目的 基于核因子E2相关因子2（nuclear factor E2 related factor 2，Nrf2）-抗氧化反应元件（antioxidant response element，ARE）信号通路研究竹节参多糖（Panax japonicus polysaccharide）保护四氯化碳（carbon tetrachloride，CCl₄）所致大鼠急性肝损伤的作用机制。方法 通过CCl₄间隔诱导法建立急性肝损伤大鼠模型，给予水提醇沉法制备的竹节参多糖治疗7 d后取材，通过苏木素-伊红（HE）染色观察肝组织病理变化；全自动生化仪检测大鼠血清中肝功能相关指标；ELISA法检测肝组织氧化应激水平；免疫组化法观察大鼠肝组织Nrf2表达；Western blotting测定大鼠肝组织Nrf2-ARE通路相关蛋白表达。结果 与模型组比较，竹节参多糖组大鼠血清中肝功能相关指标呈不同程度的降低（P<0.05、0.01），肝组织中Nrf2-ARE信号通路明显激活（P<0.01），肝脏中脂类过氧化产物丙二醛（malondialdehyde，MDA）水平降低（P<0.01），抗氧化酶活性明显升高（P<0.05、0.01），细胞质中氧化应激效应物Nrf2阳性的细胞数有所减少（P<0.01），大鼠肝脏损伤程度明显减轻。结论 竹节参多糖可激活Nrf2-ARE信号通路，增强机体的抗氧化酶系表达，减轻CCl₄引起的氧化损伤。

Objective To study the protective mechanism of Panax japonicus polysaccharide (PSPJ) against carbon tetrachloride (CCl₄) induced acute liver injury in rats through nuclear factor E2 related factor 2 (Nrf2)-antioxidant response element (ARE) signal pathway. Methods A rat model of acute liver injury was established using the CCl₄ interval induction method. After 7 d of treatment with PSPJ prepared by water extraction and alcohol precipitation method, samples were taken and liver tissue pathological changes were observed by hematoxylin eosin (HE) staining; Liver function related indicators in serum of rat were detected by fully automated biochemical analyzer; ELISA method was used to detect oxidative stress level in liver tissue; Immunohistochemical method was used to observe the expression of Nrf2 in liver tissue of rats; Western blotting was used to determine the expressions of Nrf2-ARE pathway related proteins in liver tissue of rats. Results Compared with model group, liver function related indicators in serum of rats treated with PSPJ showed varying degrees of decrease (P < 0.05, 0.01), Nrf2-ARE signaling pathway was significantly activated in liver tissue (P< 0.01), level of lipid peroxidation product malondialdehyde (MDA) in liver was reduced (P < 0.01), and activity of antioxidant enzymes was significantly increased (P < 0.05, 0.01), the number of cells with Nrf2 positive oxidative stress effector in cytoplasm was decreased (P < 0.01), and the degree of liver damage in rats was significantly reduced. Conclusion PSPJ can activate the Nrf2-ARE signaling pathway, enhance the expression of antioxidant enzymes in body, and alleviate oxidative damage caused by CCl₄.

R285.5

湖北省自然科学基金青年项目（2019CFB358）；国家自然科学基金青年基金项目（81801979）