Zou Liyi, Chen Shaoru, Li Li, Wu Tie
School of Pharmacy, Guangdong Medical University, Dongguan 523-808, China.
State key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.
Exp Toxicol Pathol. 2017 Sep 5;69(7):451-460. doi: 10.1016/j.etp.2017.04.001. Epub 2017 Apr 20.
Hyperoside was used to treat cardiovascular disease for many years in China. It was shown great effect on regulation of lipid metabolism. But there is lack of reports about the effects of hyperoside on liver diseases.
This study was designed to investigate the potentially protective effects of hyperoside and the role of transcription factor nuclear factor-erythroid 2(NF-E2)-related factor 2 (Nrf2) signaling in the regulation on Carbon Tetrachloride (CCl)-induced chronic liver fibrosis in mice.
All mice were divided into six groups containing 6 animals per group. Mice in different group were given relative processing for 4 weeks. The potentially protective effects of hyperoside on CCl-induced chronic liver fibrosis in mice were depicted histologically and biochemically.
CCl administration caused a marked increase in the levels of serum aminotransferases, serum monoamine oxidase (MAO) and lipid peroxidation, MAO in mouse liver homogenates. Also decreased activities of cellular antioxidant defense enzymes were found after CCl exposure. Histopathological changes induced by CCl including regenerative nodules, deteriorated parenchyma. Hyperoside and silymarin reduced these changes and attenuated the pathological effects of CCl induced liver injury. In addition, hyperoside exhibited antioxidant effects in vitro. In Western blot analysis, the protein level of Nrf2 was downregulated after CCl administration and reversed by hyperoside.
Hyperoside increased the activity of the antioxidant and phase II detoxifying enzymes through the activation of Nrf2 nuclear translocated in the CCl-induced liver fibrosis mice.
在我国，金丝桃苷多年来一直用于治疗心血管疾病。它在调节脂质代谢方面显示出显著效果。但关于金丝桃苷对肝脏疾病影响的报道较少。
本研究旨在探讨金丝桃苷的潜在保护作用以及转录因子核因子红系2相关因子2（Nrf2）信号通路在调节四氯化碳（CCl）诱导的小鼠慢性肝纤维化中的作用。
将所有小鼠分为六组，每组6只。对不同组的小鼠进行相关处理4周。通过组织学和生化方法描述金丝桃苷对CCl诱导的小鼠慢性肝纤维化的潜在保护作用。
给予CCl后，小鼠血清转氨酶、血清单胺氧化酶（MAO）水平及脂质过氧化水平显著升高，小鼠肝脏匀浆中的MAO也升高。CCl暴露后还发现细胞抗氧化防御酶活性降低。CCl诱导的组织病理学变化包括再生结节、实质恶化。金丝桃苷和水飞蓟宾减轻了这些变化，减弱了CCl诱导的肝损伤的病理效应。此外，金丝桃苷在体外表现出抗氧化作用。在蛋白质印迹分析中，给予CCl后Nrf2蛋白水平下调，而金丝桃苷可使其逆转。
在CCl诱导的肝纤维化小鼠中，金丝桃苷通过激活Nrf2核转位增加了抗氧化酶和Ⅱ相解毒酶的活性。
