Effects of short-chain acyl-CoA dehydrogenase on cardiomyocyte apopto-sis
10.3969/j.issn.1000-4718.2015.09.010
- VernacularTitle:短链酰基辅酶 A 脱氢酶在心肌细胞凋亡中的作用
- Author:
Zhenhua ZENG
;
Qiuju HUANG
;
Jinxian HUANG
;
Zhaohui SHU
;
Peiqing LIU
;
Shaorui CHEN
;
Bing LIU
;
Sigui ZHOU
- Publication Type:Journal Article
- Keywords:
Short-chain acyl-CoA dehydrogenase;
Cardiomyocytes;
Apoptosis;
Heart failure;
Energy metabo-lism;
Tert-butyl hydroperoxide
- From:
Chinese Journal of Pathophysiology
2015;(9):1589-1594
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the change of short-chain acyl-CoA dehydrogenase (SCAD) expression during cardiomyocyte apoptosis and to explore the relationship between SCAD and cardiomyocyte apoptosis .METHODS: The neonatal rat cardiomyocytes treated by tert-butyl hydroperoxide (tBHP) were used as the model of cardiomyocyte apoptosis . The cell viability , the expression of SCAD at mRNA and protein levels , the activity of SCAD and the content of free fatty acids were determined .RESULTS:The mRNA and protein expression of SCAD decreased in the cardiomyocyte apoptosis model.Compared with negative control group , SCAD expression and activity were both significantly decreased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the cardiomyocytes .Meanwhile, SCAD siRNA treatment triggered the same apoptosis as cardiomyocytes treated with tBHP .CONCLUSION: Down-regulation of SCAD may play an important role in primary cardiomyocyte apoptosis .Increase in the expression of SCAD may become an impor-tant part in intervening cardiomyocyte apoptosis .
