Effect of stellate ganglion block on cardiomyocyte apoptosis and expression of Bcl-2/Bax protein in spontaneously hypertensive rats.
10.3969/j.issn.1672-7347.2013.09.005
- Author:
Yongquan CHEN
1
;
Guangxiang HU
;
Qun FU
;
Xiaoju JIN
Author Information
1. Department of Anesthesiology, The First Affiliated Hospital, Wannan Medical College, Wuhu Anhui 241001,China chenyq263@163.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Apoptosis;
Autonomic Nerve Block;
Blood Pressure;
Heart Ventricles;
Male;
Myocardium;
Myocytes, Cardiac;
cytology;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
Rats;
Rats, Inbred SHR;
Stellate Ganglion;
physiopathology;
bcl-2-Associated X Protein;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2013;38(9):896-901
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the relationship between apoptosis of myocardial cells in spontaneously hypertensive rats (SHRs) and the expressions of Bcl-2 and Bax protein, and the protective effect of stellate ganglion block on apoptosis of myocardial cells.
METHODS:A total of 32 ten-week-old male SHRs were assigned randomly into 4 groups: a left stellate ganglion block group (group LS), a right stellate ganglion block group (group RS), a captopril group (group D) and a control group (group C). The arterial systolic blood pressure was measured by ALC-NIBP system. After 10 weeks, all rats were anaesthetized by 3% pentobarbital sodium, cardiomyocyte apoptosis index of left ventricle was assessed by TUNEL, and the localization of myocardium Bcl-2, Bax was investigated by immunohistochemistry.
RESULTS:Compared with group LS and C, the apoptotic index decreased (P<0.05). SHR myocardial expression of Bcl-2 significantly increased (P<0.05), Bax expression significantly decreased (P<0.05) and Bcl-2/Bax was significantly higher (P<0. 05) in group RS.
CONCLUSION:Bcl-2 and Bax play an important role in the apoptosis of myocardial cells in SHRs. Right stellate ganglion block can reduce the apoptosis of myocardial cells and reverse the reconstruction of the left ventricle in SHRs via regulation of apoptosis-related gene proteins.
