[Changes of mast cells and protease activated receptor-2 in experimental rat liver fibrosis]

Zhonghua Gan Zang Bing Za Zhi. 2006 Oct;14(10):753-6.
[Article in Chinese]

Abstract

Objective: To explore the quantity of mast cells and the role of protease activated receptor-2 (PAR-2) in experimental rat liver fibrosis.

Methods: Rats were sacrificed at 0, 2, 4, 8, and 12 weeks after subcutaneous injection of CCl(4). Mast cells were displayed by toluidine blue stain. The content of liver hydroxyproline was measured by the method of base hydrolyzate. The mRNA expression and the protein expression of PAR-2 in livers were detected by RT-PCR and immunohistochemistry at each time point.

Results: In normal rat livers there were a few mast cells (2.5+/-1.0) distributed along the hepatic portal areas. In the cirrhosis model group the number of mast cells in the livers increased degree by degree (2 weeks vs 4 weeks vs 8 weeks, 9.1+/-0.5 vs 15.7+/-3.0 vs 32.0+/-3.3; P less than 0.05), and they were distributed densely around the hepatic portal areas and the central veins. The content of liver hydroxyproline increased progressively from 0 to 12 weeks. In normal livers PAR-2 mRNA was hardly detected, at 2 weeks there was some expression of PAR-2 mRNA (PAR-2/beta-actin 0.15+/-0.01, P less than 0.05), at 4 weeks its expression increased (PAR-2/beta-actin 0.35+/-0.02, P less than 0.05) and it maintained a higher level (PAR-2/beta-actin 0.80+/-0.02, P less than 0.05) since then. The changing trend of the protein expression of PAR-2 was the same as that of PAR-2 mRNA expression.

Conclusions: PAR-2 mRNA expression and the protein expression of PAR-2 were consistent with the increase of the mast cells, and the content of liver hydroxyproline may play an important role in mediating liver fibrosis.

Publication types

  • English Abstract

MeSH terms

  • Animals
  • Hydroxyproline / metabolism
  • Liver / metabolism
  • Liver Cirrhosis, Experimental / metabolism*
  • Male
  • Mast Cells / metabolism*
  • Rats
  • Rats, Sprague-Dawley
  • Receptor, PAR-2 / metabolism*

Substances

  • Receptor, PAR-2
  • Hydroxyproline