The Hepatoprotection by Oleanolic Acid Preconditioning: Focusing on PPARαActivation

Author:

Wang Wenwen1,Chen Kan1ORCID,Xia Yujing1ORCID,Mo Wenhui2,Wang Fan3,Dai Weiqi45,Niu Peiqin16ORCID

Affiliation:

1. Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China

2. Department of Gastroenterology, Minhang Hospital, Fudan University, Shanghai 201100, China

3. Department of Oncology, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200080, China

4. Department of Gastroenterology, Zhongshan Hospital, Fudan University, Shanghai 200032, China

5. Shanghai Institute of Liver Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China

6. Shanghai Tenth People’s Hospital Chongming Branch, Tongji University School of Medicine, Shanghai 202157, China

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 PPARαand downregulation of JNK signaling.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Pharmacology (medical),Drug Discovery

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