhances the functions of various anticancer drugs such as 5-fluorouracil in CRC [146] and cisplatin in MCF-7 cells
*BG↓, ALA was shown to lower the blood glucose levels in patients with type 2 diabetes
toxicity↓, Some sedation, ptosis and ataxia were observed in Sprague-Dawley rats 15–20 minutes of administering a herbal concoction that contained WS at a large dose of 1–2 g/kg body weight [36]
TumW↓, Induction of apoptosis by WA has been noted in some in vivo models where treatment with 4 mg/kg WA, i.p. 5 times for 2 weeks markedly reduced MDA-MB-231 tumor weights in nude mice as well as increased apoptosis compared to tumors in control mice [56
Dose?, 20 mg/kg, oral 3X/wk for 14 wk Hamster Head and Neck Example
eff↝, showed that this chemopreventive capacity was dependent on a circadian pattern where hamsters dosed with WA at 8 AM and 12 PM showed 100% protection from oral tumor formation while those treated at 12 AM showed 50% incidence in oral tumors
Ki-67↓, WA treatment resulted in retarded tumor growth; reduction in cell proliferation marker Ki-67, survivin, and XIAP,
survivin↓,
XIAP↓,
PERK↑, higher protein expression of pERK, pRSK, CHOP and DR-5 was also observed in the WA-treated group compared to control.
p‑RSK↑,
CHOP↑,
DR5↑,
Dose↝, Clinically diagnosed schizophrenia patients who had received antipsychotic medications for 6 months or more received either a capsule with 400 mg of WS extract (n=15), three times daily, for 1 month [80]
BG↓, Results after one month showed significant reduction in serum triglycerides and fasting blood glucose levels in the WS extract- treated group compared to the placebo
DNMTs↓, in MCF7 and MDA-MB-231 breast cancer cells WA treatment suppressed transcription of DNMT.
*hepatoP↑, berberine (Lip-BBR) to aid in ameliorating hepatic damage and steatosis, insulin homeostasis, and regulating lipid metabolism in type 2 diabetes (T2DM)
*LC3II↑, Lip-BBR treatment promoted autophagy via the activation of LC3-II and Bclin-1 proteins and activated the AMPK/mTOR pathway in the liver tissue of T2DM rats.
*Beclin-1↑,
*AMPK↑,
*mTOR↑,
*ER Stress↓, It decreased the endoplasmic reticulum stress by limiting the CHOP, JNK expression, oxidative stress, and inflammation.
*CHOP↓,
*JNK↓,
*ROS↓,
*Inflam↓,
*BG↓, Oral supplementation of diabetic rats either by Lip-BBR or Vild, 10 mg/kg of each, significantly (p < 0.001) lowered the blood glucose levels of tested diabetic rats compared to the diabetic group.
*SOD↑, when the diabetic rats received Lip-BBR, the decrements were less pronounced compared to the diabetic group by 1.16 fold, 2.52 fold, and 67.57% for SOD, GPX, and CAT, respectively.
*GPx↑,
*Catalase↑,
*IL10↑, Treatment of the diabetic rats with Lip-BBR significantly (p < 0.001) elevated serum IL-10 levels by 37.01% compared with diabetic rats.
*IL6↓, Oral supplementation of Lip-BBR could markedly (p < 0.0001) reduce the elevated serum levels of IL-6 and TNF-α when it is used as a single treatment by 55.83% and 49.54%,
*TNF-α↓,
*ALAT↓, ALT, AST, and ALP in the diabetic group were significantly higher (p < 0.0001) by 88.95%, 81.64%, and 1.8 fold, respectively, compared with those in the control group, but this was reversed by the treatment with Lip-BBR
*AST↓,
*ALP↓,
BG↓, Dichloroacetate (DCA), which is known to increase the rate of pyruvate oxidation, has been shown to lower plasma glucose concentrations in normal fasting subjects
glucoNG↓, These results suggest that DCA may decrease gluconeogenesis by limiting the availability of the precursor substrates lactate and alanine.
eff↑, recommend combining prolonged periodic fasting with a standard conventional therapeutic approach to promote cancer‐free survival, treatment efficacy, and reduce side effects in cancer patients.
