Journal of Capital Medical University ›› 2010, Vol. 31 ›› Issue (3): 304-309.

• 消化疾病发病机制和治疗的进展 • Previous Articles     Next Articles

Adiponectin Modulates MMP-13 and TIMP-1 Expression via p38MAPK Pathway in Rat Hepatic Stellate Cell Line

CHEN Hui, MA Chao, ZHANG Yu-xian, MA Hong*   

  1. Liver Research Center, Beijing Friendship Hospital, Capital Medical University
  • Received:1900-01-01 Revised:1900-01-01 Online:2010-06-21 Published:2010-06-21
  • Contact: MA Hong

Abstract: Objective To investigate the effects of adiponectin on adiponectin receptor 1(AdipoR1) gene and protein expression in hepatic stellate cells(HSCs), and to evaluated the changes of p38MAPK pathway and its influence on matrix metalloproteinase-13(MMP-13) and tissue inhibitor of metalloproteinase-1(TIMP-1) expression in HSCs on the treatment of adiponectin. Methods HSCs proliferation was detected by MTT assay. AdipoR1, MMP-13 and TIMP-1 mRNA levels were detected by real-time RT-PCR. Western blotting was used to detect AdipoR1, MMP-13, TIMP-1, phospho-p38MAPK and phospho-pATF-2 protein expressions in HSCs. Results Adiponectin at concentrations 0.5 μg/mL-2.0 μg/mL had no effect on HSCs proliferation, however, AdipoR1 gene and protein expressions was up-regulated in adiponectin groups compared with control group. Adiponectin could increase phospho-p38MAPK protein expressions in dose and time dependent manners and had a maximal effect after 120 min treatment with adiponectin. Compared with control group, adiponectin could significantly increase MMP-13 gene and protein expressions, moreover, the blocker of p38MAPK could inhibit this effect of adiponectin in HSCs. The mRNA and protein level of TIMP-1 was decreased on the treatment with adiponectin, and this effect of adiponectin could be inhibited by p38MAPK's blocker. Conclusion Adiponectin could up-regulate AdipoR1 expression in HSCs. MMP-13 and TIMP-1 expressions in HSCs could be regulated by adiponectin through activation of p38MAPK pathway.

Key words: adiponectin, hepatic stellate cell, liver fibrosis, matrix metalloproteinase

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