Research Article

Effects of hydroxycamptothecin on the expression of matrix metalloproteinase-1 (MMP-1), tissue inhibitor of MMP-1, and type I collagen in rats with pulmonary fibrosis

Published: May 04, 2015
Genet. Mol. Res. 14 (2) : 4625-4632 DOI: https://doi.org/10.4238/2015.May.4.21
Cite this Article:
(2015). Effects of hydroxycamptothecin on the expression of matrix metalloproteinase-1 (MMP-1), tissue inhibitor of MMP-1, and type I collagen in rats with pulmonary fibrosis. Genet. Mol. Res. 14(2): gmr5140. https://doi.org/10.4238/2015.May.4.21
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Abstract

The aim of this study was to investigate the effects of hydroxycamptothecin (HCPT) on the expression of matrix metalloproteinase-1 (MMP-1), tissue inhibitor of MMP-1 (TIMP-1), and type I collagen in the lung tissue of rats with pulmonary fibrosis induced by bleomycin A5. We used hematoxylin eosin staining to observe the degree of pulmonary fibrosis in rats; Masson staining, reverse transcription polymerase chain reaction, and immunohistochemistry were used to observe the expression of collagen, MMP-1, and TIMP-1, and type I collagen. The expression of MMP-1 in the model group decreased significantly, while the expression of TIMP-1 and type I collagen significantly increased. After treatment with HCPT, the degree of pulmonary fibrosis and the expression of TIMP-1 and type I collagen decreased in all treatment groups. However, the expression of MMP-1 increased in a dose-dependent manner. Our results showed that HCPT decreased the pulmonary fibrosis induced by bleomycin A5 in rats, and an increase in MMP-1 expression and decrease in the TIMP-1 and type I collagen expression may be the mechanism that regulates the metabolism of the extracellular matrix.

The aim of this study was to investigate the effects of hydroxycamptothecin (HCPT) on the expression of matrix metalloproteinase-1 (MMP-1), tissue inhibitor of MMP-1 (TIMP-1), and type I collagen in the lung tissue of rats with pulmonary fibrosis induced by bleomycin A5. We used hematoxylin eosin staining to observe the degree of pulmonary fibrosis in rats; Masson staining, reverse transcription polymerase chain reaction, and immunohistochemistry were used to observe the expression of collagen, MMP-1, and TIMP-1, and type I collagen. The expression of MMP-1 in the model group decreased significantly, while the expression of TIMP-1 and type I collagen significantly increased. After treatment with HCPT, the degree of pulmonary fibrosis and the expression of TIMP-1 and type I collagen decreased in all treatment groups. However, the expression of MMP-1 increased in a dose-dependent manner. Our results showed that HCPT decreased the pulmonary fibrosis induced by bleomycin A5 in rats, and an increase in MMP-1 expression and decrease in the TIMP-1 and type I collagen expression may be the mechanism that regulates the metabolism of the extracellular matrix.