Tanshinone IIA protects against methylglyoxal-induced injury in human brain microvascular endothelial cells

International Journal of Clinical and Experimental Medicine

Wen-Jing Zhou¹  Qi-Feng Gui¹  Yue Wu¹  Yun-Mei Yang¹ 

关键词: Tanshinone IIA;    methylglyoxal;    human brain microvascular endothelial cells;    apoptosis;    MAPK;   

DOI  :  

学科分类：医学（综合）

来源: e-Century Publishing Corporation

【 摘 要 】

Tanshinone IIA is one of the major diterpenes from Salvia miltiorrhiza Bunge and has been shown to possess a protective effect on the endothelial cells. The present study aimed to investigate whether tanshinone IIA could protect against methylglyoxal (MGO)-induced injury in human brain microvascular endothelial cells (HBMEC). Using cultured HBMEC, cell viability was measured by MTT assay and trypan blue dye exclusion test. Cellular oxidative stress was measured by production of reactive oxygen species (ROS), thiobarbituric acid reactive substances (TBARS) and H₂O₂. AnnexinV/PI staining and western blot were performed to determine cell apoptosis and protein expression. We found that MGO treatment caused a concentration and time-dependent decrease in cell viability, which was inhibited by pretreatment with tanshinone IIA. Exposure to MGO promoted the accumulation of AGEs, and production of ROS, TBARS and H₂O₂ in the cultured HBMEC, which were inhibited by tanshinone IIA pretreatment. Addition of tanshinone IIA significantly reduced MGO-induced cell apoptosis as shown by flow cytometry. On the molecular level, tanshinone IIA administration altered the expression of apoptosis-related proteins such as p53, Bax, Bcl-2 and cyto C. In addition, MGO treatment remarkably increased the phosphorylation of MAPK family including p38, JNK and ERK. By contrast, addition of tanshinone IIA inhibited the activation of MAPK family members. These data indicated that tanshinone IIA could protect against MGO-induced cell injury through inhibiting MAPK activation in HBMEC.

【 授权许可】

Unknown