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作 者:吴贵福[1] 董春萍[1] 高珊[1] 李辉[1] WU Guifu;DONG Chunping;GAO Shan(Department of Endocrinology,Shaanxi Provincial People’s Hospital, Shaanxi, Xi’an 710068,China)
出 处:《河北医药》2020年第13期1925-1929,1934,共6页Hebei Medical Journal
摘 要:目的探讨薯蓣皂苷对高糖诱导的大鼠视网膜血管内皮细胞(RRVEC)损伤的保护作用及作用机制。方法采用不同浓度薯蓣皂苷干预高糖诱导RRVEC细胞以及构建miR-146a过表达的RRVEC细胞,流式细胞仪检测细胞凋亡,Western Blot法检测凋亡相关蛋白表达,流式细胞仪检测ROS相对含量,酶联免疫吸附法检测MDA含量和SOD活性,qRT-PCR检测miR-146a表达。结果高糖诱导的大鼠RRVEC细胞miR-146a呈低表达。薯蓣皂苷干预、过表达miR-146a均可降低高糖诱导的大鼠RRVEC细胞凋亡率(P<0.05),促进高糖诱导的RRVEC细胞Bcl-2蛋白表达,抑制Bax和Cleaved-caspase-3蛋白表达(P<0.05),降低ROS水平和MDA含量(P<0.05),提高SOD活性(P<0.05)。薯蓣皂苷干预还能促进miR-146a表达,抑制miR-146a表达逆转了薯蓣皂苷(30μg/ml)对高糖诱导的RRVEC损伤的影响。结论薯蓣皂苷通过调控miR-21表达抑制高糖诱导的大鼠视网膜血管内皮细胞损伤。Objective To investigate the protective effect of diosgenin on the injury of rat retinal vascular endothelial cells(RVEC)induced by high glucose,and to explore its action mechanism.Methods The different concentrations of diosgenin were used to interfere with the high glucose-induced rat RVEC cells and to construct RVEC cells with miR-146a overexpression.Flow cytometry was used to detect apoptosis,and western Blot method was used to detect the expression of apoptosis-related proteins.Flow cytometry was used to detect the relative ROS content,and enzyme-linked immunosorbent assay was used to detect MDA content and SOD activity.In addition,qRT-PCR was used to detect miR-146a expression.Results The miR-146a expression in RVEC cells in high glucose-induced rat was lower.The diosgenin intervention and over-expression of miR-146a could reduce the apoptosis rate of RVEC cells induced by high glucose in rats(P<0.05),promote the expression of Bcl-2 protein in RVEC cells induced by high glucose,and inhibit Bax and Cleaved caspase 3 protein expression(P<0.05).Moreover,it could reduce ROS level and MDA content(P<0.05),and increase SOD activity(P<0.05).The diosgenin intervention could also promote miR-146a expression,and inhibit miR-146a expression to reverse the effect of diosgenin(30μg/ml)on high glucose-induced RVEC injury.Conclusion The diosgenin can inhibit the high glucose-induced RVEC injury in rats by regulating miR-21 expression.
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