Zou Li, Liu Ke, Zhu Hui-Feng, Feng Shan
Sichuan Vocational College of Health and Rehabilitation, Zigong 643000, China.
College of Pharmaceutical Sciences & Chinese Medicine, Southwest University, Chongqing 400715, China.
Zhongguo Zhong Yao Za Zhi. 2018 Oct;43(20):4118-4124. doi: 10.19540/j.cnki.cjcmm.20180510.001.
This paper aimed to observe the protective effect of catalpol on the high glucose induced destruction of tight junctions of rat primary brain microvascular endothelial cells (BMECs). Catalpol co-administrated with high glucose increased BMECs survival, decreased its ET-1 secretion, and improved transmembrane electrical resistance in a time-dependent manner. Furthermore, transmission electron microscopy was used to observe catalpol's protective effect on tight junction. Fluorescence staining displayed that catalpol reversed the rearrangement of the cytoskeleton protein F-actin and up-regulated the tight junction proteins claudin-5 and ZO-1, which were further demonstrated by the mRNA expression levels of claudin-5, occludin, ZO-1, ZO-2, ZO-3, -actintin, vinculin and cateinins. This study indicated that catalpol reverses the disaggregation of cytoskeleton actin in BMECs and up-regulates the expression of tight junction proteins, such as claudin-5, occludin, and ZO-1, and finally alleviates the increase in high glucose-induced BMECs injury.
本文旨在观察梓醇对高糖诱导的大鼠原代脑微血管内皮细胞（BMECs）紧密连接破坏的保护作用。梓醇与高糖共同作用可提高BMECs的存活率，降低其ET-1分泌，并呈时间依赖性地改善跨膜电阻。此外，采用透射电子显微镜观察梓醇对紧密连接的保护作用。荧光染色显示，梓醇可逆转细胞骨架蛋白F-肌动蛋白的重排，并上调紧密连接蛋白claudin-5和ZO-1，claudin-5、occludin、ZO-1、ZO-2、ZO-3、α-肌动蛋白、纽蛋白和连环蛋白的mRNA表达水平进一步证实了这一点。本研究表明，梓醇可逆转BMECs中细胞骨架肌动蛋白的解聚，上调紧密连接蛋白如claudin-5、occludin和ZO-1的表达，最终减轻高糖诱导的BMECs损伤增加。
