Lei Zhang1,*, Yuhua Jia2,*, 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.
Danshensu, human umbilical vein endothelial cells, oxidized low-density lipoprotein.