The protective effect of hyperoside on carbon tetrachloride-induced chronic liver fibrosis in mice via upregulation of Nrf2

Q2 Medicine
Liyi Zou , Shaoru Chen , Li Li , Tie Wu
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引用次数: 36

Abstract

Context

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.

Objective

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 (CCl4)-induced chronic liver fibrosis in mice.

Materials and methods

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 CCl4-induced chronic liver fibrosis in mice were depicted histologically and biochemically.

Results

CCl4 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 CCl4 exposure. Histopathological changes induced by CCl4 including regenerative nodules, deteriorated parenchyma. Hyperoside and silymarin reduced these changes and attenuated the pathological effects of CCl4 induced liver injury. In addition, hyperoside exhibited antioxidant effects in vitro. In Western blot analysis, the protein level of Nrf2 was downregulated after CCl4 administration and reversed by hyperoside.

Conclusion

Hyperoside increased the activity of the antioxidant and phase II detoxifying enzymes through the activation of Nrf2 nuclear translocated in the CCl4-induced liver fibrosis mice.

金丝桃苷通过上调Nrf2对四氯化碳诱导的小鼠慢性肝纤维化的保护作用
在中国,花蔷薇苷用于治疗心血管疾病已有多年历史。对脂质代谢有明显的调节作用。但是关于金丝桃苷对肝脏疾病的影响还缺乏报道。目的探讨金丝桃苷对小鼠慢性肝纤维化的潜在保护作用及转录因子核因子-红细胞2(NF-E2)相关因子2(Nrf2)信号通路在四氯化碳(CCl4)诱导的小鼠慢性肝纤维化中的作用。材料与方法将小鼠分为6组,每组6只。各组小鼠给予相对加工4周。从组织学和生化角度描述了金丝桃苷对ccl4诱导的小鼠慢性肝纤维化的潜在保护作用。暴露于CCl4后,细胞抗氧化防御酶活性降低。CCl4引起的组织病理学改变包括再生结节,恶化的实质。金丝桃苷和水飞蓟素减轻了这些变化,减轻了CCl4诱导的肝损伤的病理影响。此外,金丝桃苷在体外也表现出抗氧化作用。Western blot分析显示,CCl4给药后Nrf2蛋白水平下调,金丝桃苷逆转Nrf2蛋白水平。结论金丝桃苷通过激活ccl4诱导的肝纤维化小鼠Nrf2核易位,提高抗氧化酶和II期解毒酶的活性。
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来源期刊
CiteScore
2.08
自引率
0.00%
发文量
0
审稿时长
5.3 weeks
期刊介绍: Cessation. The international multidisciplinary journal is devoted to the publication of studies covering the whole range of experimental research on disease processes and toxicology including cell biological investigations. Its aim is to support progress in the interdisciplinary cooperation of researchers working in pathobiology, toxicology, and cell biology independent of the methods applied. During the past decades increasing attention has been paid to the importance of toxic influence in the pathogenesis of human and animal diseases. This is why Experimental and Toxicologic Pathology meets the urgent need for an interdisciplinary journal felt by a wide variety of experts in medicine and biology, including pathologists, toxicologists, biologists, physicians, veterinary surgeons, pharmacists, and pharmacologists working in academic, industrial or clinical institutions.
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