ChemoSideEff↓, lowered levels of IGF1 and insulin have the potential to protect healthy cells from side effects
ChemoSen↑,
Insulin↓, causes insulin levels to drop and glucagon levels to rise
HDAC↓, Histone deacetylases are inhibited by ketone bodies, which may slow tumor development.
IGF-1↓, FGF21 rises during intermittent fasting, and it plays a vital role in lowering IGF1 levels by inhibiting phosphorylated STAT5 in the liver
STAT5↓,
BG↓, Fasting suppresses glucose, IGF1, insulin, the MAPK pathway, and heme oxygenase 1
MAPK↓,
HO-1↓,
ATG3↑, while increasing many autophagy‐regulating components (Atgs, LC3, Beclin1, p62, Sirt1, and LAMP2).
Beclin-1↑,
p62↑,
SIRT1↑,
LAMP2↑,
OXPHOS↑, Fasting causes cancer cells to release oxidative phosphorylation (OXPHOS) through aerobic glycolysis
ROS↑, which leads to an increase in reactive oxygen species (ROS), p53 activation, DNA damage, and cell death in response to chemotherapy.
P53↑,
DNAdam↑,
TumCD↑,
ATP↑, and causes extracellular ATP accumulation, which inhibits Treg cells and the M2 phenotype while activating CD8+ cytotoxic T cells.
Treg lymp↓,
M2 MC↓,
CD8+↑,
Glycolysis↓, By lowering glucose intake and boosting fatty acid oxidation, fasting can induce a transition from aerobic glycolysis to mitochondrial oxidative phosphorylation in cancerous cells, resulting in increased ROS
GutMicro↑, Fasting has been shown to have a direct impact on the gut microbial community's constitution, function, and interaction with the host, which is the complex and diverse microbial population that lives in the intestine
GutMicro↑, Fasting also reduces the number of potentially harmful Proteobacteria while boosting the levels of Akkermansia muciniphila.
Warburg↓, Fasting generates an anti‐Warburg effect in colon cancer models, which increases oxygen demand but decreases ATP production, indicating an increase in mitochondrial uncoupling.
Dose↝, Those patients fasted for 36 h before treatment and 24 h thereafter, having a total of 350 calories per day. Within 8 days of chemotherapy, no substantial weight loss was recorded, although there was an improvement in quality of life and weariness.
TumCG↓, Accumulating evidence suggests that FMDs attenuate tumor growth by altering the energy metabolism of cancer cells
toxicity∅, FMD reduces risk factors and markers for aging, cardiovascular disease, diabetes, and cancer without serious adverse effects in healthy adults.
BG↓, dramatic downregulation of blood glucose
IGF-1↓, prolonged fasting downregulated IGF-1
mTOR↓, inhibits cellular mTOR activity.
M2 MC↓, In addition, alternate-day fasting inhibited colorectal cancer growth by suppressing adenosine-induced M2 macrophage polarization in the tumor microenvironment
eff↑, large prospective cohort study of breast cancer patients, a longer nightly fasting duration was associated with a decreased risk of breast cancer recurrence, so the FMD may also be beneficial after the eradication of the initial tumo
ChemoSen↑, Combining fasting cycles with chemotherapeutic agents markedly prevented the progression of subcutaneous breast cancer, melanoma, and glioma in mouse models
QoL↑, Fasting for 60 hours seemed to improve the patients' fatigue and quality of life during chemotherapy
RadioS↑, In response to stress, cancer cells engage antioxidant and DNA repair mechanisms in an energy-demanding manner, facilitating cancer cell survival. Thus, restriction of the energy supply would improve the antitumor activity of radiotherapy.
selectivity↑, Recently, short-term starvation was shown to increase the DNA damage induced by a single exposure to high-dose radiation in metastatic cancer cell lines, whereas healthy cells were not affected by starvation medium
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in-vitro, |
GBM, |
LN229 |
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in-vitro, |
neuroblastoma, |
SH-SY5Y |
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selectivity↑, Short-term starved S. cerevisiae or cells lacking proto-oncogene homologs were up to 1,000 times better protected against oxidative stress or chemotherapy drugs than cells expressing the oncogene homolog Ras2
selectivity↑, Finally, short-term starvation provided complete protection to mice but not to injected neuroblastoma cells against a high dose of the chemotherapy drug/pro-oxidant etoposide
ROS↑, promote oxidative stress and DNA damage
DNAdam↑,
BG↓, blood glucose level for both mice and humans is ≈1.0 g/liter but can reach 0.5 g/liter after starvation.
