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Preliminary Research for the Effect of Growth Hormone Releasing Peptide on Myocardial Cell Apoptosis in Heart Failure Rats / 中国循环杂志
Chinese Circulation Journal ; (12): 692-696, 2017.
Artigo em Chinês | WPRIM | ID: wpr-616969
ABSTRACT
To explore the effect of growth hormone releasing peptide (GHRP) on myocardial cell apoptosis in heart failure (HF) rats.

Methods:

Rat's HF model was established by the ligation of left anterior descending coronary artery induced ischemia. 40 male SD rats were randomly assigned into 4 groups Normal control group, Sham operation group, HF group and GHRP treated HF group. n=10 in each group and the rats were fed for 4 weeks after the operation. Cardiac function was examined and myocardial cell morphology was observed; protein expressions of Smac/DIABL0 and Bcl-2 were measured by Western blot analysis; cell apoptosis was evaluated by FCM technique. The differences for above parameters were compared among groups to explore the effect of GHRP on myocardial cell apoptosis in HF rats.

Results:

Compared with HF group, GHRP treated HF group showed the less heart dilation, higher LVEF, lighter pathological changes in myocardial cells and decreased protein expression of Smac/DIABL0, all P<0.05. Bcl-2 level was lower in HF group than the other 3 groups, P<0.05. Compare with Normal control group, GHRP treated HF group had elevated Bcl-2 level, all P<0.05. Myocardial cell apoptosis index was different between HF group and GHRP treated HF group, P<0.05.

Conclusion:

The effect of GHRP on anti-HF should be via inhibiting myocardial cell apoptosis; the mechanism may partly be through promoting Bcl-2 protein expression and depressing Smac/DIABLO mediated mitochondrial pathway of apoptosis.

Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Circulation Journal Ano de publicação: 2017 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: WPRIM (Pacífico Ocidental) Idioma: Chinês Revista: Chinese Circulation Journal Ano de publicação: 2017 Tipo de documento: Artigo