Basic Research
Copyright ©The Author(s) 2004. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Apr 1, 2004; 10(7): 1015-1018
Published online Apr 1, 2004. doi: 10.3748/wjg.v10.i7.1015
Antiproliferative and proapoptotic effects of somatostatin on activated hepatic stellate cells
Qin Pan, Ding-Guo Li, Han-Ming Lu, Liang-Yong Lu, Yu-Qin Wang, Qin-Fang Xu
Qin Pan, Ding-Guo Li, Han-Ming Lu, Yu-Qin Wang, Qin-Fang Xu, Department of Gastroenterology, Xinhua Hospital, Shanghai Second Medical University, Shanghai 200092, China
Liang-Yong Lu, Research Center for Hepatic Diseases, Nanjing Military Command, Shanghai 200233, China
Author contributions: All authors contributed equally to the work.
Supported by the Scientific Development Programs of Science and Technology Commission Foundation of Shanghai, No. 004119047
Correspondence to: Dr. Qin Pan, Department of Gastroenterology, Xinhua Hospital, 1665 KongJiang Rd., Shanghai 200092, China.
Telephone: +86-21-65790000-5319 Fax: +86-21-55571294
Received: July 17, 2003
Revised: August 6, 2003
Accepted: August 25, 2003
Published online: April 1, 2004

AIM: To assess the effects of somatostatin on proliferation and apoptosis of activated rat hepatic stellate cells (HSCs).

METHODS: HSCs isolated from the livers of adult Sprague-Dawley rats (weighing 400-500 g) by in situ perfusion and purified by single-step density gradient centrifugation with Nycodenz, became activated after 10 days’ cultivation. Then the apoptotic rate of HSCs treated with different doses of somatostatin for 72 h, was assayed by acridine orange/ ethidium bromide fluorescent staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, transmission electron microscopy and flow cytometry, while the proliferation of HSCs was measured by MTT assay. Furthermore, the mechanisms of somatostatin were investigated by cytodynamic analysis.

RESULTS: Somatostatin at the concentration of 10-6-10-9 mol/L could decrease the proliferative rate, and promote the apoptosis of activated rat HSCs in a dose-dependent way. Its action was most significant when the concentration reached 10-6 mol/L or 10-7 mol/L (P < 0.05-0.01). An obvious cell-cycle arrest (G0/G1 arrest) was the important way for somatostatin to exert its action.

CONCLUSION: Antiproliferative and proapoptotic effects of low-dose somatostatin on activated rat HSCs can be obtained. These findings reveal its potential antifibrotic action.

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