Protective role of adiponectin against ethanol-induced gastric injury in mice

Author:

Yamamoto Shunsuke1,Watabe Kenji1,Araki Hiroshi2,Kamada Yoshihiro1,Kato Motohiko1,Kizu Takashi1,Kiso Shinichi1,Tsutsui Shusaku2,Tsujii Masahiko1,Kihara Shinji3,Funahashi Tohru4,Shimomura Iichiro5,Hayashi Norio6,Takehara Tetsuo1

Affiliation:

1. Department of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine;

2. Department of Gastroenterology and Hepatology, Itami City Hospital;

3. Department of Biomedical Informatics,

4. Departments of 4Metabolism and Atherosclerosis and

5. Metabolic Medicine, Osaka University Graduate School of Medicine, Osaka; and

6. Kansai Rosai Hospital, Hyogo, Japan

Abstract

Adiponectin is an anti-inflammatory molecule released from adipocytes, and serum adiponectin concentrations are reduced in obesity. We previously reported that gastric erosion occurs in association with obesity and low serum adiponectin levels. In the present study, we examined adiponectin-knockout (APN-KO) mice to elucidate the role of adiponectin in gastric mucosal injury. Gastric injury was induced by oral administration of ethanol in wild-type (WT) and APN-KO mice. Ethanol treatment induced severe gastric injury in APN-KO mice compared with WT mice. In APN-KO mice, increased apoptotic cells and decreased expression of prostaglandin E2 (PGE2) were detected in the injured stomach. We next assessed the effect of adiponectin on the cellular response to ethanol treatment and wound repair in rat gastric mucosal cells (RGM1). Adiponectin induced the expression of PGE2 and cyclooxygenase 2 (COX-2) in ethanol-treated RGM1 cells. RGM1 cells exhibited efficient wound repair accompanied by increased PGE2 expression in the presence of adiponectin. Coadministration of adiponectin with celecoxib, a COX-2 inhibitor, inhibited efficient wound repair. These findings indicate that adiponectin has a protective role against ethanol-induced gastric mucosal injury in mice. This effect may be partially mediated by the efficient wound repair of epithelial cells via increased PGE2 expression.

Publisher

American Physiological Society

Subject

Physiology (medical),Gastroenterology,Hepatology,Physiology

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