Effects of exendin-4 on rat cardiomyocyte apoptosis early after severe scald injury.
- Author:
Yun-hui CHEN
1
;
Jia-han WANG
;
Zhi-qing LI
;
Zhao-hui YI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Burns; pathology; Caspase 3; metabolism; Myocytes, Cardiac; cytology; pathology; Peptides; pharmacology; Rats; Rats, Sprague-Dawley; Venoms; pharmacology
- From: Journal of Southern Medical University 2011;31(6):1101-1104
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of exendin-4 on cardiomyocyte apoptosis in the early stage after scald injury in rats and explore the mechanisms.
METHODSFifty-four healthy adult SD rats were randomly divided into normal control group (n=6), scald group (n=24) and scald with exendin-4 treatment group (n=24). In the latter two groups, the rats were subjected to 30% TBSA full-thickness scald burns on the back, and Parkland formula was used for determining the resuscitation fluid volume. In exendin-4 treatment group, the rats received intraperitoneal injection of 5 µg/kg exendin-4 after the scald. Apoptosis of the cardiomyocytes from the left ventricle was determined by TUNEL assay and the activity of caspase-3 in the myocardium was assessed.
RESULTSIn the scald group, the apoptotic index of the cardiomyocytes was increased at 6 h post-burn, reaching the peak level at 12 h, and maintained a significantly higher level than that in the normal control at 48 h (P<0.05). Myocardial caspase-3 activity in the scald group was increased at 6 h post-burn and reached the peak at 12 h, still maintaining a high levels at 24 h (P<0.05). In exendin-4 treatment group, the apoptotic index of the cardiomyocytes was significantly lower than that in the scald group at 6, 12, 24 and 48 h post-burn (P<0.05), and so was the caspase-3 activity at 6, 12 and 48 h (P<0.05). A significant positive correlation was found between the apoptotic index of the cardiomyocytes and myocardial caspase-3 activity in the rats (P<0.05).
CONCLUSIONExdendin-4 can inhibit rat cardiomyocyte apoptosis early after scald injury possibly by suppressing caspase-3 activity in the myocardium.