The findings of this study indicate that resveratrol supplementation increased some key bone biomarkers.

PMID: 

Ann N Y Acad Sci. 2019 Sep 6. Epub 2019 Sep 6. PMID: 31490554

Abstract Title: 

Effects of resveratrol supplementation on bone biomarkers: a systematic review and meta-analysis.

Abstract: 

The current study presents a comprehensive systematic review and meta-analysis of randomized controlled trials (RCTs) on resveratrol and bone health biomarkers. PubMed, Scopus, and Web of Science (until September 2018) were searched to identify the potential RCTs with information on resveratrol supplementation and bone metabolism biomarkers. Mean differences (MD) were analyzed using a random-effects model. Pooling six RCTs (eight treatment arms with 264 subjects) together identified no significant reduction of serum Ca, osteocalcin, C-terminal telopeptide of type I collagen, and procollagen I N-terminal propeptide values after resveratrol supplementation over placebo treatment. However, a significant increase in serum alkaline phosphatase (ALP) (MD: 5.69 mg/mL, 95% CI: 3.58-7.80, I = 95.7%, P

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Resveratrol may counteract LPS-mediated oxidative stress in MC3T3E1 cells by modulating SOCS-1 protein.

PMID: 

Shanghai Kou Qiang Yi Xue. 2019 Jun ;28(3):237-240. PMID: 31489408

Abstract Title: 

[Resveratrol counteracts lipopolisaccharide-mediated oxidative stress by upregulating SOCS-1 production].

Abstract: 

PURPOSE: To investigate the protective effect and mechanism of resveratrol on oxidative stress of MC3T3-E1.METHODS: The levels of reactive oxygen species in the cells were observed by fluorescence microscope and flow cytometry. The expression of SOCS-1 protein was detected by Western blot. SOCS-1 transient transfected cell line was established, and the levels of reactive oxygen species in transfected cells were observed by fluorescence microscopy and flow cytometry. The data were analyzed using SPSS22.0 software package.RESULTS: The level of ROS in LPS group was significantly higher than that in the blank group and LPS+RES group (P

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Resveratrol normalizes the deterioration of smooth muscle contractility following intestinal ischemia and reperfusion injury.

PMID: 

Ann Vasc Surg. 2019 Aug 23. Epub 2019 Aug 23. PMID: 31449943

Abstract Title: 

Resveratrol normalizes the deterioration of smooth muscle contractility following intestinal ischemia and reperfusion in rats associated with an anti-oxidative effect and modulating TNF-α activity.

Abstract: 

BACKGROUND: The aim of the current study was to investigate the effect of resveratrol on cytokine levels and oxidative stress in intestinal ischemia/reperfusion injuries.METHODS: To induce intestinal I/R, the superior mesenteric artery was occluded for 30 min and then reperfused for 150 min or 24 h. The therapeutic effects of resveratrol on the damage from intestinal ischemia/reperfusion were investigated using an isolated organ bath, along with oxidant/antioxidant and inflammatory factors such as glutathinone (GSH), malondialdehyhde (MDA), myeloperoxidase (MPO), interleukin-1β (IL-1β), and tumor necrosis factor alpha (TNF-α).RESULTS: Ischemia/reperfusion (I/R) control animals demonstrated severe deterioration of smooth muscle motor function as a significant decrease in KCl- and Ach-induced acontractile responses, high oxidative stress as an increase in lipid peroxidation and a decrease in GSH level, and an increase of MPO, IL-1β, and TNF-α activity. Pretreatment of animals with resveratrol restored intestinal dysfunction; reduced elevated MDA, MPO, IL-1β, and TNF-α levels; and reversed the depleted intestine GSH levels after both 150 min and 24 h reperfusion periods.CONCLUSIONS: The results indicated that resveratrol can reverse the effects of disrupted smooth muscle contractility, probably due to its antioxidant and anti-inflammatory effects on MPO, IL-1β, and TNF-α activities.

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Resveratrol is a potential therapeutic agent for preventing renal fibrosis.

PMID: 

Br J Pharmacol. 2019 Aug 27. Epub 2019 Aug 27. PMID: 31454852

Abstract Title: 

Resveratrol suppresses the myofibroblastic phenotype and fibrosis formation in kidneys via proliferation-related signalling pathways.

