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目的:观察肝缺血再灌注损伤中肾组织中琥珀酸脱氢酶(SDH)、乳酸脱氢酶(LDH)的变化及葛根素预处理对其影响及机制。方法:建立肝缺血再灌注损伤动物模型,健康雄性SD大鼠32只随机分为假手术组、缺血再灌注组(I/R组)、葛根素预处理组(PUE组)和生理盐水预处理组(N组),应用HE染色观察肝、肾组织病理组织学改变,分光光度计法测定肾组织中SDH、LDH的活性变化。结果:PUE组肾小球系膜区上皮细胞部分肿胀,间质充血,未见明显上皮细胞坏死。I/R组SDH活性比对照组明显下降(P<0.05),PUE组与I/R组比较,SDH活性有差异(P<0.05),N组SDH活性与假手术组及PUE组比较,也有显著差异(P<0.05)。I/R组LDH活性比对照组明显下降(P<0.05),PUE组LDH活性比I/R组明显升高(P<0.05)。结论:肝缺血再灌注损伤可引起肝、肾组织形态结构改变,其造成能量代谢障碍是导致肾损伤的主要病理生理基础之一,葛根素可通过改善肾组织能量代谢而减轻肾组织的损伤。
Objective: To observe the changes of superoxide dismutase (SDH) and lactate dehydrogenase (LDH) and the effect of puerarin preconditioning on hepatic ischemia-reperfusion injury and its mechanism. Methods: The animal model of liver ischemia-reperfusion injury was established. Thirty-two healthy male Sprague-Dawley rats were randomly divided into sham operation group, ischemia / reperfusion group (I / R group), puerarin pretreatment group Pretreatment group (N group), the pathological changes of liver and kidney were observed by HE staining. The changes of SDH and LDH activity in renal tissue were measured by spectrophotometer. Results: The epithelial cells in the glomerular mesangial area of PUE group were partly swollen and interstitial hyperemia. No obvious epithelial cell necrosis was found. SDH activity in I / R group was significantly lower than that in control group (P <0.05), SDH activity was different in PUE group and I / R group (P <0.05), and SDH activity in N group was also lower than that in sham operation group and PUE group Significant difference (P <0.05). LDH activity in I / R group was significantly lower than that in control group (P <0.05). LDH activity in PUE group was significantly higher than that in I / R group (P <0.05). CONCLUSION: Hepatic ischemia / reperfusion injury can cause the morphological changes of liver and kidney tissues. The resulting energy metabolism disorder is one of the major pathophysiological bases leading to renal injury. Puerarin can reduce renal tissue damage by improving energy metabolism of kidney tissue .