Ursolic acid ameliorates CCl4-induced liver fibrosis through the NOXs/ROS pathway

被引:69
作者
Gan, Dakai [1 ]
Zhang, Wang [2 ]
Huang, Chenkai [2 ]
Chen, Jiang [2 ]
He, Wenhua [2 ]
Wang, Anjiang [2 ]
Li, Bimin [2 ]
Zhu, Xuan [2 ]
机构
[1] Ninth Hosp Nanchang, Dept Liver Dis 1, Nanchang, Jiangxi, Peoples R China
[2] Nanchang Univ, Affiliated Hosp 1, Dept Gastroenterol, 17 Yongwai Main St, Nanchang 330006, Jiangxi, Peoples R China
基金
中国国家自然科学基金;
关键词
hepatic stellate cells; hepatocytes; Kupffer cells; ursolic acid; NADPH OXIDASES; OXIDATIVE STRESS; DYSFUNCTION; ACTIVATION; APOPTOSIS; INJURY; RAT;
D O I
10.1002/jcp.26541
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Liver fibrosis is a reversible wound-healing response that occurs after liver injury. NADPH oxidases (NOXs) and reactive oxygen species (ROS) which are expressed in hepatocytes (HCs), hepatic stellate cells (HSCs), and Kupffer cells (KCs) play an important role in the development of hepatic fibrosis. In in vitro studies, we had shown that ursolic acid (UA) could reverse liver fibrosis by inhibiting the activation of NOX-mediated fibrotic signaling networks in HSCs. In this study, we verified that UA could alleviate CCl4-induced liver fibrosis by reducing the expression of NOXs/ROS in HCs, HSCs, KCs. Meanwhile, the phagocytic index and clearance index K which represent phagocytosis of KCs were unchanged. Together, all our data demonstrated that UA induced the proliferation of HCs, promoted apoptosis in HSCs, and prevented activation of KCs in vivo by reducing the expression of NOXs/ROS in HCs, HSCs, KCs. Besides, UA had no effect on the host defense function.
引用
收藏
页码:6799 / 6813
页数:15
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