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目的研究鲨鱼肝刺激物(sHSS)对硫代乙酰胺(TAA)所致大鼠急性肝损伤和肝线粒体功能的影响。方法雄性SD大鼠,体质量(200±20)g,随机分3组对照组、模型组、治疗组,每组8只。以400mg/kgTAA2次腹腔注射建立大鼠急性肝损伤模型,治疗组在注射TAA前1h腹腔注射80mg/kgsHSS,对照组注射等体积的生理盐水,24h后观察大鼠血清中丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)活性和肝中丙二醛(MDA)含量的变化,以及TAA和sHSS对肝线粒体呼吸功能、线粒体肿胀和膜电位的影响。结果治疗组大鼠血清中ALT、AST的水平明显低于模型组,而模型组MDA含量明显高于治疗组和正常组(P<0.05);治疗组大鼠肝脏线粒体ADP诱导的3态氧消耗、呼吸控制率(RCR)、氧化磷酸化率(OPR)明显高于TAA模型组(P<0.05);注射TAA和sHSS后,线粒体肿胀和跨膜电位没有明显的变化。结论sHSS能明显抑制TAA造成的急性肝损伤和脂质过氧化,改善因TAA而受损的线粒体呼吸功能。
Objective To investigate the effects of shark liver stimulant (sHSS) on acute liver injury and hepatic mitochondrial function induced by thioacetamide (TAA) in rats. Methods Male SD rats weighing 200 ± 20 g were randomly divided into 3 groups: control group, model group and treatment group, with 8 rats in each group. The model of acute liver injury was established by intraperitoneal injection of 400mg / kg TAA2. The rats in the treatment group were intraperitoneally injected with 80mg / kgsHSS 1h before TAA injection, and the control group were injected with equal volume of normal saline. After 24 hours, the alanine aminotransferase (ALT), aspartate aminotransferase (AST) and malondialdehyde (MDA) content in the liver, as well as the effects of TAA and sHSS on mitochondria respiratory function, mitochondria swelling and membrane potential. Results The levels of ALT and AST in the serum of rats in the treatment group were significantly lower than those in the untreated group, while the levels of MDA in the model group were significantly higher than those in the untreated group and the normal group (P <0.05) , Respiratory rate (RCR) and oxidative phosphorylation rate (OPR) in TAA model group were significantly higher than those in TAA model group (P <0.05). There was no significant change in mitochondrial swelling and transmembrane potential after TAA and sHSS injection. Conclusion sHSS can significantly inhibit TAA-induced acute liver injury and lipid peroxidation, and improve mitochondrial respiratory function damaged by TAA.