Changes of c-fos and c-jun mRNA Expression in Angiotensin Ⅱ-induced Cardiomyocyte Hypertrophy and Effects of Sodium Tanshinone Ⅱ A Sulfonate
10.1007/s11596-008-0509-7
- Author:
ZHOU DAIXING
1
;
LIANG QIANSHENG
;
HE XUEXIN
;
ZHAN CHENGYE
Author Information
1. Department of Emergency Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology,Wuhan 430030, China
- Keywords:
sodium tanshinone Ⅱ A sulfonate;
angiotensin Ⅱ;
cardiomyocyte hypertrophy;
c-fos;
c-jun
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2008;28(5):531-534
- CountryChina
- Language:Chinese
-
Abstract:
Summary: The changes of proto-oncogene c-fos and c-jun mRNA expression in angiotensin Ⅱ (Ang Ⅱ)-induced hypertrophy and effects of sodium tanshinone Ⅱ A sulfonate (STS) in the primary culture of neonatal rat cardiomyocytes were investigated. Twelve neonatal clean grade Wistar rats were selected. The cardiomyocytes were isolated, cultured and divided according to different treatments in the medium. The cardiomyocyte size was determined by phase contrast microscope, and the rate of protein synthesis was measured by [3H]-Leucine incorporation. The c-fos and c-jun mRNA expression in cardiomyocytes was detected by reverse transcription polymerase chain reaction (RT-PCR). It was found after cardiomyocytes were treated with Ang Ⅱ for 30 min, the c-fos and c-jun mRNA expression in cardiomyocytes was increased significantly (P<0.01). After treatment with Ang Ⅱ for 24 h, the rate of protein synthesis in Ang Ⅱ group was significantly increased as compared with control group (P<0.01). After treatment with Ang Ⅱ for 7 days, the size of cardiomyocytes in Ang Ⅱ group was increased obviously as compared with control group (P<0.05). After pretreatment with STS or Valsartan before Ang Ⅱ treatment, both of them could inhibit the above effects of Ang Ⅱ (P<0.05 or P<0.01). It was suggested that STS could ameliorate Ang Ⅱ-induced cardiomyocyte hypertrophy by inhibiting c-fos and c-jun mRNA expression and reducing protein synthesis rate of cardiomyocytes.
