2010Zhonghua shiyan waike zazhiRequires access

The effects of preconditioning on cardiomyocyte apoptosis in rats and the mechanisms

Weixing Wang, Siping Hu, Zhipeng Meng, He Liu, Yang Liu

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Abstract

Objective To observe the possible roles of apoptosis and its mechanisms in myocardial ischemia-reperfusion injury and preconditioning protection in rats. Methods Forty rats were randomly divided into four groups : control group (group A), 60 min ischemia-reperfusion group (group B), 120 min ischemia-reperfusion group (group C), and ischemic-preconditioning group (group D). Apoptosis was treasured by using terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling (TUNEL). The pathological changes of the heart were observed under the light and and electron microscopies. The expression of tumor necrosis factor (TNF)-α, bcl-2, and bax was detected. Results Apoptosis index and the expression of TNF-α, bcl-2, and bax in group D were significantly lower than those in the group B and group C. Conclusion Ischemic-preconditioning can relieve the apoptosis of myocardial ischemia-reperfu-sion. Inhibiting the expression of TNF-α, bcl-2, and bax accounts for the mechanisms of preconditioning protection. Key words: Myocardium; Isehemia preconditioning; Reperfusion injury; Apoptosis; Immunohistochemistry

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Objective To observe the possible roles of apoptosis and its mechanisms in myocardial ischemia-reperfusion injury and preconditioning protection in rats. Methods Forty rats were randomly divided into four groups : control group (group A), 60 min ischemia-reperfusion group (group B), 120 min ischemia-reperfusion group (group C), and ischemic-preconditioning group (group D). Apoptosis was treasured by using terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling (TUNEL). The pathological changes of the heart were observed under the light and and electron microscopies. The expression of tumor necrosis factor (TNF)-α, bcl-2, and bax was detected. Results Apoptosis index and the expression of TNF-α, bcl-2, and bax in group D were significantly lower than those in the group B and group C. Conclusion Ischemic-preconditioning can relieve the apoptosis of myocardial ischemia-reperfu-sion. Inhibiting the expression of TNF-α, bcl-2, and bax accounts for the mechanisms of preconditioning protection. Key words: Myocardium; Isehemia preconditioning; Reperfusion injury; Apoptosis; Immunohistochemistry

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Available abstract

Objective To observe the possible roles of apoptosis and its mechanisms in myocardial ischemia-reperfusion injury and preconditioning protection in rats. Methods Forty rats were randomly divided into four groups : control group (group A), 60 min ischemia-reperfusion group (group B), 120 min ischemia-reperfusion group (group C), and ischemic-preconditioning group (group D). Apoptosis was treasured by using terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling (TUNEL). The pathological changes of the heart were observed under the light and and electron microscopies. The expression of tumor necrosis factor (TNF)-α, bcl-2, and bax was detected. Results Apoptosis index and the expression of TNF-α, bcl-2, and bax in group D were significantly lower than those in the group B and group C. Conclusion Ischemic-preconditioning can relieve the apoptosis of myocardial ischemia-reperfu-sion. Inhibiting the expression of TNF-α, bcl-2, and bax accounts for the mechanisms of preconditioning protection. Key words: Myocardium; Isehemia preconditioning; Reperfusion injury; Apoptosis; Immunohistochemistry

Key concepts: TUNEL assay, Apoptosis, Terminal deoxynucleotidyl transferase, Ischemia, Ischemic preconditioning, Reperfusion injury, Tumor necrosis factor alpha, Immunohistochemistry

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