Association between dietary selenium intake and severe abdominal aortic calcification in the United States: a cross-sectional study.

Abdominal aortic calcification (AAC) is an important predictor of cardiovascular disease. The purpose of the current study was to detect the association between dietary selenium intake and severe AAC. We included 2651 participants from the National Health and Nutrition Examination Survey (NHANES, 2013-2014). Dietary selenium intake was measured using the 24-hour recall method. AAC was quantified using the Kauppila score system based on dual-energy X-ray absorptiometry, with a score of >6 indicating severe AAC. The association between dietary selenium intake and severe AAC was analyzed by using a weighted multivariate logistic regression model, smooth curve fitting, and stratified subgroup analysis. After adjusting for multiple covariates, we found that higher dietary selenium intake was negatively associated with severe AAC incidence. When selenium intake was converted into tertiles, the highest tertile of dietary selenium intake was significantly associated with the incidence of severe AAC (odds ratio = 0.66). Smooth curve fitting revealed that this relationship was nonlinear. Subgroup analysis revealed that this negative association was present in participants with chronic kidney disease, but was absent when participants had hypertension or diabetes mellitus. Higher dietary selenium intake was negatively associated with severe AAC incidence in a nonlinear pattern, except in participants with diabetes mellitus or hypertension. However, further cohort studies are required to validate these findings.

Green tea polyphenols alleviate early BBB damage during experimental focal cerebral ischemia through regulating tight junctions and PKCalpha signaling.

BACKGROUND: It has been supposed that green tea polyphenols (GTPs) have neuroprotective effects on brain damage after brain ischemia in animal experiments. Little is known regarding GTPs' protective effects against the blood-brain barrier (BBB) disruption after ischemic stroke. We investigated the effects of GTPs on the expression of claudin-5, occludin, and ZO-1, and the corresponding cellular mechanisms involved in the early stage of cerebral ischemia. METHODS: Male Wistar rats were subjected to a middle cerebral artery occlusion (MCAO) for 0, 30, 60, and 120 min. GTPs (400 mg/kg/day) or vehicle was administered by intragastric gavage twice a day for 30 days prior to MCAO. At different time points, the expression of claudin-5, occludin, ZO-1, and PKCα signaling pathway in microvessel fragments of cerebral ischemic tissue were evaluated. RESULTS: GTPs reduced BBB permeability at 60 min and 120 min after ischemia as compared with the vehicle group. Transmission electron microscopy also revealed that GTPs could reverse the opening of tight junction (TJ) barrier at 60 min and 120 min after MACO. The decreased mRNA and protein expression levels of claudin-5, occludin, and ZO-1 in microvessel fragments of cerebral ischemic tissue were significantly prevented by treatment with GTPs at the same time points after ischemia in rats. Furthermore, GTPs could attenuate the increase in the expression levels of PKCα mRNA and protein caused by cerebral ischemia. CONCLUSIONS: These results demonstrate that GTPs may act as a potential neuroprotective agent against BBB damage at the early stage of focal cerebral ischemia through the regulation of TJ and PKCα signaling.