Effect of ischemic preconditioning on apoptosis and expression of bcl-2, bax protein in sino-atrial node cells during ischemia/reperfusion in rabbits
Zhikun Guo
Abstract
Zhikun Guo
Abstract
Objective:To investigate the effects of apoptosis and expression of bcl-2, bax protein in sino-atrial node cells during ischemia/reperfusion (I/R) in rabbits. Method:I/R and IP model of SAN was established by occluding or loosening the root of right coronary artery. Thirty healthy adult rabbits were divided randomly into the following three groups: Control group, I/R group and IP group. Apoptosis index (AI) and protein expression of bcl-2, bax were measured. Occurrence and outcome of the arrhythmia were observed. Result:①The incidence of ischemia-reperfusion arrhythmia was decreased significantly in IP group as compared with that of I/R group; ②AI was increased, bcl-2 A was increased, but bax A was reduced significantly in IP group as compared with that of I/R group (P 0.01or P 0.05) .Conclusion: IP can decrease ischemia and induce sino-atrial node cells apoptosis induced by I/R and this action is mediated by the increase of bcl-2 and reduction of bax protein expression.
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Objective:To investigate the effects of apoptosis and expression of bcl-2, bax protein in sino-atrial node cells during ischemia/reperfusion (I/R) in rabbits. Method:I/R and IP model of SAN was established by occluding or loosening the root of right coronary artery. Thirty healthy adult rabbits were divided randomly into the following three groups: Control group, I/R group and IP group. Apoptosis index (AI) and protein expression of bcl-2, bax were measured. Occurrence and outcome of the arrhythmia were observed. Result:①The incidence of ischemia-reperfusion arrhythmia was decreased significantly in IP group as compared with that of I/R group; ②AI was increased, bcl-2 A was increased, but bax A was reduced significantly in IP group as compared with that of I/R group (P 0.01or P 0.05) .Conclusion: IP can decrease ischemia and induce sino-atrial node cells apoptosis induced by I/R and this action is mediated by the increase of bcl-2 and reduction of bax protein expression.
Key concepts: Apoptosis, Medicine, BAX Protein, Ischemia, Ischemic preconditioning, Internal medicine, Artery, Bcl-2-associated X protein