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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。
Objective To investigate the effect of chronic aluminum overload on liver function and morphology in rats and to observe its mechanism. Methods Wistar rats were given aluminum aluminum gluconate (Al3 + 200 mg / kg) once a day for 5 days a week for 20 weeks. A chronic aluminum overload rat model was established. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), glutamyl transpeptidase (GGT), and hepatic superoxide (SOD) activity and malondialdehyde (MDA) content in the liver tissue were measured. The content of Al3 + in liver tissue was detected by plasma atomic emission spectrophotometer. The pathological changes of liver tissue were observed by HE staining. Results Chronic aluminum overload induced a significant increase of aluminum content in rat liver tissue. Hepatic cells showed obvious vacuolar degeneration, granular degeneration and punctate necrosis, plasma ALT and AST concentrations increased, ALP and GGT levels were significantly increased, and liver tissue SOD activity was significantly decreased and MDA content increased significantly (both P <0.01). Conclusion Chronic aluminum overload can cause hepatic injury in rats, and its mechanism may be related to the promotion of oxidative stress by aluminum.