Abstract: 

BACKGROUND AND PURPOSE: Renal fibrosis acts as the common pathway leading to the development of end-stage renal disease. Previous studies have shown that resveratrol has anti-fibrotic activity, but its potential molecular mechanisms of action are not well understood.EXPERIMENTAL APPROACH: The anti-fibrotic effects of resveratrol were assayed in a rat model of unilateral ureteral obstruction (UUO) in vivo, and in fibroblasts and tubular epithelial cells (TECs) stimulated by TGF-β1 in vitro. Gene and protein expression levels were analysed by PCR, western blotting and immunohistochemical staining.KEY RESULTS: Resveratrol inhibits the myofibroblastic phenotype and fibrosis formation in UUO kidneys by targeting fibroblast-to-myofibroblast differentiation (FMD) and epithelial-mesenchymal transition (EMT). The anti-fibrotic effects of resveratrol correlated with inhibited proliferation of TECs in the interstitium and tubules, resulting in suppressed activity of the proliferation-related signalling pathways, including that of the MAPK, PI3K/Akt, Wnt/β-catenin, and JAK2/STAT3 pathways. Resveratrol treatment suppressed TGF-β1-induced FMD and the expression of the myofibroblastic phenotype in fibroblasts in vitro by antagonizing the activation of proliferation-related signalling. Similarly, TGF-β1-mediated overactivation of the proliferation-related signalling in TECs induced EMT and the myofibroblastic phenotype was suppressed by resveratrol. The anti-fibrotic and anti-proliferative effects of resveratrol were associated with the inactivation of Smad2/3 signalling, and resulted in a partial reversal of FMD and EMT and the inhibition of the myofibroblastic phenotype.CONCLUSIONS AND IMPLICATIONS: Resveratrol suppresses the myofibroblastic phenotype and fibrosis formation in vivo and in vitro via proliferation-related pathways, making it a potential therapeutic agent for preventing renal fibrosis.

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Resveratrol induces apoptosis of benign prostatic hyperplasia epithelial cell line (BPH-1).

PMID: 

BMC Complement Altern Med. 2019 Aug 29 ;19(1):233. Epub 2019 Aug 29. PMID: 31464618

Abstract Title: 

Resveratrol induces apoptosis of benign prostatic hyperplasia epithelial cell line (BPH-1) through p38 MAPK-FOXO3a pathway.

Abstract: 

BACKGROUND: Resveratrol is reported to inhibit the growth of prostate, which is characteristic of benign prostatic hyperplasia (BPH) condition. However, the mechanism remains unclear. This study aimed to identify the effects and probable mechanism of resveratrol on BPH.METHODS: We used the BPH epithelial cell line BPH-1 to investigate the effect of resveratrol. Cells were treated with various concentrations of resveratrol, and its effects on cells viability, apoptosis, ROS accumulation, and cell cycle were assessed. Western blot was used to examine activation of p38 MAPK and protein levels of FOXO3a, Bcl2, Bcl-XL, and caspase3. Cells were also co-treated with the p38 MAPK inhibitor SB203580 or ROS scavenger N-Acetyl-L-cysteine (NAC) to further investigate the mechanism.RESULTS: Resveratrol treatment inhibited the growth of BPH-1 and increased apoptosis of cells. In addition, levels of phosphorylated p38 MAPK level was elevated and FOXO3a repression was observed. Concomitantly, ROS was accumulated. All of these resveratrol-mediated effects were suppressed by additional treatment with SB203580 or NAC. Resveratrol was also found to induce cell cycle arrest at S phase.CONCLUSIONS: Resveratrol can activate p38 MAPK and repress FOXO3a, thereby causing repression of SOD2, catalase, and increase of ROS accumulation, leading to apoptosis in BPH-1 cells.

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This study suggests that vaccinations in early childhood are protective against asthma (0.66). However, the same protective effect (0.67) is also seen for tobacco smoke exposure early in life.

PMID: 

J Allergy Clin Immunol. 2014 Apr ;133(4):979-88. Epub 2014 Jan 22. PMID: 24461583

Abstract Title: 

Early-life determinants of asthma from birth to age 20 years: a German birth cohort study.

