目的 探究金盞銀盤Bidens biternata（Lour.）Merr.&Sherff.水提液對四氯化碳誘導(dǎo)的急性肝損傷改善作用及其機(jī)制。方法 將60只雄性昆明小鼠隨機(jī)分為對照組、模型組、水飛薊素（0.15 g/kg）組和金盞銀盤低、高劑量（3.9、7.8 g/kg）組，每組12只。各組小鼠連續(xù)ig給予相應(yīng)藥物7 d，末次給藥后除對照組外均ip 0.4%四氯化碳構(gòu)建急性肝損傷小鼠模型。24 h后收集小鼠血清及肝臟組織。用生化試劑盒檢測血清中天門冬氨酸氨基轉(zhuǎn)移酶（AST）、丙氨酸氨基轉(zhuǎn)移酶（ALT）、超氧化物歧化酶（SOD）活性及丙二醛（MDA）含量，并取肝組織勻漿檢測谷胱甘肽過氧化物酶（GSH-Px）活性。采用蘇木精-伊紅染色（HE）切片觀察小鼠肝臟病理變化。Western blotting測定肝組織中核因子E₂相關(guān)因子2（Nrf2）、抗體Kelch樣ECH相關(guān)蛋白1（Keap1）、血紅素氧合酶1（HO-1）蛋白的表達(dá)情況。結(jié)果 與模型組比較，金盞銀盤水提液組小鼠組織病理學(xué)觀察發(fā)現(xiàn)肝臟炎癥細(xì)胞浸潤明顯減少，血清AST、ALT、MDA水平降低，血清SOD和肝組織GSH-Px活性升高（P＜0.05、0.01）；金盞銀盤水提液組可以增加小鼠肝臟Nrf2和HO-1蛋白表達(dá)，抑制Keap1蛋白表達(dá)。結(jié)論 金盞銀盤能夠有效改善四氯化碳誘導(dǎo)的急性肝損傷，作用機(jī)制與激活Nrf2/Keap1信號通路抑制氧化應(yīng)激損傷有關(guān)。

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

中山市醫(yī)學(xué)科研項(xiàng)目（2021A020743）