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目的探讨缺血后处理对腹腔镜气腹模型大鼠肝脏氧化应激损伤的保护作用。方法将24只雄性SD大鼠随机分为4组,即气腹组(P)、缺血预处理组(IP)、缺血后处理组(IPo)、对照组(C)。对照组为假手术组,其余各组建立CO2气腹模型,气腹压力15 mm Hg。P组充气60 min后放气30 min;IP组先进行10 min充气和10 min放气,然后充气60 min,再放气30min;IPo组在充气60 min后行3个循环的放气1 min/充气1 min,再放气30 min。检测各组大鼠血清天冬氨酸转氨酸(AST)、丙氨酸转氨酶(ALT)及肝脏组织匀浆丙二醛(MDA)、还原型谷胱甘肽(GSH)、一氧化氮(NO);免疫组织化学方法检测诱导型一氧化氮合酶(iNOS)在肝脏中的表达。结果P组、IP组、IPo组较C组血清ALT、AST、肝组织匀浆MDA含量升高,差异均有统计学意义(P<0.05)。IP组、IPo组与P组相比,血清ALT、AST、肝组织匀浆MDA、NO含量下降,GSH含量升高,差异有统计学意义(P<0.05);IP组与IPo组相比,除GSH外其他生化指标差异无统计学意义(P>0.05)。免疫组织化学结果显示:IPo组iNOS表达,明显低于P组,差异有统计学意义(P<0.05)。结论缺血后处理能使机体GSH含量升高并且抑制iNOS表达减少NO的生成,从而减低CO2气腹所致大鼠肝脏氧化应激损伤;缺血后处理较预处理GSH升高更显著,提示后处理可能对氧化应激更具保护作用。
Objective To investigate the protective effect of ischemic postconditioning on liver oxidative stress injury induced by laparoscopic pneumoperitoneum in rats. Methods Twenty-four male Sprague-Dawley rats were randomly divided into 4 groups: pneumoperitoneum group, IP group, IPo group and control group. The control group was sham operation group, the other groups were established CO2 pneumoperitoneum model, pneumoperitoneum pressure 15 mm Hg. Group P was inflated for 60 min and then deflated for 30 min. The IP group was inflated for 10 min and deflated for 10 min, then inflated for 60 min and then deflated for 30 min. IPo group was deflated for 3 cycles for 60 min after inflation Inflated for 1 min, then deflated for 30 min. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) and liver homogenate malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide NO). Immunohistochemistry was used to detect the expression of inducible nitric oxide synthase (iNOS) in the liver. Results The levels of ALT, AST and the content of MDA in liver homogenate of P group, IP group and IPo group were significantly higher than those of C group (P <0.05). Compared with P group, the levels of ALT, AST, MDA and NO in liver homogenate of IP group and IPo group were significantly decreased (P <0.05) There were no significant differences in other biochemical indexes except GSH (P> 0.05). The results of immunohistochemistry showed that the expression of iNOS in IPo group was significantly lower than that in P group, the difference was statistically significant (P <0.05). Conclusion Ischemic postconditioning can increase the body’s GSH content and inhibit the expression of iNOS, reduce the production of NO, thereby reducing the oxidative stress injury induced by CO2 pneumoperitoneum. The ischemic postconditioning is more significant than the pretreatment GSH, suggesting that Post-treatment may be more protective of oxidative stress.