ChemoSideEff↓, Ten volunteers with different types of cancers were starved for 48–140 hours before chemotherapy and five–56 hours after. Overall, all patients showed decreased side effects of chemotherapy.
*toxicity↓, A case report showed that short-term starvation of up to five days followed by chemotherapy is not only safe and feasible, but also helps to ameliorate chemotherapy related side-effects.3
mTOR↓, reduction in mTOR activity
IGF-1↓, Studies reveal that starvation reduces levels of IGF-1 significantly. Short-term starvation of 72 hours reduces circulating IGF-1 by 70%
IGFBP1↑, and increases the level of IGF binding protein (IGFBP-1) an IGF-1 inhibitor, by 11-fold
BG↓, glucose levels were reduced by 41%
ROS↑, Increased metabolic rate as a result of DR causes increased ROS production
*toxicity∅, Data suggest overall good compliance, no malnutrition, minimal side effects. No significant changes were identified to suggest increased harm.
QoL∅, unchanged quality of life (QOL),
eff↑, improved endocrine parameters
eff↝, mixed results for cancer outcomes
ChemoSideEff↓, decreasing chemotherapy-related side effects
TumCG↓, limiting tumor growth
Dose↑, When fasting is used as an adjunct to chemotherapy, a minimum fasting period of at least 48 hours is currently recommended for nutritional interventions in order to achieve a measurable metabolic response at the cellular level
toxicity↝, The increased risk for poor outcomes associated with malnutrition, weight loss, and cachexia poses an obvious safety concern for patients with cancer who participate in calorie-restricted fasting
eff↑, short-term fasting involving water-only or limited daily calorie consumption for less than a week has the potential to achieve positive metabolic changes while avoiding malnutrition and significant weight loss
IGF-1↑, statistically significant decrease in IGF-1 among participants compliant with fasting compared with regular diet during the middle of therapy
*OXPHOS↑, Healthy cells also use mitochondrial oxidative phosphorylation for metabolism while cancer cells use aerobic glycolysis, also known as the Warburg effect
BG↓, statistically significant decrease in glucose among participants compliant with fasting compared with controls
Insulin↓, statistically significant decrease in insulin among participants compliant with fasting compared with regular diet before the first cycle of chemotherapy (p = .001), as well as during the middle of therapy
RadioS↑, A complete or partial radiographic response was also noted more often among fasting participants compared with normal diet participants
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in-vitro, |
BC, |
SUM159 |
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in-vitro, |
BC, |
4T1 |
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PI3K↑, FMD activates PI3K-AKT, mTOR, and CDK4/6 as survival/growth pathways, which can be targeted by drugs to promote tumor regression.
Akt↑,
mTOR↑,
CDK4↑,
CDK6↑,
hyperG↓, FMD cycles also prevent hyperglycemia and other toxicities caused by these drugs.
TumCG↓, cycles of FMD significantly slowed down tumor growth, reduced tumor size, and caused an increased expression of intratumor Caspase3
TumVol↓,
Casp3↑,
BG↓, confirming our hypothesis that lowering intracellular glucose levels (through reduced extracellular levels or reduced uptake) reduces CSC survival
eff↑, 2DG potentiated the effect of FMD both in terms of delaying tumor progression and in decreasing the number of mammospheres derived by tumor masses,
eff∅, metformin did not show any additive or synergistic antitumor effect when combined with the FMD, thus suggesting that FMD and metformin have redundant effects on blood glucose levels
PKA↓, We have previously shown that prolonged fasting reduces the activity of protein kinase A (PKA) in different types of normal cells
KLF5↓, PKA inhibition resulted in the downregulation of KLF5, a potential therapeutic target for TNBC
p‑GSK‐3β↑, (GSK3β) phosphorylation
Nanog↓, stemness-associated genes NANOG and OCT4, and KLF2 and TBX3,
OCT4↓,
KLF2↓,
eff↑, Combining FMD cycles with PI3K/AKT/mTOR inhibitors results in long-term animal survival and reduces treatment-induced side effects
ROS↑, FMD resulted in an increased expression of pro-apoptotic molecules, such as BIM, and ASK1, a critical cellular stress sensor frequently activated by ROS, whose production was previously shown to be increased by the FMD
BIM↑,
ASK1↑,
PI3K↑, FMD cycles upregulate PI3K-AKT and mTOR pathways and downregulate CCNB-CDK1 while upregulating CCND-CDK4/6 signaling axes
Akt↑,
mTOR↑,
CDK1↓,
CDK4↑,
CDK6↑,
eff↑, combining STS with pictilisib, ipatasertib, and rapamycin, selective inhibitors for PI3K, AKT, and mTOR, respectively, resulted in enhanced cancer cell death and reduction of mammosphere numbers in SUM159 cells
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in-vitro, |
Colon, |
CT26 |
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in-vivo, |
NA, |
NA |
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selectivity↑, Short-term-starvation (STS) was shown to protect normal cells and organs but to sensitize different cancer cell types to chemotherapy
ChemoSen↑, STS potentiated the effects of OXP on the suppression of colon carcinoma growth and glucose uptake in both in vitro and in vivo models.