Abstract: 

BACKGROUND: The lack of longitudinal data analyses from birth to adulthood is hampering long-term asthma prevention strategies.OBJECTIVE: We aimed to determine early-life predictors of asthma incidence up to age 20 years in a birth cohort study by applying time-to-event analysis.METHODS: In 1990, the Multicenter Allergy Study included 1314 newborns in 5 German cities. Children were evaluated from birth to age 20 years at 19 time points. Using a Cox regression model, we examined the associations between 36 early-life factors and onset of asthma based on a doctor's diagnosis or asthma medication (primary outcome), typical asthma symptoms, or allergic asthma (including positive IgE measurements).RESULTS: Response at 20 years was 71.6%. Two hundred eighteen subjects met the primary outcome criteria within 16,257 person years observed. Asthma incidence was lower in participants who were vaccinated (measles, mumps, and rubella vaccine/tick-borne encephalitis vaccine/BCG vaccine: adjusted hazard ratio [HR], 0.66 [95% CI, 0.47-0.93]). Up to age 20 years, asthma incidence was higher in subjects who had parents with allergic rhinitis (adjusted HR, 2.24 [95% CI, 1.67-3.02]), started day care early or late (before 18 months: adjusted HR, 1.79 [95% CI, 1.03-3.10]; after 3 years: adjusted HR, 1.64 [95% CI, 0.96-2.79]), had mothers who smoked during pregnancy (adjusted HR, 1.79 [95% CI, 1.20-2.67]), had poor parents (adjusted HR, 1.55 [95% CI, 1.09-2.22]), and had parents with asthma (adjusted HR, 1.65 [95% CI, 1.17-2.31]). Not associated with asthma were aspects of diet and breast-feeding, pet ownership, presence of older siblings, and passive smoking.CONCLUSION: Parental asthma and nasal allergy increase asthma incidence in offspring up to adulthood. Avoiding tobacco smoke exposure during pregnancy, receiving vaccinations in early childhood, and starting day care between 1.5 and 3 years of age might prevent or delay the development of asthma.

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This poorly-designed study is touted as a true “vaxxed vs. unvaxxed study”, however, it only included 94 unvaccinated children, of which were children who had no “documented vaccinations”, compared to a vaccinated group of 13,499.

PMID: 

Dtsch Arztebl Int. 2011 Feb ;108(7):99-104. Epub 2011 Feb 18. PMID: 21412506

Abstract Title: 

Vaccination status and health in children and adolescents: findings of the German Health Interview and Examination Survey for Children and Adolescents (KiGGS).

Abstract: 

BACKGROUND: Whether unvaccinated children and adolescents differ from those vaccinated in terms of health is subject to some discussion.METHOD: We evaluated data on diseases that are preventable by vaccination, infectious and atopic diseases, and vaccinations received that had been collected between 2003 and 2006 in a representative sample of 17 641 subjects aged 0 to 17 years in the framework of the German Health Interview and Examination Survey for Children and Adolescents (Kinder- und Jugendgesundheitssurvey, KiGGS).RESULTS: Evaluable data on vaccinations were available for 13 453 subjects aged 1-17 years from non-immigrant families. 0.7% of them (95% confidence interval: 0.5%-0.9%) were not vaccinated. The lifetime prevalence of diseases preventable by vaccination was markedly higher in unvaccinated than in vaccinated subjects. Unvaccinated children aged 1-5 years had a median number of 3.3 (2.1-4.6) infectious diseases in the past year, compared to 4.2 (4.1-4.4) in vaccinated children. Among 11- to 17-year-olds, the corresponding figures were 1.9 (1.0-2.8) (unvaccinated) versus 2.2 (2.1-2.3) (vaccinated). The lifetime prevalence of at least one atopic disease among 1- to 5-year-olds was 12.6% (5.0%-28.3%) in unvaccinated children and 15.0% (13.6%-16.4%) in vaccinated children. In older children, atopy was more common, but its prevalence was not found to depend on vaccination status: among 6- to 10-year-olds, the prevalence figures were 30.1% (12.9%-55.8%) for unvaccinated children versus 24.4% (22.8%-26.0%) for vaccinated children, and the corresponding figures for 11- to 17-year-olds were 20.3% (10.1%-36.6%) versus 29.9% (28.4%-31.5%).CONCLUSION: The prevalence of allergic diseases and non-specific infections in children and adolescents was not found to depend on vaccination status.

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Resveratrol supplementation produced useful effects on some cardio-metabolic parameters in patients with T2DM.

