Combination of Astragaloside Ⅳ and Tanshinone Ⅱa Promote Angiogenesis after Oxygen-Glucose Deprivation Injury in Endothelial Cells
10.11842/wst.20230724006
- VernacularTitle:黄芪甲苷与丹参酮IIA配伍拮抗内皮细胞糖氧剥夺损伤促进血管新生
- Author:
Lei ZHANG
1
;
Lin LIN
;
Jibiao WU
;
Chao LI
Author Information
1. 山东中医药大学中医学院 济南 250355
- Keywords:
Oxygen-glucose deprivation injury;
Astragaloside Ⅳ;
Tanshinone Ⅱa;
Angiogenesis;
Endothelial cells;
Enos;
NO
- From:
World Science and Technology-Modernization of Traditional Chinese Medicine
2024;26(5):1279-1289
- CountryChina
- Language:Chinese
-
Abstract:
Objective The present study was designed to investigate the protection of Astragaloside Ⅳ(AS-Ⅳ)and Tanshinone Ⅱa(Tan Ⅱa)on human umbilical vein endothelial cells(HUVECs)after oxygen-glucose deprivation(OGD)injury and underlying mechanism.Methods HUVECs were cultured in vitro to establish the OGD injury model.The cells were divided into control group,model group,AS-Ⅳ group,Tan ⅡA group,and AS-Ⅳ+Tan ⅡA treatment group.The protective effect of AS-Ⅳ and Tan ⅡA combination on HUVECs after oxygen-glucose deprivation injury was observed,and the proliferation,migration,and tube formation of endothelial cells were analyzed.Apoptosis of HUVECs was determined using an AnnexinV-FITC apoptosis detection kit.The protein expressions of VE-cadherin,TGF-β1,VEGFA and Enos were detected by Western blotting.The expression of the proteins CD31 and Enos were detected by immunofluorescence.The concentration of nitric oxide(NO)in cell culture supernatants was also measured by ELISA.Results Compared with the control group,oxygen-glucose deprivation induced HUVECs dysfunction and apoptosis,and decreased the protein expression levels of VE-cadherin,TGF-β1,VEGFA,CD31,Enos as well as NO content(P<0.01).Compared with the model group,treatment group improved proliferation,migration and tube formation abilities of HUVECs,inhibited apoptosis,and increased the protein expression levels of VE-cadherin,TGF-β1,VEGFA,CD31,Enos as well as NO content(P<0.05).Conclusion AS-Ⅳ and Tan ⅡA can alleviate OGD-induced damage and may promote angiogenesis of HUVECs via upregulating the expression of Enos and enhancing the release of NO.
