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目的观察肢体缺血预处理(LIPC)对大鼠肝缺血-再灌注(I-R)损伤的延迟性保护作用。方法雄性SD大鼠36只,随机分为对照组(S组),I-R组,LIPC组,每组12只。S组仅行开腹,不作其他处理;I-R组行肝缺血1h,再灌注3h;LIPC组先行双后肢缺血5min,反复3次24h后行肝缺血1h,再灌注3h。手术完毕,腹主动脉采血用于检测总超氧化物歧化酶(T-SOD)、丙二醛(MDA)、血清ALT与AST;切取肝组织,测定肝脏的湿干比(W/D),免疫组化检测肿瘤坏死因子α(TNF-α)的表达,同时光电镜观察肝组织显微、超微结构的变化。结果与I-R组比较,LIPC组T-SOD活性增加(P<0.01),MDA水平、ALT、AST、W/D值及TNF-α的阳性表达均明显降低(P<0.01),肝脏的显微及超微结构损伤减轻。结论 LIPC对大鼠肝脏I-R损伤有明显的延迟性保护作用。其机制可能与增加机体抗氧化能力、抑制肝脏炎症反应、减轻肝脏水肿、抑制TNF-α的表达和改善肝组织微循环有关。
Objective To observe the delayed protective effect of limb ischemic preconditioning (LIPC) on liver ischemia-reperfusion (I-R) injury in rats. Methods Thirty-six male SD rats were randomly divided into control group (S group), I-R group and LIPC group, with 12 rats in each group. Group S was only laparotomized for no other treatment. Group I-R was subjected to 1 h of ischemia and 3 h of reperfusion; LIPC group was subjected to ischemia of both hindlimbs for 5 minutes and then to liver ischemia for 1 hour and reperfusion for 3 hours. At the end of surgery, blood samples were taken from abdominal aorta for detecting total superoxide dismutase (T-SOD), malondialdehyde (MDA) and serum ALT and AST. Liver tissues were harvested and the wet / dry ratio (W / D) Immunohistochemistry was used to detect the expression of tumor necrosis factor-α (TNF-α), and the changes of the microstructure and ultrastructure were observed by light microscope. Results Compared with IR group, the activity of T-SOD in LIPC group was significantly increased (P <0.01), and the levels of MDA, ALT, AST, W / D and TNF- And ultrastructure damage reduction. Conclusion LIPC has obvious delayed protective effect on rat liver I-R injury. The mechanism may be related to increasing body antioxidant capacity, inhibiting liver inflammation, reducing liver edema, inhibiting TNF-α expression and improving microcirculation of liver tissue.