BG↓, glucose and amino acid deficiency conditions imposed by STS promote an anti-Warburg effect
AminoA↓,
Warburg↓,
OCR↑, characterized by increased oxygen consumption but failure to generate ATP, resulting in oxidative damage and apoptosis.
ATP↓,
ROS↑, a significant increase in O2consumption rate (OCR), indicative of an increased oxidative metabolism, was observed
Apoptosis↑,
GlucoseCon↓, STS was as effective as oxaliplatin (OXP) in reducing the average tumor glucose consumption
PI3K↓, STS and in particular STS+OXP down-regulated the expression of PI3K
PTEN↑, and up-regulated PTEN expression
GLUT1↓, STS induced a profound reduction in GLUT1 , GLUT2 , HKII , PFK1, PK
GLUT2↓,
HK2↓,
PFK1↓,
PKA↓,
ATP:AMP↓, Accordingly, the ATP/AMP ratio, a good indicator of cellular energy charge, was dramatically reduced by the two STS settings
Glycolysis↓, results strongly support the effect of STS on reducing glycolysis and lactate production and increasing respiration at Complexes I-IV resulting in superoxide production/oxidative stress but in reduced ATP generation.
lactateProd↓,
BG↓, In 101 patients, the FMD was safe, feasible, and resulted in a consistent decrease of blood glucose and growth factor concentration
AntiCan↑, mediate fasting/FMD anticancer effects in preclinical experiments
IFN-γ↑, enrichment of IFNγ
eff↑, Cyclic FMD Is Safe in Combination with Standard Anticancer Treatments
Dose↝, five-day FMD followed by 16 to 23 days of refeeding
CD14↓, end of five-day FMD, we found a significant decrease of total monocytes (CD14+)
IGF-1↓, Preclinical evidence in tumor-bearing mice suggests that fasting/FMD-induced reduction of blood glucose and insulin/IGF1 concentration
IGFR↓, induced reduction of serum IGF1 levels is associated with the downregulation of total and activated IGF1R at the tumor level
CD8+↑, where five-day fasting/FMD in patients with breast cancer increased total and activated intratumor CD8+ T cells, aDCs, NK cells, and Tem cells,
NK cell↑,
BG↓, KD alone significantly decreased blood glucose, slowed tumor growth, and increased mean survival time by 56.7% in mice with systemic metastatic cancer.
TumCG↓,
OS↑,
eff↑, While HBO2T alone did not influence cancer progression, combining the KD with HBO2T elicited a significant decrease in blood glucose, tumor growth rate, and 77.9% increase in mean survival time compared to controls.
Dose∅, Mice undergoing HBO2T received 100% O2 for 90 minutes at 1.5 ATM gauge (2.5 ATM absolute) three times per week (M, W, F) in a hyperbaric chamber (Model 1300B, Sechrist Industries, Anaheim, CA).
