【摘要】 目的探讨慢性铝过负荷对大鼠肝功能和形态学影响,并初步观察其机制。方法 Wistar大鼠灌胃给予葡萄糖酸铝(Al3+200 mg/kg),1次/d,每周5 d,连续20 w,建立慢性铝过负荷大鼠模型。采用生化方法检测大鼠血浆丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALP)、谷氨酰转肽酶(GGT),以及肝超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量;采用等离子体原子发射光谱分光光度仪检测肝组织Al3+含量;采用HE染色观察大鼠肝组织病理形态变化。结果慢性铝过负荷致大鼠肝组织铝含量明显增高,肝细胞出现明显空泡变性、颗粒变性和点状坏死,血浆ALT和AST浓度有增高的趋势,ALP和GGT水平显著升高,肝组织SOD活性明显降低和MDA含量明显增加(均P<0.01)。结论慢性铝过负荷可致大鼠肝损伤,其机制可能与铝促进氧化应激有关。更多还原

【Abstract】 Objective To investigate effects of chronic aluminum overload on rat liver function and histomorphology and explore its mechanisms.Methods Wistar rats were intragastric administered aluminum gluconate(200 mg Al3+/kg),once a day,5 days a week for 20 weeks.Biochemistry method was used to detect activity of serum ALT,AST,ALP,GGT and liver SOD and the content of liver MDA.Morphologic changes of liver were evaluated by HE staining.The aluminum level was measured by ICP-AES.Results Aluminum content significantly was increased in chronic aluminum overload rat liver.Liver cells showed a significant vacuolar degeneration,granular degeneration and necrosis.Serum ALP and GGT level were significantly increased while ALT and AST levels had a trend of increase.SOD activity of liver was significantly decreased and MDA content was significantly increased in chronic aluminum overload rat.Conclusions Chronic aluminum overload can induce liver injury in rat and its mechanism involves in the pro-oxidation of aluminum.更多还原