Japanese herbal medicine, Saiko-keishi-to, prevents gut ischemia/reperfusion-induced liver injury in rats via nitric oxide

doi:10.3748/wjg.v10.i15.2241

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Aug 1, 2004 (publication date) through Nov 5, 2024

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World Journal of Gastroenterology

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1007-9327

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Gastroenterol. Aug 1, 2004; 10(15): 2241-2244
Published online Aug 1, 2004. doi: 10.3748/wjg.v10.i15.2241

Japanese herbal medicine, Saiko-keishi-to, prevents gut ischemia/reperfusion-induced liver injury in rats via nitric oxide

Yoshinori Horie, Mikio Kajihara, Shuka Mori, Yoshiyuki Yamagishi, Hiroyuki Kimura, Hironao Tamai, Shinzo Kato, Hiromasa Ishii

Yoshinori Horie, Mikio Kajihara, Shuka Mori, Yoshiyuki Yamagishi, Hiroyuki Kimura, Hironao Tamai, Shinzo Kato, Hiromasa Ishii, Department of Internal Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan

Supported by the Grants from Tsumura Co. Ltd

Correspondence to: Yoshinori Horie, M.D., Department of Internal Medicine, School of Medicine, Keio University, 35 Shinanomachi Shinjuku-ku, Tokyo 160-8582, Japan. yhorie@sc.itc.keio.ac.jp

Telephone: +81-3-5363-3789 Fax: +81-3-3356-9654

Received: February 6, 2004
Revised: February 23, 2004
Accepted: March 26, 2004
Published online: August 1, 2004

Abstract

AIM: To determine whether Saiko-keishi- to (TJ-10), a Japanese herbal medicine, could protect liver injury induced by gut ischemia/reperfusion (I/R), and to investigate the role of NO.

METHODS: Male Wistar rats were exposed to 30-min gut ischemia followed by 60 min of reperfusion. Intravital microscopy was used to monitor leukocyte recruitment. Plasma tumor necrosis factor (TNF) levels and alanine aminotransferase (ALT) activities were measured. TJ- 10 1 g/(kg·d) was intragastrically administered to rats for 7 d. A NO synthase inhibitor was administered.

RESULTS: In control rats, gut I/R elicited increases in the number of stationary leukocytes, and plasma TNF levels and ALT activities were mitigated by pretreatment with TJ-10. Pretreatment with the NO synthase inhibitor diminished the protective effects of TJ-10 on leukostasis in the liver, and the increase of plasma TNF levels and ALT activities. Pretreatment with TJ-10 increased plasma nitrite/nitrate levels.

CONCLUSION: TJ-10 attenuates the gut I/R-induced hepatic microvascular dysfunction and sequential hepatocellular injury via enhancement of NO production.

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