KeyT↑, only the KD+HBO2T animals showed significantly increased ketones compared to controls
eff↑, we hypothesized that combining these non-toxic treatments would provide a powerful, synergistic anti-cancer effect.
cachexia↓, While low carbohydrate or ketogenic diets promote weight loss in overweight individuals, they are also known to spare muscle wasting during conditions of energy restriction and starvation
ChemoSen↑, KD improves quality of life and enhances the efficacy of chemotherapy treatment in the clinic
*ROS↓, ketone body metabolism protects cells from oxidative damage by decreasing ROS production. cancer cells are unable to effectively metabolize ketone bodies; we do not expect that ketones would confer the same protective effects onto the cancer cells
ROS↑, HBO2T increases ROS production within the cell which can lead to membrane lipid peroxidation and cell death
lipid-P↑,
selectivity↑, KD weakens cancer cells by glucose restriction and the inherent anti-cancer effects of ketone bodies while simultaneously conferring a protective advantage to the healthy tissue capable of ketone metabolism.
toxicity∅, HBO2T should be considered a safe treatment for patients with varying malignancies and that there is no convincing evidence its use promotes cancer progression or recurrence
*GutMicro↓, pecific taxa changes due to the diet were observed at the 1 or 18‐week time points, including Ileibacterium, Odoribacter, Lachnoclostridium, Marinifilaceae, and Lactobacillaceae.
*OS↑, MR diet feeding was also found to boost healthspan and lifespan in progeroid mice
Weight↓, This reduction in body weight coincided with reductions in BMD and percent fat mass, and an increase in percent lean mass
BG↓, MR mice had significantly reduced blood glucose levels at all time points except at 5 and 15 min indicating an increase in insulin sensitivity
*BG↓, Fisetin treatment showed a significant decline in the levels of blood glucose, glycosylated hemoglobin (HbA1c), NF-kB p65 unit (in pancreas) and IL-1β (plasma), serum nitric oxide (NO) with an elevation in plasma insulin
*NF-kB↓,
*IL1β↓,
*NO↓,
*Insulin↑,
*SOD↑, Furthermore, the levels of activities of
enzymatic antioxidants such as SOD, CAT, GPx, and GST
were significantly improved in fisetin treated diabetic rats.
*Catalase↑,
*GPx↑,
*GSTs↑,
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Review, |
Nor, |
NA |
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AD, |
NA |
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NA, |
Diabetic, |
NA |
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NA, |
Stroke, |
NA |
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NA, |
LiverDam, |
NA |
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NA, |
Park, |
NA |
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*mtDam↓, The mitochondrial decay, which is responsible for aging, can be reversed by the increased levels of nicotinamide adenine dinucleotide (NAD+) in the body.
*BioAv↝, NMN is a precursor of NAD+ that acts as an intermediate in NAD+ biosynthesis, while dietary supplements of NMN are found to increase the NAD+ levels in the body
*BioAv↑, molecular weight is 334.22 g/mol. It is fairly acidic and water-soluble compound. The solubility has been reported to be 1.8 mg/mL
*OS↑, plays a vital role in a variety of biological processes of the body including cell death, aging, gene expression, neuroinflammation and DNA repair, which indicating a significance role of NAD+ in longevity and health of human life
*eff↑, NMN has therapeutic effects towards a range of diseases, including age-induced type 2 diabetes, obesity, cerebral and cardiac ischemia, heart failure and cardiomyopathies
*eff↑, Alzheimer’s disease and other neurodegenerative disorders, corneal injury, macular degeneration and retinal degeneration, acute kidney injury and alcoholic liver disease
*cognitive↑, cognitive impairments, DNA damage and sirtulin gene inactivation, are brought about by aging which can be evaded by enhancing NAD+ count in the body
*DNAdam↓,
*SIRT1↑, NMN, the NAMPT reaction product, is able to be utilised to trigger the SIRT1 activity
*cardioP↑, NMN also can restore gene expression linked to circadian rhythm, inflammatory response and oxidative stress, and improve hepatic insulin sensitivity, partially by SIRT1 activation.
*ROS↓, NMN has been proven to reduce DNA damage and accumulation of ROS
*Dose↝, NMN in available commercial products vary from 50 to 150 mg/capsule, whereas some consumers take two 150 mg capsules per day
*BioAv↑, NMN was speedily absorbed in the small intestine by a specific transporter, which was encoded by the Slc12a8 gene as demonstrated in in vitro and in vivo studies
*hepatoP↑, NMN supplementation has been found to have significant recovering effects on hepatocyte functions and liver pathologies in early-stage of ethanol toxicity, instead of causing adverse effects to the liver
*eff↑, supplementation of NMN has been found to be a promising therapeutic remedy for PD
*BG↓, Oral administration of NMN increased serum bilirubin contents and decreased blood glucose, chloride and serum creatinine levels, but within the normal range.
