Effects of Tanshinone II A on the myocardial apoptosis and the miR-133 levels in rats with heart failure.
- Author:
Jun FENG
1
;
Shu-Sheng LI
;
Qian-Sheng LIANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Diterpenes, Abietane; pharmacology; Heart Failure; metabolism; Male; MicroRNAs; metabolism; Myocytes, Cardiac; drug effects; metabolism; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Integrated Traditional and Western Medicine 2012;32(7):930-933
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effects of Tanshinone II A (Tan II A) on the myocardial apoptosis in rats with heart failure and its mechanisms for regulating the miR- 133 levels.
METHODSThe heart failure rat model was established by thoracic aorta constriction (TAC). Tan II A Injection was applied for 12 successive weeks. Meanwhile, partial heart failure rats were subcutaneously implanted with osmotic pump of antagonist to observe its inhibition on the miR-133 level. Twelve weeks later, the hemodynamic conditions, the myocardial apoptosis (using TUENL method), myocardial pro-apoptotic genes (Bax and Caspase-3), and the expressions of anti-apoptosis genes (Bcl-2) (using Western blot and RT-PCR method) were analyzed.
RESULTSCompared with the sham-operation group, TAC operation could deteriorate the heart function (except the mean arterial pressure), elevate the myocardial apoptosis level, increase the protein and mRNA levels of Bax and Caspase-3, and down-regulate the protein and mRNA levels of miR-133 and Bcl-2. TAC rats treated by Tan II A could significantly improve all indices with statistical difference except the heart rate. Subcutaneously pumping of antagonist could partially abolish the anti-apoptosis effect of Tan II A.
CONCLUSIONTan II A could decrease the myocardial apoptosis level of heart failure rats, which was possibly realized by up-regulating the miR-133 level.