Effects of sevoflurane preconditioning on p-IκBα in a rat model of myocardial ischemia-reperfusion
Xue mei Wu, Xia Liu, Chen Wang, Hong Xie
Abstract
Xue mei Wu, Xia Liu, Chen Wang, Hong Xie
Abstract
Objective To observe the effect of sevoflurane preconditioning on the expression of p-IκBα in a rat model of myocardial ischemia-reperfusion (I/R). Methods Eighty -four male SD rats after setting up the model of I/R, randomly were divided into seven groups: ①Control group; ② Simple-Ischemic group received 30 min I/R merely; ③ SEVO group inhaled 1.0 MAC sevoflurane for 30 min and 15 min wash-out followed by a 30 min I/R; ④ SEVO 165' group inhaled 1.0 MAC sevoflurane for 30 min and then stoped for 165 min; ⑤ PTN group received PTN 500 μg/kg(NF-κB inhibitor) intraperitoneally 60 min before I/R; ⑥ PTN±SEVO group and⑦SEVO+PTN group received PTN 500 μg/kg 15 min before and after sevoflurane preconditioning. Myocardium sample of all groups were collected before and after the time of I/R or the corresponding point in time. p- IκBα was determined by Western Blotting. Results The expression of p- IκBαwas significantly up-regulated in SEVO group(22±3)and SEVO 165'group(20±4) than that in Control group (15±3) before I/R(P<0.05); After perfusion the expression of p- IκBαin Simple-Ischemic group(44±6)and SEVO group (30±3) was significantly up-regulated than that in Control group( 15±4,P<0.05);but the up-regulated adjustment of SEVO group was smaller than that in Simple-Ischemic group (P<0.05). Conclusion This study further confirmed NF-κB participates in the I/R injury and it may play an important role in the mechanism of sevoflurane-induced cardioprotection. Key words: Anaesthetic,Inhalation; Myocardial reperfusion injury; Preconditioning; p-IκBα
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Objective To observe the effect of sevoflurane preconditioning on the expression of p-IκBα in a rat model of myocardial ischemia-reperfusion (I/R). Methods Eighty -four male SD rats after setting up the model of I/R, randomly were divided into seven groups: ①Control group; ② Simple-Ischemic group received 30 min I/R merely; ③ SEVO group inhaled 1.0 MAC sevoflurane for 30 min and 15 min wash-out followed by a 30 min I/R; ④ SEVO 165' group inhaled 1.0 MAC sevoflurane for 30 min and then stoped for 165 min; ⑤ PTN group received PTN 500 μg/kg(NF-κB inhibitor) intraperitoneally 60 min before I/R; ⑥ PTN±SEVO group and⑦SEVO+PTN group received PTN 500 μg/kg 15 min before and after sevoflurane preconditioning. Myocardium sample of all groups were collected before and after the time of I/R or the corresponding point in time. p- IκBα was determined by Western Blotting. Results The expression of p- IκBαwas significantly up-regulated in SEVO group(22±3)and SEVO 165'group(20±4) than that in Control group (15±3) before I/R(P<0.05); After perfusion the expression of p- IκBαin Simple-Ischemic group(44±6)and SEVO group (30±3) was significantly up-regulated than that in Control group( 15±4,P<0.05);but the up-regulated adjustment of SEVO group was smaller than that in Simple-Ischemic group (P<0.05). Conclusion This study further confirmed NF-κB participates in the I/R injury and it may play an important role in the mechanism of sevoflurane-induced cardioprotection. Key words: Anaesthetic,Inhalation; Myocardial reperfusion injury; Preconditioning; p-IκBα
Key concepts: Sevoflurane, Anesthesia, Ischemia, Ischemic preconditioning, Perfusion, Medicine, Inhalation, Group A