Brief Report
Copyright ©The Author(s) 1997. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 15, 1997; 3(2): 103-103
Published online Jun 15, 1997. doi: 10.3748/wjg.v3.i2.103
Effect of amygdalin on proliferation of rat hepatic fat-storing cells and collagen production in vitro
Lie-Ming Xu, Cheng Liu, Ping Liu
Lie-Ming Xu, Cheng Liu, Ping Liu, Liver Diseases Research Center, Shanghai Academy of Traditional Chinese Medicine, Shanghai 200032, China
Author contributions: All authors contributed equally to the work.
Received: August 25, 1996
Revised: January 31, 1997
Accepted: March 1, 1997
Published online: June 15, 1997
Abstract

AIM: To study the anti-fibrotic mechanism of amygdalin, a component of Semen Persicae, on fat-storing cells (FSC).

METHODS: Livers of normal adult rats were perfused with Pronas E and collagenase in situ. FSC were isolated by centrifugation with 11% Metrizamide. The subcultured FSC were incubated with 10-4-10-8 mol/L amygdalin for 72 h, and then FSC proliferation and collagen production were assayed, respectively.

RESULTS: Low doses of amygdalin reduced incorporation of L-[3H]-thymidine into FSC and L-[5-3H]-proline into secreted collagenase-sensitive proteins and cell layer-associated collagenase-sensitive proteins. the strongest effects were seen for the 10-8 mol/L dose of amygdalin, which inhibited the proliferation of FSC by 25.0%, and decreased collagen production in medium and cell layer by 24.2% and 26.8%, respectively.

CONCLUSION: An anti-fibrotic mechanism of amygdalin is to inhibit the proliferation and collagen production of active FSC.

Keywords: Amygdalin; Pharmacology; Liver; Drug effects; Cirrhosis; Drug therapy; Collagen; Biosynthesis