CAJ | 학술논문

目的评价缺血后处理对大鼠肝缺血再灌注时线粒体损伤的影响.方法雄性SD大鼠30只,体重180～230 g,随机分为3组(n=10):假手术组(S组)、肝缺血再灌注组(IR组)和缺血后处理组(Ipo组).IR组和Ipo组采用阻断肝门60 min再灌注6 h的方法制备肝缺血再灌注模型,Ipo组缺血60 min时再灌注10 s、缺血10 s,反复6次,进行缺血后处理.于再灌注6 h时取静脉血样,测定血清谷丙转氨酶(ALT)及天门冬氨酸氨基转移酶(AST)活性,然后取肝组织,制备病理切片及分离肝细胞,电镜下观察线粒体超微结构,测定线粒体膜电位及线粒体Na+-K+-ATP酶活性.结果与S组比较,IR组和Ipo组血清ALT和AST活性升高,线粒体Na+-K+-ATP酶活性及线粒体膜电位降低(P<0.01);与IR组比较,Ipo组血清ALT和AST活性降低,线粒体Na+-K+-ATP酶活性及线粒体膜电位升高(P<0.05或0.01).Ipo组线粒体损伤程度轻于IR组.结论缺血后处理可减轻大鼠肝缺血再灌注时肝细胞线粒体损伤.
목적 평개결혈후처리대대서간결혈재관주시선립체손상적영향.방법 웅성SD대서30지,체중180～230 g,수궤분위3조(n=10):가수술조(S조)、간결혈재관주조(IR조)화결혈후처리조(Ipo조).IR조화Ipo조채용조단간문60 min재관주6 h적방법 제비간결혈재관주모형,Ipo조결혈60 min시재관주10 s、결혈10 s,반복6차,진행결혈후처리.우재관주6 h시취정맥혈양,측정혈청곡병전안매(ALT)급천문동안산안기전이매(AST)활성,연후취간조직,제비병리절편급분리간세포,전경하관찰선립체초미결구,측정선립체막전위급선립체Na+-K+-ATP매활성.결과 여S조비교,IR조화Ipo조혈청ALT화AST활성승고,선립체Na+-K+-ATP매활성급선립체막전위강저(P<0.01);여IR조비교,Ipo조혈청ALT화AST활성강저,선립체Na+-K+-ATP매활성급선립체막전위승고(P<0.05혹0.01).Ipo조선립체손상정도경우IR조.결론 결혈후처리가감경대서간결혈재관주시간세포선립체손상.
Objective To evaluate the effects of ischemic postconditioning on hepatocyte mitochondria injury induced by liver ischemia-reperfusion (IR) in rats.Methods Thirty male SD rats weighing 180-230 g were randomly divided into 3 groups (n = 10 each): sham operation group (group S), IR group and ischemic postconditioning group (group Ipo). The animals were anesthetized with intraperitoneal 3% pentobarbital 30 mg/kg. Hepatic IR was produced by occlusion of the hepatic hilum for 60 min in group IR and Ipo. In group Ipo, 60 min ischemia was followed by six cycles of 10-s reperfusion and 10-s ischemia. Blood samples were obtained from the inferior cava vena at 6 h of reperfusion for determination of the serum activities of ALT and AST. Pathological sections of the liver tissues were prepared and the mitochondrial ultrastructure was observed with electron microscope. Mitochondrial Na+-K+ -ATPase activity and mitochondrial membrane potential were also measured. Results Compared with group S, the serum AST and ALT activities were significantly increased and mitochondrial Na+ -K+ -ATPase activity and mitochondrial membrane potential were significantly decreased in group IR and Ipo (P<0.01). Compared with group IR, the serum AST and ALT activities were significantly decreased and mitochondrial Na+ -K+ -ATPase activity and mitochondrial membrane potential were significantly increased in group Ipo (P<0.05 or 0.01). The mitochondria injury was less severe in group Ipo than in group IR. Conclusion Ischemic postconditioning can attenuate the hepatocyte mitochondria injury induced by liver IR in rats.