目的 探究金盏银盘Bidens biternata（Lour.）Merr.&Sherff.水提液对四氯化碳诱导的急性肝损伤改善作用及其机制。方法 将60只雄性昆明小鼠随机分为对照组、模型组、水飞蓟素（0.15 g/kg）组和金盏银盘低、高剂量（3.9、7.8 g/kg）组，每组12只。各组小鼠连续ig给予相应药物7 d，末次给药后除对照组外均ip 0.4%四氯化碳构建急性肝损伤小鼠模型。24 h后收集小鼠血清及肝脏组织。用生化试剂盒检测血清中天门冬氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）、超氧化物歧化酶（SOD）活性及丙二醛（MDA）含量，并取肝组织匀浆检测谷胱甘肽过氧化物酶（GSH-Px）活性。采用苏木精-伊红染色（HE）切片观察小鼠肝脏病理变化。Western blotting测定肝组织中核因子E₂相关因子2（Nrf2）、抗体Kelch样ECH相关蛋白1（Keap1）、血红素氧合酶1（HO-1）蛋白的表达情况。结果 与模型组比较，金盏银盘水提液组小鼠组织病理学观察发现肝脏炎症细胞浸润明显减少，血清AST、ALT、MDA水平降低，血清SOD和肝组织GSH-Px活性升高（P＜0.05、0.01）；金盏银盘水提液组可以增加小鼠肝脏Nrf2和HO-1蛋白表达，抑制Keap1蛋白表达。结论 金盏银盘能够有效改善四氯化碳诱导的急性肝损伤，作用机制与激活Nrf2/Keap1信号通路抑制氧化应激损伤有关。

Objective To explore the protective effect and mechanism of Bidens biternata water extract on the acute liver injury in mice induced by CCl₄. Methods 60 Male Kunming mice were randomly divided into control group, model group, silymarin (0.15 g/kg), low and high-dose (3.9 and 7.8 g/kg) of B. biternata water extract, each group had 12 mice. Mice in each group were given the corresponding drug intragastrically for 7 days. After the last administration, all mice except the control group were given 0.4% CCl₄ to establish the model of acute liver injury. The serum and liver tissues of mice were collected 24 h later. The activities of AST, ALT, SOD, and MDA in serum were detected by biochemical kit, and GSH-Px activity was detected by liver homogenate. The pathological changes of liver were observed by hematoxylin - eosin staining (HE) sections. The expressions of Nrf2, Keap1, and HO-1 protein in liver were determined by Western blotting. Results Compared with model group, histopathological observation in B. biternata water extract group showed that liver inflammatory cell infiltration was significantly decreased, serum AST, ALT, and MDA levels were decreased, but SOD and liver GSH-Px activities were increased (P < 0.05, 0.01). The expression of Nrf2 and HO-1 protein was increased, and Keap1 protein was inhibited in the B. biternata water extract group. Conclusion B. biternata can effectively improve acute liver injury induced by CCl₄, and its mechanism is related to the activation of Nrf2/Keap1 signaling pathway to inhibit oxidative stress injury.

R285.5

中山市医学科研项目（2021A020743）