Liu Song, Wu Xiang-feng, Zhang Wen-zhong, Sun Ying-xian, Cai Shang-lang
Cardiology Department of Affiliated Hospital of Qingdao University-Medical College, Qingdao 266003, China.
Zhonghua Xin Xue Guan Bing Za Zhi. 2007 Aug;35(8):757-60.
To observe the effects of renal ischemic postconditioning (RI-Post) on myocardial apoptosis in rabbits with acute myocardial ischemia and reperfusion.
All rabbits were subjected to 60 minutes ischemia by left anterior descending coronary artery occlusion (LADO) and 6 hours reperfusion. The rabbits are randomly divided into 3 groups (n = 8 in each group): (1) Ischemia-reperfusion (IR): LADO and reperfusion without additional intervention; (2) RI-Post: after 60 minutes of LADO, the left renal artery was occluded for 30 seconds and reperfused for 30 seconds and repeated 3 times, then the coronary artery was reperfused for 6 hours; (3) Medication intervention (MI): 10 minutes before coronary reperfusion, rabbits were treated with PKC antagonist GF109203X (0.05 mg/kg, IV), followed by RI-Post treatment and 6 hours coronary reperfusion. Myocardial apoptosis was measured by TUNEL and the myocardial Bcl-2 and Bax protein expressions were assessed by immunohistochemistry.
Compared with the IR group and the MI group, myocardial apoptosis was significantly reduced (P < 0.05) and the Bcl-2 protein expression increased (P < 0.01) while the Bax protein expression decreased (P < 0.05) in the RI-Post group.
Remote renal postconditioning applied right before the onset of coronary artery reperfusion can reduce the myocardial apoptosis induced by myocardial ischemia and reperfusion and up-regulate Bcl-2 while down-regulate Bax expression possibly by activation of protein kinase C.
观察肾缺血后处理(RI-Post)对急性心肌缺血再灌注家兔心肌细胞凋亡的影响。
所有家兔均通过左冠状动脉前降支闭塞(LADO)60分钟并再灌注6小时。将家兔随机分为3组(每组n = 8):(1)缺血再灌注(IR)组:LADO及再灌注,无额外干预;(2)RI-Post组:LADO 60分钟后,左肾动脉闭塞30秒再灌注30秒,重复3次,然后冠状动脉再灌注6小时;(3)药物干预(MI)组:冠状动脉再灌注前10分钟,家兔接受蛋白激酶C拮抗剂GF109203X(0.05 mg/kg,静脉注射)治疗,随后进行RI-Post处理及冠状动脉再灌注6小时。采用TUNEL法检测心肌细胞凋亡,免疫组织化学法评估心肌Bcl-2和Bax蛋白表达。
与IR组和MI组相比,RI-Post组心肌细胞凋亡明显减少(P < 0.05),Bcl-2蛋白表达增加(P < 0.01),Bax蛋白表达减少(P < 0.05)。
在冠状动脉再灌注开始前即刻进行远隔肾后处理可减少心肌缺血再灌注诱导的心肌细胞凋亡,上调Bcl-2表达,下调Bax表达,可能是通过激活蛋白激酶C实现的。