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23-乙酰泽泻醇B对急性酒精性肝损伤小鼠的保护作用及机制
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| 篇名： | 23-乙酰泽泻醇B对急性酒精性肝损伤小鼠的保护作用及机制 |
| TITLE： | Protective effects and mechanism of alisol B 23-acetate on acute alcoholic liver injury in mice |
| 摘要： | 目的 探讨23-乙酰泽泻醇B对急性酒精性肝损伤小鼠的保护作用及潜在机制。方法将50只雄性昆明小鼠分为空白组、模型组和23-乙酰泽泻醇B低、中、高剂量组（10、20、40mg/kg），每组10只。各组小鼠灌胃相应药液或生理盐水，每天1次，持续2周。于实验第15天，空白组小鼠灌胃生理盐水，其余4组小鼠灌胃12mL/kg的白酒，共2次（间隔6h）以建立急性酒精性肝损伤小鼠模型。实验期间，监测小鼠体重；于实验第16天，计算各组小鼠肝脏指数，检测其血清中丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、总胆固醇（TC）、甘油三酯（TG）、丙二醛（MDA）、谷胱甘肽（GSH）水平，观察其肝组织病理形态并进行评分，检测肝组织中细胞色素P4502E1（CYP2E1）、Kelch样环氧氯丙烷相关蛋白1（Keap1）、核转录因子红系2相关因子2（Nrf2）、NAD（P）H：醌氧化还原酶1（NQO1）蛋白的表达水平。结果与模型组比较，23-乙酰泽泻醇B各剂量组小鼠体重均有不同程度恢复；肝组织炎症细胞浸润、脂肪空泡等病理改变均有不同程度改善；其肝脏指数，肝组织病理形态评分，血清ALT、AST、TC、TG、MDA水平，以及肝组织中CYP2E1、Keap1蛋白的表达水平均显著降低（P＜0.05或P＜0.01）；血清GSH水平及肝组织中Nrf2（23-乙酰泽泻醇B低剂量组除外）、NQO1蛋白的表达水平均显著升高（P＜0.05或P＜0.01），且上述定量指标的变化呈剂量依赖趋势。结论23-乙酰泽泻醇B能改善酒精急性暴露所引发的小鼠肝损伤，其机制可能与调控Keap1/Nrf2/NQO1信号通路以发挥抗氧化应激作用，同时改善肝脏脂质代谢有关。 |
| ABSTRACT： | OBJECTIVE To investigate the protective effects and potential mechanism of alisol B 23-acetate on acute alcoholic liver injury in mice. METHODS Fifty male Kunming mice were divided into the blank group， model group， and alisol B 23-acetate low-， medium- and high-dose groups （10， 20， 40 mg/kg）， with 10 mice in each group. Each group was given relevant drug solution or normal saline intragastrically， once a day， for 2 consecutive weeks. On the 15th day， mice in the blank group were given normal saline intragastrically， while the other four groups were given 12 mL/kg white wine intragastrically， twice at six-hour intervals， to establish an acute alcoholic liver injury model. On the 16th day of the experiment， the liver indexes of mice in each group were calculated； the serum levels of alanine transaminase （ALT）， aspartate transaminase （AST）， total cholesterol （TC）， triglycerides （TG）， malondialdehyde （MDA） and glutathione （GSH） were also determined. The histopathological morphology of their liver tissues was observed and scored. The protein expressions of cytochrome P450 2E1 （CYP2E1）， Kelch-like ECH-associated protein 1 （Keap1）， nuclear factor erythroid 2-related factor 2 （Nrf2） and NAD（P）H： quinone oxidoreductase 1 （NQO1） were measured in liver tissue. RESULTS Compared with model group， mice in each dosage group of alisol B 23-acetate showed varying degrees of recovery in body weight， along with improvements in pathological changes in liver tissues such as inflammatory cell infiltration and fatty vacu oles. Their liver indexes， histopathological scores of liver tissue， serum levels of ALT， AST， TC， TG and MDA， as well as the protein expressions of CYP2E1 and Keap1 in liver tissue， were all significantly decreased （ P ＜0.05 or P ＜0.01）. The serum GSH levels and the protein expressions of Nrf2 （except for the alisol B 23-acetate low-dose group） and NQO1 in liver tissue were significantly increased （ P ＜0.05 or P ＜0.01）， and the changes in the above quantitative indicators showed a dose-dependent pattern. CONCLUSIONS Alisol B 23-acetate can ameliorate acute alcoholic liver injury in mice， and its mechanism may be related to improving antioxidant capacity by regulating the Keap1/Nrf2/NQO1 signaling pathway while simultaneously improving liver lipid metabolism-related indexes. |
| 期刊： | 2026年第37卷第06期 |
| 作者： | 魏小果；慕淑丽；杨帆；李海娥；罗舒丹；车晓娜 |
| AUTHORS： | WEI Xiaoguo，MU Shuli，YANG Fan，LI Hai’e，LUO Shudan，CHE Xiaona |
| 关键字： | 23-乙酰泽泻醇B；急性酒精性肝损伤；抗氧化；脂质代谢；Keap1/Nrf2/NQO1信号通路 |
| KEYWORDS： | alisol B 23-acetate； acute alcoholic liver injury； antioxidant； lipid metabolism； Keap1/Nrf2/NQO1 signaling |
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