*creat↓,
*Inflam↓,
*AntiCan↑,
*antiOx↑,
*hyperG↓, flavanone glycoside found in propolis, has been reported to have insulin-like and lipid-reducing properties that reduce both insulin resistance and hyperglycemia
*BG↓, These flavonoids, including apigenin, naringin, chrysin, galangin, kaempferol, luteolin, genistein, and quercetin help to reduce blood glucose concentration
*HbA1c↓, propolis showed significant effects, reducing the blood glucose levels, serum insulin, and serum glycosylated haemoglobin (HbA1c) levels of T2DM patients
*NF-kB↓, propolis can also suppress inflammatory cascades by blocking the NF-κB pathway and reducing ROS by enhancing antioxidants
*ROS↓,
*TGF-β↑, formation of the transforming growth factor-β1 (TGF-β1) of the cells are promoted by the caffeic acid, CAPE, hesperidin, and quercetin of propolis
*selectivity↑, CAPE is a very significant compound of propolis that has anti-inflammatory properties and also acts as the selective inhibitor of NF-κB activation
pH↑, found that interstitial fluid pH in ascites, liver, and skeletal muscle was higher in rats fed propolis diet than rats fed normal diet.
BP↓, Propolis significantly reduced systolic arterial pressures in both 0.1% and 0.5%-propolis contained diet groups compared with normal diet (p < 0.05)
BG↓, decreased levels of blood glucose and plasma insulin
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in-vivo, |
Nor, |
NA |
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in-vitro, |
NA, |
NA |
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*BG↓, Two doses of quercetin increased rat body weight and testicular weight, decreased blood glucose, and inhibited oxidative stress.
*ROS↓,
*SOD↑, Both doses of quercetin reduced reactive oxygen species and malondialdehyde levels, and increased superoxide dismutase level in HG-treated cells.
*MDA↓,
*ER Stress↓, quercetin inhibits endoplasmic reticulum stress
*iNOS↓, Quercetin could eliminate the upregulation of iNOS, ET-1, and AR mRNA levels in HG-treated cells
*CHOP↓, HG treatment increased CHOP and Grp78 mRNA and protein levels in HG-treated cells, and two doses (5 or 10 μM) of quercetin all decreased these levels
*GRP78/BiP↓,
*antiOx↓, Quercetin is a natural polyphenol compound with anti-inflammatory [37], anti-oxidant [38], and blood sugar lowering properties
*Inflam↓,
*JAK2↑, Our results in vitro showed that quercetin treatment upregulated the phosphorylation levels of JAK2 and STAT3 in HG treated cells. (activating of the JAK2/STAT3 pathway could inhibit ER stress)
*STAT3?,
TumCP↓, including in tumor cell proliferation, apoptosis, metastasis, and inflammation
Apoptosis↑,
TumMeta↓,
Inflam↓,
*antiOx↑, RA is therefore considered to be the strongest antioxidant of all hydroxycinnamic acid derivatives
*AntiAge↑, , it also exerts powerful antimicrobial, anti-inflammatory, antioxidant and even antidepressant, anti-aging effects
*ROS↓, RA and its metabolites can directly neutralize reactive oxygen species (ROS) [10] and thereby reduce the formation of oxidative damage products.
BioAv↑, RA is water-soluble, and according to literature data, the efficacy of secretion of this compound in infusions is about 90%
Dose↝, Accordingly, it is possible to consume approximately 110 mg RA daily, i.e., approximately 1.6 mg/kg for adult men weighing 70 kg.
NRF2↑, liver cancer cell line, HepG2, transfected with plasmid containing ARE-luciferin gene, RA predominantly enhances ARE-luciferin activity and promotes nuclear factor E2-related factor-2 (Nrf2) translocation from cytoplasm to the nucleus
P-gp↑, and also increases MRP2 and P-gp efflux activity along with intercellular ATP level
ATP↑,
MMPs↓, RA concurrently induced necrosis and apoptosis and stimulated MMP dysfunction activated PARP-cleavage and caspase-independent apoptosis.
