Effect of Dilong on expression of fibrogenic factors TGF-β1 and α-SMA in lung tissue of mice with pulmonary fibrosis.
10.19540/j.cnki.cjcmm.20190716.402
- Author:
Hui-Hui WANG
1
;
Yan-Li MENG
1
;
Zhi-Min YANG
1
;
Xiao-Xi WANG
1
;
Hui-Xing XU
1
;
Wei-Ming WANG
1
Author Information
1. Heilongjiang Academy of Chinese Medicine Sciences Harbin 150036,China.
- Publication Type:Journal Article
- Keywords:
Biacore technology;
Dilong(geosaurus);
TGF-β1;
pulmonary fibrosis;
α-SMA
- MeSH:
Actins/metabolism*;
Animals;
Bleomycin;
Lung;
Medicine, Chinese Traditional;
Mice;
Mice, Inbred C57BL;
Oligochaeta;
Pulmonary Fibrosis/metabolism*;
Random Allocation;
Transforming Growth Factor beta1/metabolism*
- From:
China Journal of Chinese Materia Medica
2019;44(24):5473-5478
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this paper was to investigate the effect of Dilong( geosaurus) on the expressions of fibrotic factors TGF-β1 and α-SMA in bleomycin-induced pulmonary fibrosis mice. The binding ability of Dilong to fibrotic factor TGF-β1 was initially detected by Biacore technology and verified by in vivo pharmacodynamics. A total of 60 SPF C57 mice were randomly divided into 6 groups. Except the blank group( injecting 0. 08 m L·kg-1 sodium chloride in the trachea),the other five groups were given bleomycin( 4 mg·kg-1) to replicate the pulmonary fibrosis model. After 14 days of drug treatment,the expressions of TGF-β1 and α-SMA were detected by Masson staining,immunohistochemistry and RT-PCR. The results of Biacore experiment showed that the extract of Dilong was well bound to TGF-β1 protein in vitro,and the binding value reached 619. 3. Compared with the model group,Masson's results showed that cellulose deposition in high-dose,medium-dose and low-dose Dilong groups decreased to varying degrees. RT-PCR results showed that different doses of Dilong could reduce protein and mRNA expressions of TGF-β1 and α-SMA to a certain extent in a dose-dependent manner. In conclusion,Dilong could delay the process of pulmonary fibrosis by binding to target protein TGF-β1 and inhibiting the expression of α-SMA.
