Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (20): 3711-3714.doi: 10.3969/j.issn.1673-8225.2011.20.024

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Correlation between acetaldehyde-induced proliferation of hepatic stellate cells and p38 mitogen-activated protein kinase signal transduction pathway

Zheng Ren-yuan1, Jiang Ming-de2, Mei Zhe-chuan1, Zhuo Qiang1, Ye Ping2, Tang Wen2   

  1. 1Department of Gastroenterology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing  400016, China
    2Department of Gastroenterology, General Hospital of Chengdu Military Area Command, Chengdu  610083, Sichuan Province, China
  • Received:2011-01-06 Revised:2011-04-13 Online:2011-05-14 Published:2011-05-14
  • Contact: Mei Zhe-chuan, Chief physician, Professor, Master’s supervisor, Department of Gastroenterology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China meizhechuan@21cn.com
  • About author:Zheng Ren-yuan★, Studying for master’s degree, Assistant researcher, Department of Gastroenterology, the Second Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China zry@cmc.edu.cn

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Abstract:

BACKGROUND: Activation and proliferation of hepatic stellate cells (HSCs) leads to hepatic fibrosis, and p38 mitogen-activated protein kinase (p38MAPK) signaling pathway has a role in regulating cell proliferation.
OBJECTIVE: To explore the p38MAPK activity and cell proliferation of acetaldehyde-induced rat HSCs treated with SB203580.
METHODS: Rat HSC strains were cultured in vitro, and divided into blank group, acetaldehyde control group and SB203580 group. The proliferation of HSCs was evaluated by MTT colorimetric assay and the variability of phosphorylated-p38 was examined by Western blot.
RESULTS AND CONCLUSION: p38 activity increased in acetaldehyde-induced HSCs, and HSCs proliferated significantly; SB203580 (5, 10, 20 μmol/L) could block the activity of p38 in the cells, and inhibit acetaldehyde-induced HSCs proliferation     (P < 0.05), when the concentration was increased to 30 μmol/L, its inhibitive effect on HSCs proliferation was more significant, and the expression of p-p38 decreased relatively (P < 0.05). The results showed that inhibition of p38MAPK activity can affect HSCs proliferation; p38 signaling pathway may play an important role in the regulation of HSCs proliferation.

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