cl‑PARP↓,
Hif1a↓, inhibits transcription factor hypoxia-inducible factor-1α (HIF-1α) expression
GlucoseCon↓, it also suppressed glucose consumption and lactate production in colorectal cells
lactateProd↓,
Warburg↓, may suppress the Warburg effects through an inflammatory pathway involving activator of transcription-3 (STAT3) and signal transducer of interleukin (IL)-6
TNF-α↓, RA supplementation also reduced tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2) and IL-6 levels, and modulated p65 expression [
COX2↓,
IL6↓,
HDAC2↓, RA induced the cell cycle arrest and apoptosis in prostate cancer cell lines (PCa, PC-3, and DU145) [31]. These effects were mediated through modulation of histone deacetylases expression (HDACs), specifically HDAC2;
GSH↑, RA can also inhibit adhesion, invasion, and migration of Ls 174-T human colon carcinoma cells through enhancing GSH levels and decreasing ROS levels
ROS↓,
ChemoSen↑, RA also enhances chemosensitivity of human resistant gastric carcinoma SGC7901 cells
*BG↓, RA significantly increased insulin index sensitivity and reduced blood glucose, advanced glycation end-products, HbA1c, IL-1β, TNFα, IL-6, p-JNK, P38 mitogen-activated protein kinase (MAPK), and NF-κB levels
*IL1β↓,
*TNF-α↓,
*IL6↓,
*p‑JNK↓,
*p38↓,
*Catalase↑, The reduced activities of CAT, SOD, glutathione S-transferases (GST), and glutathione peroxidase (GPx) and the reduced levels of vitamins C and E, ceruloplasmin, and GSH in plasma of diabetic rats were also significantly recovered by RA application
*SOD↑,
*GSTs↑,
*VitC↑,
*VitE↑,
*GSH↑,
*GutMicro↑, protective effects of RA (30 mg/kg) against hypoglycemia, hyperlipidemia, oxidative stress, and an imbalanced gut microbiota architecture was studied in diabetic rats.
*cardioP↑, Cardioprotective Activity: RA also reduced fasting serum levels of vascular cell adhesion molecule 1 (VCAM-1), inter-cellular adhesion molecule 1 (ICAM-1), plasminogen-activator-inhibitor-1 (PAI-1), and increased GPX and SOD levels
*ROS↓, Finally, in H9c2 cardiac muscle cells, RA inhibited apoptosis by decreasing intracellular ROS generation and recovering mitochondria membrane potential
*MMP↓,
*lipid-P↓, At once, RA suppresses lipid peroxidation (LPO) and ROS generation, whereas in HSC-T6 cells it increases cellular GSH.
*NRF2↑, Additionally, it significantly increases Nrf2 translocation
*hepatoP↑, Hepatoprotective Activity
*neuroP↑, Nephroprotective Activity
*P450↑, RA also reduced CP-produced oxidative stress and amplified cytochrome P450 2E1 (CYP2E1), HO-1, and renal-4-hydroxynonenal expression.
*HO-1↑,
*AntiAge↑, Anti-Aging Activity
*motorD↓, A significantly delays motor neuron dysfunction in paw grip endurance tests,
*glucose↓, Vitamin C supplementation resulted in significant decreases in blood glucose 16, BP 17, TG and LDL-C 1
*BG↓,
*antiOx↑, vitamin C is a powerful antioxidant because it acts as a reducing agent preventing other compounds from being oxidised.
