Protective effect of oil from Cornus wilsoniana fruits against carbon tetrachloride-induced hepatic fibrosis in mice

Protective effect of oil from Cornus wilsoniana fruits against carbon tetrachloride-induced hepatic fibrosis in mice
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山茱萸果油对四氯化碳所致小鼠肝纤维化的保护作用

DOI:
10.29219/fnr.v64.4205
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发表时间:
2020-05-08
影响因子:
3.3
通讯作者:
Xu, Xundi
Xu, Xundi
中科院分区:
农林科学3区
文献类型:
--
作者:
Liu, Qiang;Lei, Xiaohua;Xu, Xundi

文献摘要

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背景:毛皮是中国南部分布广泛的木本油料植物,几百年来,从其果实中提取的油脂一直是当地居民食用油的主要来源。已有研究表明,山茱萸油(CWO)对大鼠具有降血脂作用。然而,CWO的保肝作用及其机制尚不清楚。目的:探讨CWO对四氯化碳(CCl4)诱导的小鼠肝纤维化的保护作用及其机制。方法:以1 m L/kg CCl4(橄榄油1:4混合液)腹腔注射复制小鼠肝纤维化模型,每周2次,共6周。同时给予CWO(0.5,2mL/kg)灌胃,1次/d,连续6周。检测肝脏的血清学变化、氧化应激、炎症反应和组织学改变。结果:血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、III型前胶原、IV型胶原、透明质酸、层粘连蛋白等血清学指标显示,CWO可显著减轻CCl4诱导的小鼠血清学改变。同时,CWO显著改善了CCl4诱导的肝组织学改变,苏木精伊红(H&E)、天狼星红和Masson‘s三色染色检测到了这一点。此外,使用CWO治疗可减少肝脏中的氧化应激和炎症。此外,CwO还可降低CCl4诱导的肝组织细胞外基质的表达,转化生长因子-β1/Smad3信号通路可能参与了该过程。结论:CWO通过减轻肝脏氧化应激,减轻肝脏炎症反应,抑制肝内转化生长因子-β1/Smad3信号通路,从而减轻CCl4诱导的肝纤维化。CWO可能是一种潜在的有益于肝纤维化辅助治疗的食用油。
Background: Cornus wilsoniana Wanger is a widely distributed woody oil plant in south China; oil extracted from its fruits has been the main source of edible oil for local residents for hundreds of years. Previous studies have demonstrated that Cornus wilsoniana oil (CWO) has hypolipidemic activity in rats. However, the hepatoprotective effects of CWO and their underlying mechanisms are not clear. Objective: The purpose of this study was to explore the protective effects and mechanisms of the CWO against carbon tetrachloride (CCl4)-induced hepatic fibrosis in mice. Methods: Hepatic fibrosis mouse model was induced by intraperitoneal injection with 1 mL/kg CCl4 (mixed 1:4 in olive oil) twice a week for 6 weeks. In the meantime, the mice were orally administrated with CWO (0.5, 2 mL/kg) once daily for 6 weeks. Serological changes as well as oxidative stress, inflammatory, and histological alteration in the liver were determined. Results: The results showed that CWO significantly attenuated CCl4-induced serological changes in mice, as assessed by serum markers, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), procollagen III, collagen type IV, hyaluronic acid, and laminin. At the same time, CWO significantly improved CCl4-induced liver histological changes, as detected by hematoxylin and eosin (H&E), Sirius red, and Masson’s trichrome staining. In addition, treatment with CWO reduced oxidative stress and inflammation in the liver. Furthermore, CWO also reduced the expression of extracellular matrix (ECM) in liver induced by CCl4, and TGF-β1/Smad3 signaling may be involved in the process. Conclusions: CWO ameliorates CCl4-induced hepatic fibrosis by attenuating hepatic oxidative stress, reducing hepatic inflammation and inhibiting TGF-β1/Smad3 signaling pathway in liver. CWO may be a potentially beneficial edible oil for the adjuvant treatment of hepatic fibrosis.