Danshensu mitigates oxidized low-Density lipoprotein-induced human vascular endothelial cell injury through activation of p38/JNK signaling

Lei Zhang^1,*, Yuhua Jia^2,*, Xiaoshan Zhao², Yunyun Pan², Qiang Wan³, Fenghua Zhou², Dandan Zhao², Yu Zhang², Zhijie Su²

¹Nursing school, Henan University of Traditional Chinese Medicine, Zhengzhou 450000, Henan, China - ²School of traditional chinese medicine, southern medical university, Guangzhou 510515, China - ³Cardiovascular medicine department, Jiangxi Provincial People's Hospital, Nanchang 330006, Jiangxi, China

Introduction: This study investigated the effect of Danshensu (DSS) on oxidized low-density lipoprotein (ox-LDL) induced injury of cultured human umbilical vein endothelial cells (HUVEC). 

Materials and methods: The results showed that ox-LDL suppressed HUVEC viability, induced apoptosis and upregulated phosphorylation of p38 MAPK and c-Jun N-terminal kinase (JNK). DSS showed a protective effect against ox-LDL induced loss in cell viability and an increase in apoptosis. Furthermore, the suppressed cell viability and increased apoptosis induced by ox-LDL could be rescued by inhibitor of p38 (SB203580) and JNK (SP600125), which can effectively inhibit the protective effect of DSS on cell viability loss and apoptosis induced by ox-LDL. In vivo experiment with genetically deficient apolipoprotein E (ApoE) male mice of C57BL/6J strain (Apo E-/-) was also conducted which received DSS. 

Results: The aorta was harvested for hematoxylin and eosin staining and the result showed that DSS treatment ameliorated atherosclerotic lesions. Moreover, Western blot results revealed that DSS inhibits injury to HUVEC induced by ox-LDL, and the expression of p38 and JNK in apo E-/- mice was also deregulated. 

Conclusion: Collectively, we suggested that the protective effect of DSS against ox-LDL induced HUVEC apoptosis might, at least in part, be obtained via inhibition of the p38/JNK signaling pathway.