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Aim To investigate the effect of XNST and its monomeric components on the barrier structure and tight junction protein expression of brain microvascular endothelial cells damaged by oxygen glucose deprivation/reoxygenation (OGD/R) and the possible mechanism. Methods The mouse brain microvascular endothelial cell line bEnd. 3 was inoculated in the upper layer of the Transwell chamber to establish an OGD/R damage model, and the effect of the drug on the integrity of the endothelial cell barrier was investigated by the transmembrane resistance value and fluorescein-so-dium transmittance. Claudin-5 immunofluorescence staining was used to observe the changes of tight junction structure between endothelial cells. RT-PCR and Western blot were employed to detect mRNA and protein expression levels of tightly linked proteins Claudin-5 , Occludin, ZO-1. Western blot was applied to detect the expression levels of MAPKs (JNK, p38, ERK) , I kappa B a, I kappa B kinase phosphorylated protein expression, and Western blot and immunofluorescence were utilized to detect NF-K.B/p65 nucleation expression. Results XNST and its three monomers could significantly increase endothelial cell resistance and de- crease fluorescein-sodium transmittance. Claudin-5 fluorescence staining showed that the tight junction between cells in the model group was significantly damaged , while XNST and its monomer components could significantly improve its tight structure. RT-PCR and Western blot results showed that it could significantly upregulate the expression of mRNA and protein of Claudin-5, Occludin and ZO-1, and further study on the mechanism showed that XNST and its monomer components could significantly inhibit the phosphoryla-tion of JNK, p38 and ERK, inhibit the phosphorylation of I kappa B a and I kappa B kinases, and significantly inhibit the nuclear translocation of NF-KB/p65. Conclusion Both XNST and its monomeric components can exert cerebroprotective effects by increasing the tight junction structure between cells to promote barrier integrity, and the mechanism may be related to inhibition of NF-kB and MAPKs signaling pathway activation.
RESUMO
Objective To observe the effects of Gross Saponins of Tribulus terrestris(GSTT)on energy metabolism and lactic acid metabolism in hyperlipemic rats with acute myocardial infarction(AMI).Methods Rats were fed with high fat diet for 15 days to induce hyperlipidemia,then left anterior descending branch of coronary artery of rats were ligated.Rats showed ST segment elevation in lead Ⅱof electrocardiogram were proved to be AMI rats.AMI rats with hyperlipidemia were divided randomly into five groups(normal group,model group,24.3 mg?kg-1 GSTT group,12.15 mg?kg-1 GSTT group,Simvastatin group)and test drugs were given in succession for 28 days.Left ventricular ischemic myocardium were harvested to prepare myocardial mitochondria.Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity and lactic acid content were measured.Results Compared with the normal group,Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity significantly lowered in model group(P