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Role of transforming growth factor-ß1 (TGF-ß1) in endotoxin-induced hepatic failure after extensive hepatectomy in rats

Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan, yosinobo{at}isis.ocn.ne.jp

Shinji Togo

Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Toru Kubota

Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Nobuyuki Kamimukai

Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Shuji Saito

Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Yasuhiko Nagano

Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Itaru Endo

Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Hitoshi Sekido

Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Yoji Nagashima

Department of Molecular Pathology and Oncology, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Hiroshi Shimada

Department of Gastroenterological Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan

Postoperative infections after hepatectomy sometimes lead to fatal hepatic failure, but the mechanism of the hepatic failure is unclear. Wistar rats underwent 90% hepatectomy, and were then divided into three groups: (i) the SAL group, injected with normal saline; (ii) the LPS group, injected with lipopolysaccharide (LPS) every day for 1 week; and (iii) the LPS plus TGF-Ab (LPS+TGF-Ab) group, injected with LPS with anti-transforming growth factor-ß1 (TGF-ß1) antibody. We investigated survival rates, TGF-ß1 expression in the liver, liver regeneration by proliferating cell nuclear antigen labeling index, hepatocyte apoptosis by single stranded DNA labeling index, and perisinusoidal fibrosis using Masson's trichrome staining. The LPS group (30.4%) had a significantly lower survival rate than the SAL group (84%) and tended to be lower than the LPS+TGF-Ab group (49.4%). Liver regeneration in the LPS group was significantly lower than in the other groups. In the LPS group, hepatocyte apoptosis and perisinusoidal fibrosis was significantly more remarkable, and TGF-ß1 expression was significantly higher than in the SAL group. TGF-ß1 enhanced by LPS plays an important role in the mechanism of hepatic failure by infections after hepatectomy, especially in inhibition of liver regeneration, and induction of hepatocyte apoptosis and perisinusoidal fibrosis.

Key Words: TGF-ß1 • endotoxin • hepatic failure • hepatectomy • rats • liver regeneration • hepatocyte apoptosis • perisinusoidal fibrosis

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