Naoluo Xintong Decoction promotes proliferation of rat brain microvascular endothelial cells after oxygen-glucose deprivation by activating the HIF-1α/VEGF signaling pathway
10.12122/j.issn.1673-4254.2025.09.17
- VernacularTitle:脑络欣通通过激活HIF-1α/VEGF信号通路促进氧糖剥夺/复氧复糖损伤后大鼠的脑微血管内皮细胞增殖
- Author:
Yu ZHANG
1
;
Yinqi HU
;
Peipei LI
;
Xiao SHI
;
Wei XU
;
Jianpeng HU
Author Information
1. 新安医学教育部重点实验室,安徽 合肥 230012;安徽中医药大学中医学院,安徽 合肥 230012
- Publication Type:Journal Article
- Keywords:
ischemic stroke;
Naoluo Xintong Decoction;
HIF-1α/VEGF signaling pathway;
oxygen-glucose deprivation/reoxygenation injury;
cerebral microvascular endothelial cells
- From:
Journal of Southern Medical University
2025;45(9):1980-1988
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of Naoluo Xintong Decoction(NLXTD)on proliferation of rat brain microvascular endothelial cells(BMECs)after oxygen-glucose deprivation/reoxygenation(OGD/R)injury and role of the HIF-1α/VEGF pathway in mediating its effect.Methods Using a BMEC model of OGD/R,we tested the effects of 10%NLXTD-medicated rat serum,alone or in combination with 2ME2 or 10%NAKL,on cell proliferation,migration,tube-forming ability and permeability using CCK-8 assay,Transwell chamber assay,tube formation assay and permeability assay.Cellular expressions of VEGF and Notch were detected using ELISA and laser confocal immunofluorescence analysis,and the expressions of HIF-1α,VEGFR2,Notch1,ERK and P-ERK1/2 proteins were detected with Western blotting.Results OGD/R injury significantly decreased viability of BMECs.NLXTD treatment of the cells with OGD/R could significantly promoted cell proliferation,migration and tube formation ability,but these effects were strongly attenuated by application of 2ME2.NLXTD treatment also significantly increased the percentages of VEGF-and Notch-positive cells in the cell models and obviously enhanced the expression levels of HIF-1α,VEGFR2,Notch1 and P-ERK1/2.Conclusion NLXTD promotes proliferation,migration,and tube formation of rat BMECs after OGD/R injury possibly by activating the HIF-1α/VEGF signaling pathway.
