Protective effects of Taraxasterol on oxidatively injured cardiomyocytes
10.3969/j.issn.1671-8348.2018.12.002
- VernacularTitle:蒲公英甾醇对氧化损伤心肌细胞保护作用研究
- Author:
Weiwei WANG
1
;
Hongmiao ZHANG
;
Lin WANG
;
Tianhao BAO
Author Information
1. 昆明医科大学第二附属医院心内科三病区
- Keywords:
taraxacum mongolicum;
sterols;
myocytes,cardiac;
taraxasterol;
myocardial ischemia-reperfusion injury;
ERK1/2
- From:
Chongqing Medicine
2018;47(12):1572-1574,1579
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the protective effect and mechanism of taraxasterol on cardiomyocytes in oxidative injury model caused by ischemia-reperfusion (I/R).Methods Mouse cardiomyocytes (CSC cells) were used as the study objects and divided into the normal control group,I/R group,taraxasterol treating I/R group (5,10,30 μmol/L) and positive control group.The cell viability was measured by MTT.The expressions of Caspase-3 and Bcl-2 were detected by RT-PCR.The expressions of superoxide dismutase (SOD) and malondialdehyde (MAD) were detected by biochemical methods.The expression of ERK1/2 was detected by western blot.Results MTT assay showed that 30 μmol/L taraxasterol increased the cell viability of CSC cells injured by I/R (P＜0.05).The RT-PCR results showed that the expression of Caspase-3 mRNA was decreased with 10,30 μmol/L taraxasterol treatment,the difference was statistically significant when compared with I/R group (P＜0.05).The expression of Bcl-2 mRNA was increased with 30 μmol/L taraxasterol treatment,the difference was statistically significant when compared with the I/R group (P＜0.05).The biochemical method detection showed that 30 μmol/L taraxasterol induced SOD expression was increased and MAD expression was decreased,the difference was statistically significant when compared with the I/R group (P＜0.05).Western blot detection showed that 30 μmol/L taraxasterol treatment increased the ratio of p-ERK1/2 to t-ERK1/2 in injured CSC cells (P＜0.05).Conclusion Taraxasterol might inhibit ischemia-reperfusion caused cardiomyocyte oxidative injury by up-regulation of ERK1/2 expression.