*ROS↓,
Showing Research Papers: 1 to 21 of 21
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 21
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GSH↑, 1, HO-1↓, 1, hyperG↓, 1, lipid-P↑, 2, NRF2↑, 1, OXPHOS↑, 1, ROS↓, 1, ROS↑, 7,
Metal & Cofactor Biology ⓘ
KLF5↓, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, ATP↑, 2, Insulin↓, 2, MMP↓, 1, OCR↑, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
AminoA↓, 1, ATP:AMP↓, 1, glucoNG↓, 1, GlucoseCon↓, 2, GLUT2↓, 1, Glycolysis↓, 2, HK2↓, 1, KeyT↑, 1, lactateProd↓, 2, PFK1↓, 1, SIRT1↑, 1, Warburg↓, 3,
Cell Death ⓘ
Akt↑, 2, Apoptosis↑, 3, ASK1↑, 1, BIM↑, 1, Casp3↑, 2, Casp9↑, 1, DR5↑, 1, MAPK↓, 1, p‑RSK↑, 1, survivin↓, 1, TumCD↑, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, PERK↑, 1,
Autophagy & Lysosomes ⓘ
ATG3↑, 1, Beclin-1↑, 1, LAMP2↑, 1, p62↑, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 2, DNMTs↓, 1, P53↑, 1, cl‑PARP↓, 1, PARP1↑, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 1, CDK4↑, 2,
Proliferation, Differentiation & Cell State ⓘ
p‑GSK‐3β↑, 1, HDAC↓, 1, HDAC2↓, 1, IGF-1↓, 4, IGF-1↑, 1, IGFBP1↑, 1, IGFR↓, 1, mTOR↓, 2, mTOR↑, 2, Nanog↓, 1, OCT4↓, 1, PI3K↓, 1, PI3K↑, 2, PTEN↑, 1, STAT5↓, 1, TumCG↓, 4,
Migration ⓘ
Ki-67↓, 1, KLF2↓, 1, MMPs↓, 1, PKA↓, 2, Treg lymp↓, 1, TumCP↓, 1, TumMeta↓, 1,
Angiogenesis & Vasculature ⓘ
Hif1a↓, 1,
Barriers & Transport ⓘ
GLUT1↓, 1, P-gp↑, 1,
Immune & Inflammatory Signaling ⓘ
CD14↓, 1, COX2↓, 1, IFN-γ↑, 1, IL6↓, 1, Inflam↓, 1, M2 MC↓, 2, NK cell↑, 1, TNF-α↓, 1,
Cellular Microenvironment ⓘ
pH↑, 1,
Hormonal & Nuclear Receptors ⓘ
CDK6↑, 2,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, ChemoSen↑, 6, Dose?, 1, Dose↑, 1, Dose↝, 4, Dose∅, 1, eff↑, 10, eff↝, 2, eff∅, 1, RadioS↑, 2, selectivity↑, 5,
Clinical Biomarkers ⓘ
BG↓, 13, BP↓, 1, GutMicro↑, 2, IL6↓, 1, Ki-67↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, cachexia↓, 1, ChemoSideEff↓, 3, OS↑, 1, QoL↑, 1, QoL∅, 1, RenoP↑, 1, toxicity↓, 1, toxicity↝, 1, toxicity∅, 2, TumVol↓, 1, TumW↓, 1, Weight↓, 1,
Infection & Microbiome ⓘ
CD8+↑, 2,
Total Targets: 117
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, antiOx↑, 4, Catalase↑, 3, GPx↑, 2, GSH↑, 3, GSTs↑, 2, HO-1↑, 1, hyperG↓, 1, lipid-P↓, 1, MDA↓, 1, NRF2↑, 2, OXPHOS↑, 1, ROS↓, 9, SOD↑, 4, VitC↑, 1, VitE↑, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics ⓘ
Insulin↑, 1, MMP↓, 1, mtDam↓, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, AMPK↑, 1, glucose↓, 1, SIRT1↑, 1,
Cell Death ⓘ
iNOS↓, 1, JNK↓, 1, p‑JNK↓, 1, p38↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↓, 2, ER Stress↓, 2, GRP78/BiP↓, 1,
Autophagy & Lysosomes ⓘ
Beclin-1↑, 1, LC3II↑, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State ⓘ
mTOR↑, 1, STAT3?, 1,
Migration ⓘ
TGF-β↑, 1,
Angiogenesis & Vasculature ⓘ
NO↓, 1,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
IL10↑, 1, IL1β↓, 2, IL6↓, 2, Inflam↓, 3, JAK2↑, 1, NF-kB↓, 2, TNF-α↓, 2,
Drug Metabolism & Resistance ⓘ
BioAv↑, 2, BioAv↝, 1, Dose↝, 1, eff↑, 3, P450↑, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, ALP↓, 1, AST↓, 1, BG↓, 8, creat↓, 1, GutMicro↓, 1, GutMicro↑, 1, HbA1c↓, 1, IL6↓, 2,
Functional Outcomes ⓘ
AntiAge↑, 2, AntiCan↑, 1, cardioP↑, 2, cognitive↑, 1, hepatoP↑, 3, motorD↓, 1, neuroP↑, 1, OS↑, 2, toxicity↓, 1, toxicity∅, 1,
Total Targets: 71
Scientific Paper Hit Count for: BG, Blood Glucose
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1162 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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