Experimental study on effect of Qidan granule in treatment of pulmonary fibrosis in rats.
- Author:
Chang-Jun JIN
1
;
Hong-Tao XIN
;
Dian-Jie LIN
;
Zhen WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Drugs, Chinese Herbal; therapeutic use; Lung; metabolism; pathology; Male; Phytotherapy; Pulmonary Fibrosis; drug therapy; metabolism; pathology; Rats; Rats, Sprague-Dawley; Transforming Growth Factor beta; metabolism; Tumor Necrosis Factor-alpha; metabolism
- From: Chinese Journal of Industrial Hygiene and Occupational Diseases 2007;25(1):22-25
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the therapeutic effect and mechanism of Qidan granule on blemycinA5-induced pulmonary fibrosis in rats.
METHODSA total of 70 SD rats were randomly divided into normal group, the model group, Qidan group and hydrocortisone group and observed for 28 days and 42 days, respectively. Rat pulmonary fibrosis was induced by intrabronchial injection of blemycinA5. Treatment started from day 14 to day 42 with Qidan granule and Hydrocortisone for 14 days (day 28 group) and for 28 days (day 42 group), respectively. The lung pathological grades were observed by hematoxylin and eosin (HE) staining and expressions of transforming growth factor beta (TGF-beta(1)) protein and tumor necrosis factor alpha (TNF-alpha) protein were tested by the immunohistochemical technique.
RESULTS(1) Lung pathobiology fibrosis were alleviated was alleviated significantly in Qidan granule group compared with those in model group and hydrocortisone group (p < 0.01). (2) In Qidan group and hydrocortisone group, the expression of TGF-beta(1) protein was 1.71 +/- 0.17 and 1, 78 +/- 0.17 in day 28 group and day 42 group, respectively. The expression of TNF-aprotein was 2.16 +/- 0.40 and 1.98 +/- 0.33 in day 28 group and day 42 group, respectively. The expression of TGF-beta(1) and TNF-alpha protein was significantly difference from those in the model group and the hydrocortisone group (p < 0.01).
CONCLUSIONSQidan granule ameliorate the pulmonary fibrosis by decreasing expressions of TGF-beta(1) and TNF-alpha proteins in lung tissue.
