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目的:探讨肢体远程缺血预处理(remote ischemic preconditioning,RIPC)对肝脏缺血/再灌注损伤的影响及其机制。方法:对大鼠进行局部的肝组织缺血再灌注(缺血60 min后再灌注24 h),缺血前30 min通过3个循环的双侧股动脉闭塞10 min和再灌注10 min来实现RIPC。在RIPC之前,用PPAR-γ抑制剂T0070907处理部分大鼠。结果:在再灌注结束时,局部缺血后肝损伤显著增加Suzike的损伤评分和AST及ALT释放,并伴随有氧化应激和炎症反应增加。RIPC能够改善肝脏缺血/再灌注后的肝功能,减少肝组织病理损伤,与PPAR-γ活化和自噬体增多相关。PPAR-γ抑制剂T0070907显著减少自噬体形成,抑制RIPC对肝脏缺血/再灌注损伤的保护作用。结论:肢体远程缺血预处理是通过活化的PPAR-γ激活肝脏自噬,从而对肝脏起保护作用。
Objective: To investigate the effect of limb ischemic preconditioning (RIPC) on hepatic ischemia / reperfusion injury and its mechanism. METHODS: Local ischemia-reperfusion of liver tissue was performed in rats (reperfusion 24 h after 60 min of ischemia) and occlusion of the bilateral femoral artery by 3 cycles of 10 min and reperfusion for 10 min 30 min before ischemia RIPC. Prior to RIPC, some rats were treated with PPAR-γ inhibitor T0070907. Results: At the end of reperfusion, injury of liver after ischemia significantly increased the damage score of Suzike and the release of AST and ALT accompanied by increased oxidative stress and inflammatory response. RIPC can improve hepatic function after hepatic ischemia / reperfusion, reduce pathological damage of liver tissue, which is related to activation of PPAR-γ and increase of autophagosome. PPAR-γ inhibitor T0070907 significantly reduced the formation of autophagosomes and inhibited the protection of RIPC against hepatic ischemia / reperfusion injury. CONCLUSION: Limb ischemic preconditioning activates liver autophagy through activated PPAR-γ and thus protects the liver.