缺血后处理对裸鼠肝脏缺血再灌注损伤的保护作用及其机制

The Mechanism and Protection Role of Ischemic Postconditioning in Rat Liver

目的探讨缺血后处理(ischemic postconditioning,IPO)对裸鼠肝脏的保护的机制.方法建立裸鼠肝脏缺血再灌注模型,将40只裸鼠随机分为4组:假手术组(S组,n=10)、缺血再灌注组(IR组,n=10)、缺血后处理组(IPO组,n=10)、阻断剂组(IIPO组n=10).比较各组血清肝脏功能变化(ALT、AST)变化,蛋白免疫印迹法检测肝脏组P-Akt及NF-κB P65的蛋白表达:与S组相比,其余3组血清ALT、AST含量均明显升高(P<0.05),组织P-Akt及NF-κB P65蛋白表达明显增加,与IR组相比,IPO组ALT、AST明显降低(P<0.05),P-Akt明显升高, NF-κB P65明显降低(P<0.05).结论缺血后处理机制可能通过激活PI3K的途径使Akt,表达增加,同时抑制P65蛋白表达来减轻裸鼠肝脏缺血再灌注损伤。

Objective To study the protection function and mechanism of ischemic post-conditioning in rat liver. Methods The model of liver ischemia-reperfusion in nude mice was established,and 40 nude mice were randomly divided into 4 groups： sham operation group（group S,n = 10）,ischemia reperfusion group（group IR,n = 10）,post ischemic treatment group（IPO group,n = 10）,and blocker group（IIPO group n = 10）. The changes of serum liver function（ALT, AST）were compared and the protein expression of P-Akt and NF-KB P65 in the liver group was detected by protein immunoblotting. Compared with the S group,the content of ALT and AST in the other three groups increased significantly（P 〈 0.05）, and the expression of P-Akt and NF-KB P65 protein in the tissues increased obviously. AST significantly decreased（P 〈 0.05）, P-Akt was significantly increased,NF-KB P65 was significantly reduced（P 〈 0.05）. Conclusion The mechanism of ischemic postconditioning may increase the expression of Akt by activating PI3 K, and inhibit the expression of P65 protein to reduce the liver ischemia-reperfusion injury in nude mice.