Effect of propofol on Bax and Bcl-2expression of myocardial ischemia-reperfusion injury in type 2diabetic rats
Yang Xu
Abstract
Yang Xu
Abstract
Objective To observe the effects of propofol on Bax and Bcl-2expression during myocardial ischemia-reperfusion(I/R)injury in type 2diabetic rats.Methods A total of 48 male Wistar rats were randomly divided into six equal groups as follows:the myocardial I/R group(CI), which was induced by occluding the left anterior descending coronary artery for 30min,followed by 2 h of reperfusion;the I/R+propofol group(CP),which underwent I/R and propofol infusion at 6 mg·kg-1·h-1 started 10min before reperfusion;sham operation group(CC),which underwent sham operation without tightening of the coronary sutures,and diabetic I/R group(DI),diabetic propofol group(DP),diabetic sham group(DC),of which the above mentioned procedures were applied to rats with type 2diabetic.Type 2diabetic rats were induced by a combination of high-fat and high-glucose diet with intraperitoneal STZ injection.The injured cardiac tissues were removed for microscopic examination after reperfusion.Bax and Bcl-2expression was measured with immunohistochemistry, as well as the Bcl-2/Bax ratio was also calculated.Results Compared with group CC,Bcl-2and Bax expression obviously upregualted and Bcl-2/Bax ratio decreased in group CI(P0.05).Compared with group CI,Bax expression decreased,Bcl-2expression increased,and Bcl-2/Bax ratio increased in group CP(P0.05),as well a significantly upregulated Bcl-2and Bax expression in group DI(P 0.05).Otherwise,compared with group DC,Bcl-2and Bax expression increased in group DI and DP, concomitant with a dcreased Bcl-2/Bax ratio in group DI(P0.05).Furthermore,compared with group DI,Bax expression decreased,Bcl-2expression increased,and Bcl-2/Bax ratio increased in group DP(P0.05).Conclusion Propofol could up-regulate anti-apoptosis protein Bcl-2expression and down-regulate proapoptotic protein Bax expression and ameliorate the ischemic reperfusion injury in normal and type 2diabetic rats.
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Objective To observe the effects of propofol on Bax and Bcl-2expression during myocardial ischemia-reperfusion(I/R)injury in type 2diabetic rats.Methods A total of 48 male Wistar rats were randomly divided into six equal groups as follows:the myocardial I/R group(CI), which was induced by occluding the left anterior descending coronary artery for 30min,followed by 2 h of reperfusion;the I/R+propofol group(CP),which underwent I/R and propofol infusion at 6 mg·kg-1·h-1 started 10min before reperfusion;sham operation group(CC),which underwent sham operation without tightening of the coronary sutures,and diabetic I/R group(DI),diabetic propofol group(DP),diabetic sham group(DC),of which the above mentioned procedures were applied to rats with type 2diabetic.Type 2diabetic rats were induced by a combination of high-fat and high-glucose diet with intraperitoneal STZ injection.The injured cardiac tissues were removed for microscopic examination after reperfusion.Bax and Bcl-2expression was measured with immunohistochemistry, as well as the Bcl-2/Bax ratio was also calculated.Results Compared with group CC,Bcl-2and Bax expression obviously upregualted and Bcl-2/Bax ratio decreased in group CI(P0.05).Compared with group CI,Bax expression decreased,Bcl-2expression increased,and Bcl-2/Bax ratio increased in group CP(P0.05),as well a significantly upregulated Bcl-2and Bax expression in group DI(P 0.05).Otherwise,compared with group DC,Bcl-2and Bax expression increased in group DI and DP, concomitant with a dcreased Bcl-2/Bax ratio in group DI(P0.05).Furthermore,compared with group DI,Bax expression decreased,Bcl-2expression increased,and Bcl-2/Bax ratio increased in group DP(P0.05).Conclusion Propofol could up-regulate anti-apoptosis protein Bcl-2expression and down-regulate proapoptotic protein Bax expression and ameliorate the ischemic reperfusion injury in normal and type 2diabetic rats.
Key concepts: Propofol, Medicine, Ischemic reperfusion injury, Intraperitoneal injection, BAX Protein, Apoptosis, Myocardial ischemia, Reperfusion injury