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In China, ages at menarche and menopause are not associated with diabetes. Later menarche and menopause are associated with decreasing CVD risk and earlier menopause with higher osteoporosis risk. Menarche and menopause history may help identify women with increased risk of developing CVD and osteoporosis.

Inflammation and reactive oxygen species (ROS) play important roles in the pathogenesis of atherosclerosis. Resveratrol has been shown to possess anti-inflammatory and antioxidative stress activities, but the underlying mechanisms are not fully understood. In the present study, we investigated the molecular basis associated with the protective effects of resveratrol on tumor necrosis factor-alpha (TNF-α)-induced injury in human umbilical endothelial cells (HUVECs) using a variety of approaches including a cell viability assay, reverse transcription and quantitative polymerase chain reaction, western blot, and immunofluorescence staining. We showed that TNF-α induced CD40 expression and ROS production in cultured HUVECs, which were attenuated by resveratrol treatment. Also, resveratrol increased the expression of sirtuin 1 (SIRT1); and repression of SIRT1 by small-interfering RNA (siRNA) and the SIRT1 inhibitor Ex527 reduced the inhibitory effects of resveratrol on CD40 expression and ROS generation. In addition, resveratrol downregulated the levels of p65 and phospho-p38 MAPK, but this inhibitory effect was attenuated by the suppression of SIRT1 activity. Moreover, the p38 MAPK inhibitor SD203580 and the nuclear factor (NF)-κB inhibitor pyrrolidine dithiocarbamate (PDTC) achieved similar repressive effects as resveratrol on TNF-α-induced ROS generation and CD40 expression. Thus, our study provides a mechanistic link between resveratrol and the activation of SIRT1, the latter of which is involved in resveratrol-mediated repression of the p38 MAPK/NF-κB pathway and ROS production in TNF-α-treated HUVECs.

These findings suggest that caffeine may represent a novel, protective strategy against alcoholic liver injury by attenuating oxidative stress and inflammatory response.

BackgroundSepsis combined with myocardial injury is an important cause of septic shock and multiple organ failure. However, the molecular mechanism of sepsis-induced myocardial dysfunction has not yet been thoroughly studied. Resveratrol has been an important research topic due its organ-protection function, but the specific mechanism is unclear. The purpose of this study was to explore the mechanism of organ injury in sepsis and to investigate the molecular mechanism of resveratrol in myocardial protection in sepsis.Material/MethodsA classical Sprague-Dawley rat model of sepsis peritonitis was constructed for further experiments. The PI3K inhibitor LY294002 and resveratrol were used to intervene in a rat model of cardiomyopathy. HE staining was used to observe pathological changes. Cardiomyocyte apoptosis was detected by TUNEL assay. Western blot analysis was used to detect the level of maker proteins.ResultsThe PI3K inhibitors could promote cardiac abnormalities and apoptosis, but resveratrol showed the opposite effect. The upregulation function of the PI3K inhibitor on the expression of NF-κB, IL-6, IL-1β, and TLR4 in LPS rats was not obvious, but the expression of TNF-α in LPS+LY294002 rats was increased by 22.85% compared with that in LPS rats (P<0.05). Compared with the LPS group, the expression of NF-κB, TNF-α, IL-6, IL-1β, and TLR4 in the LPS+resveratrol group was decreased. The expression of p-PI3K, p-AKT, and p-mTOR in LPS+LY294002 was reduced. The expression p-PI3K, p-AKT, and p-mTOR in the myocardium of the LPS+resveratrol group was increased.ConclusionsResveratrol can protect the myocardium in sepsis by activating the PI3K/AKT/mTOR signaling pathway and inhibiting the NF-κB signaling pathway and related inflammatory factors.

BackgroundThis study aimed to investigate the correlation between quantitative retinal vascular parameters such as central retinal arteriolar equivalent (CRAE) and retinal vascular fractal dimension (D(f)), and cardiovascular risk factors in the Chinese Han population residing in the in islands of southeast China.Methodology/Principle FindingsIn this cross-sectional study, fundus photographs were collected and semi-automated analysis software was used to analyze retinal vessel diameters and fractal dimensions. Cardiovascular risk factors such as relevant medical history, blood pressure (BP), lipids, and blood glucose data were collected. Subjects had a mean age of 51.9±12.0 years and included 812 (37.4%) males and 1,357 (62.6%) females. Of the subjects, 726 (33.5%) were overweight, 226 (10.4%) were obese, 272 (12.5%) had diabetes, 738 (34.0%) had hypertension, and 1,156 (53.3%) had metabolic syndrome. After controlling for the effects of potential confounders, multivariate analyses found that age (β = 0.06, P = 0.008), sex (β = 1.33, P = 0.015), mean arterial blood pressure (β = −0.12, P<0.001), high-sensitivity C-reactive protein (β = −0.22, P = 0.008), and CRVE (β = 0.23, P<0.001) were significantly associated with CRAE. Age (β = −0.0012, P<0.001), BP classification (prehypertension: β = −0.0075, P = 0.014; hypertension: β = −0.0131, P = 0.002), and hypertension history (β = −0.0007, P = 0.009) were significantly associated with D(f).Conclusions/SignificanceD(f) exhibits a stronger association with BP than CRAE. Thus, D(f) may become a useful indicator of cardiovascular risk.

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