Ginkgolide B inhibits apoptosis in high glucose-stimulated human umbilical vein endothelial cells
10.3969/j.issn.1001-1978.2017.03.017
- VernacularTitle:银杏内酯B抑制高糖诱导内皮细胞凋亡及机制研究
- Author:
Kun CHEN
;
Ming ZHANG
;
Beidong CHEN
;
Yanyang ZHAO
;
Wei WU
;
Ruomei QI
- Keywords:
ginkgolide B;
glucose;
HUVECs;
ROS;
ap-optosis;
p53
- From:
Chinese Pharmacological Bulletin
2017;33(3):378-383
- CountryChina
- Language:Chinese
-
Abstract:
Aim Toinvestigatetheeffectofginkgolide B on apoptosis in high glucose-treated endothelial cells.Methods Humanumbilicalveinendothelial cells(HUVECs)were used in the present study.The level of transmigration of HUVECs was analyzed by Tr-answell experiment.Apoptosis was detected by flow cy-tometry.Reactive Oxygen Species (ROS ) was meas-ured by immunofluorescence kit.The protein expres-sionwasanalyzedbyWesternblot.Result Highglu-cose treatment resulted in a reduction in transmigration of HUVECs and ginkgolide B recovered the phenome-non in glucose-treated endothelial cells.The level of ROS generation was increased in high glucose-treated group,whereas ginkgolide B inhibited ROS genera-tion.Immunofluorescence data showed high glucose in-creased apoptosis,whereas ginkgolide B inhibited ap-optosis in high glucose-treated HUVECs.Moreover, the expressions of Bax and caspase-3 were increased and Bcl-2 was reduced in high glucose-treated group. In contrast,ginkgolide B abolished the expressions of Bax and caspase-3 and increased Bcl-2 expression. Moreover,high glucose enhanced the expression and phosphorylation of p53,while ginkgolide B suppressed the expression and phosphorylation of p53 induced by highglucose.Conclusions GinkgolideBcaninhibit apoptosis and improve transmigration function in high glucose-treated HUVECs.Ginkgolide B has protection against high glucose-induced endothelial cell injury.