PMID: 

Phytother Res. 2019 Sep 1. Epub 2019 Sep 1. PMID: 31475415

Abstract Title: 

The Effect of Resveratrol Supplementation on Cardio-Metabolic Risk Factors in Patients with Type 2 Diabetes: A Randomized, Double-Blind Controlled Trial.

Abstract: 

The aim of the present randomized controlled trial was to evaluate the effect of a micronized resveratrol supplement on glycemic status, lipid profile, and body composition in patients with type 2 diabetes mellitus (T2DM). A total of 71 overweight patients with T2DM (body mass index ranged 25-30) were randomly assigned to receive 1000 mg/day trans-resveratrol or placebo (methyl cellulose) for 8 weeks. Anthropometric indices and biochemical indices including lipid and glycemic profile were measured before and after the intervention. In adjusted model (age, sex, and baseline body mass index), resveratrol decreased fasting blood sugar (-7.97±13.6 mg/dL, p=0.05) and increased high density lipoprotein (3.62±8.75 mg/dL, p=0.01) levels compared with placebo. Moreover, the mean difference in insulin levels reached significance (-0.97±1.91, μIU/mL, p= 0.02). However, no significant differences were observed for anthropometric measures. It was found that 8-week resveratrol supplementation produced useful effects on some cardio-metabolic parameters in patients with T2DM. More studies are needed to confirm these findings.

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The protective effect of resveratrol against cyclosporine A-induced oxidative stress and hepatotoxicity.

PMID: 

Arch Physiol Biochem. 2019 Sep 2:1-6. Epub 2019 Sep 2. PMID: 31475571

Abstract Title: 

The protective effect of resveratrol against cyclosporine A-induced oxidative stress and hepatotoxicity.

Abstract: 

The immunosuppressive agent cyclosporine A (CsA) has hepatotoxic potential. Increased reactive oxygen species (ROS) formation is among the causes leading to hepatotoxicity. This study aimed to investigate the effect of resveratrol (RES) on CsA-induced oxidative stress and hepatotoxicity in rats. Rats were treated with RES (10 mg/kg/day; i.p.) for 14 days. CsA (25 mg/kg/day; s.c.) was given during the last seven days together with RES. Serum alanine aminotransferase and aspartate aminotransferase activities together with hepatic histopathological examinations were performed. ROS, thiobarbituric acid reactive substances (TBARS), advanced oxidation protein products (AOPPs), ferric reducing antioxidant power, and glutathione levels as well as superoxide dismutase, and glutathione peroxidase activities were measured in the liver tissue. RES ameliorated histopathological changes and decreased hepatic ROS, TBARS, and AOPP levels significantly. However, antioxidant parameters did not change in CsA-treated rats. Our results indicate that RES treatment may be effective in decreasing CsA-induced oxidative stress and hepatotoxicity.

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Resveratrol improves cognitive dysfunction in rats with chronic cerebral hypoperfusion.

PMID: 

Front Neurosci. 2019 ;13:859. Epub 2019 Aug 20. PMID: 31481868

Abstract Title: 

Resveratrol Activates Autophagy via the AKT/mTOR Signaling Pathway to Improve Cognitive Dysfunction in Rats With Chronic Cerebral Hypoperfusion.

Abstract: 

Chronic cerebral hypoperfusion (CCH) is a main cause of vascular dementia and is also an etiological factor of neurological diseases and mental disorders. However, few treatments are available for CCH, and new medications are needed. In the present study, we employed a rat model of CCH that was based on bilateral common carotid artery occlusion and investigated the therapeutic effects of resveratrol and its detailed mechanism of action. We evaluated neurological deficit scores and performed the Morris water maze test, hematoxylin and eosin staining, TUNEL staining, enzyme-linked immunosorbent assays, and Western blot. Resveratrol reduced neurological deficit scores in CCH rats and reduced pathological damage in the frontal cortex and hippocampus. Resveratrol activated autophagy and inhibited the expression of AKT/mechanistic target of rapamycin (mTOR) signaling pathway-related proteins. Treatment with a phosphoinositide-3 kinase inhibitor reversed the protective effect of resveratrol. These findings suggest that resveratrol improves cognitive function in a rat model of CCH and reduces oxidative stress-induced neuronal damage in the frontal cortex and hippocampus by activating autophagy and inhibiting neuronal apoptosis. These effects may be regulated by the AKT/mTOR signaling pathway.

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