The Hepatoprotection by Oleanolic Acid Preconditioning: Focusing on PPARα Activation.

IF 3.5 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL PPAR Research Pub Date : 2018-04-02 eCollection Date: 2018-01-01 DOI:10.1155/2018/3180396
Wenwen Wang, Kan Chen, Yujing Xia, Wenhui Mo, Fan Wang, Weiqi Dai, Peiqin Niu
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引用次数: 19

Abstract

Objective: Previous studies have characterized the hepatoprotective and anti-inflammatory properties of oleanolic acid (OA). This study aimed to investigate the molecular mechanisms of OA hepatoprotection in concanavalin A- (ConA-) induced acute liver injury.

Materials and methods: ConA (20 mg/kg) was intravenously injected to induce acute liver injury in Balb/C mice. OA pretreatment (20, 40, and 80 mg/kg) was administered subcutaneously once daily for 3 consecutive days prior to treatment with ConA; 2, 8, and 24 h after ConA injection, the levels of serum liver enzymes and the histopathology of major factors and inflammatory cytokines were determined.

Results: OA reduced the release of serum liver enzymes and inflammatory factors and prevented ConA mediated damage to the liver. OA elevated the expression levels of peroxisome proliferator-activated receptor alpha (PPARα) and decreased the phosphorylation of c-Jun NH2-terminal kinase (JNK).

Conclusion: OA exhibits anti-inflammatory properties during ConA-induced acute liver injury by attenuating apoptosis and autophagy through activation of PPARα and downregulation of JNK signaling.

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齐墩果酸预处理对肝脏的保护作用:以PPARα激活为重点。
目的:已有研究证实齐墩果酸(OA)具有保护肝脏和抗炎的作用。本研究旨在探讨OA在刀豆蛋白A- (ConA-)诱导的急性肝损伤中保护肝的分子机制。材料与方法:采用静脉注射ConA (20 mg/kg)诱导Balb/C小鼠急性肝损伤。在ConA治疗前,OA预处理(20、40和80 mg/kg)每天皮下注射一次,连续3天;注射ConA后2、8、24 h测定大鼠血清肝酶水平及主要因子和炎症因子的组织病理学变化。结果:OA降低了血清肝酶和炎症因子的释放,防止了ConA介导的肝脏损伤。OA升高过氧化物酶体增殖物激活受体α (PPARα)的表达水平,降低c-Jun nh2末端激酶(JNK)的磷酸化水平。结论:OA在cona诱导的急性肝损伤中具有抗炎作用,其机制是通过激活PPARα和下调JNK信号通路,从而减弱细胞凋亡和自噬。
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来源期刊
PPAR Research
PPAR Research MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
6.20
自引率
3.40%
发文量
17
审稿时长
12 months
期刊介绍: PPAR Research is a peer-reviewed, Open Access journal that publishes original research and review articles on advances in basic research focusing on mechanisms involved in the activation of peroxisome proliferator-activated receptors (PPARs), as well as their role in the regulation of cellular differentiation, development, energy homeostasis and metabolic function. The journal also welcomes preclinical and clinical trials of drugs that can modulate PPAR activity, with a view to treating chronic diseases and disorders such as dyslipidemia, diabetes, adipocyte differentiation, inflammation, cancer, lung diseases, neurodegenerative disorders, and obesity.
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