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目的：探讨山莨菪碱对急性肝损伤的保护作用及其作用机制。方法：雄性Ｗｉｓｔａｒ大鼠１８只随机分为３组：正常对照组、模型组和山莨菪碱组。以Ｄ半乳糖胺加内毒素脂多糖制成大鼠急性肝损伤模型。用山莨菪碱（２０ｍｇ／ｋｇ）预处理模型鼠。观察３组大鼠肝酶含量，血清一氧化氮（ＮＯ）含量，肝组织中ＮＯ、丙二醛（ＭＤＡ）含量和超氧化物歧化酶（ＳＯＤ）活性及肝组织病理学变化。结果：山莨菪碱组大鼠丙氨酸转氨酶〔ＡＬＴ（６６６±２６７）Ｕ〕、天冬氨酸转氨酶〔ＡＳＴ（１０５９±４０８）Ｕ〕及血清总胆红素〔ＴＢＩＬ（７．２２±５．６２）μｍｏｌ／Ｌ〕均明显低于模型组〔分别为（２３５２±６９８）Ｕ，（３５４９±７１７）Ｕ和（２０．７１±５．９２）μｍｏｌ／Ｌ〕，Ｐ均＜０．０１；伴随着山莨菪碱对血及肝组织中ＮＯ过量合成的抑制，肝组织中ＭＤＡ降低、ＳＯＤ增高（Ｐ均＜０．０１）。山莨菪碱组肝组织病理改变较模型组明显减轻。结论：山莨菪碱对大鼠急性肝损伤有保护作用，保护作用可能与山莨菪碱抑制ＮＯ的过量产生及清除自由基有关。
Objective: To investigate the protective effect of anisodamine on acute liver injury and its mechanism. Methods: Eighteen male Wistar rats were randomly divided into three groups: normal control group, model group and anisodamine group. D-galactosamine plus endotoxin lipopolysaccharide was used to establish rat acute liver injury model. Model rats were pretreated with anisodamine (20 mg / kg). The levels of liver enzyme, serum nitric oxide (NO), NO, malondialdehyde (MDA) and superoxide dismutase (SOD) activity and liver histopathological changes in the three groups were observed. Results: In the anisodamine group, the levels of ALT (666 ± 267 U), aspartate aminotransferase (AST (1059 ± 408) U and TBIL (7.22 ± 5) .62) μmol / L] were significantly lower than those in the model group (2352 ± 698 U, 3549 ± 717 U and 20.71 ± 5.92 μmol / L, respectively) ; Accompanied by the inhibition of Anisodamine on the overproduction of NO in blood and liver tissue, MDA in liver tissue decreased and SOD increased (P <0.01). Anisodamine group liver pathological changes than the model group was significantly reduced. Conclusion: Anisodamine has a protective effect on acute liver injury in rats, which may be related to the inhibitory effect of anisodamine on the overproduction of NO and the scavenging of free radicals.