Protective effect of catalpolon destruction of tight junctions of high glucose induced BMECs.
10.19540/j.cnki.cjcmm.20180510.001
- Author:
Li ZOU
1
;
Ke LIU
2
;
Hui-Feng ZHU
2
;
Shan FENG
2
Author Information
1. Sichuan Vocational College of Health and Rehabilitation, Zigong 643000, China.
2. College of Pharmaceutical Sciences & Chinese Medicine, Southwest University, Chongqing 400715, China.
- Publication Type:Journal Article
- Keywords:
BMECs;
adhesion junction;
catalpol;
cytoskeleton protein;
high glucose;
tight junction
- MeSH:
Actin Cytoskeleton;
drug effects;
Actins;
metabolism;
Animals;
Brain;
cytology;
Cells, Cultured;
Claudin-5;
metabolism;
Endothelial Cells;
drug effects;
Glucose;
Iridoid Glucosides;
pharmacology;
Phosphoproteins;
Rats;
Tight Junctions;
drug effects;
Zonula Occludens-1 Protein;
metabolism
- From:
China Journal of Chinese Materia Medica
2018;43(20):4118-4124
- CountryChina
- Language:Chinese
-
Abstract:
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.
