Study on treatment effect and mechanism of Hirsutella sinensis mycelium in idiopathic pulmonary fibrosis in rats.
- Author:
Qi-Yang SHOU
1
,
2
;
Hui-Ying FU
;
Li-Zong ZHANG
;
Yue-Qin CAI
;
Fang-Ming CHEN
;
Min-Li CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Disease Models, Animal; Humans; Hypocreales; chemistry; growth & development; Idiopathic Pulmonary Fibrosis; drug therapy; genetics; metabolism; pathology; Male; Mycelium; chemistry; growth & development; Rats; Rats, Wistar; Transforming Growth Factor beta1; genetics; metabolism; Treatment Outcome; Tumor Necrosis Factor-alpha; genetics; metabolism
- From: China Journal of Chinese Materia Medica 2012;37(23):3618-3623
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study and discuss the effect and mechanism of Hirsutella sinensis mycelium (HSM) on idiopathic pulmonary fibrosis in rats.
METHODForty Wistar rats were divided into five groups: the normal control group, the model control group, the high-dose group (1.0 g x kg(-1) HSM), the low-dose group (0.5 g x kg(-1) HSM), and the positive control group (10 mg x kg(-1) hydrocortisone). In addition to rats in the normal control group, the pulmonary fibrosis model was established by injecting 5 mg x kg(-1) bleomycin into rat tracheas for consecutively 28 days, in order to observe their lung function, lung tissue hydroxyproline, cytokines and pathology.
RESULTAfter rats were administered with HSM, 0.5 g x kg(-1) and 1.0 g x kg(-1) HSM could significantly decrease lung index and hydroxyproline content (P<0.01), while notably improving pulmonary function, alveolus inflammation and fibrosis degree (P<0.05, P<0.01); 1.0 g x kg(-1) HSM could decrease significantly protein expressions of TNF-alpha, IL-1beta and TGF-beta1 in lung tissues, while increasing significantly protein expressions of IFN-gamma (P<0.05).
CONCLUSIONHSM have better effect in treating idiopathic pulmonary fibrosis in rats. Its treatment effect and mechanism are related to the regulation of TNF-alpha, IL-1beta and TGF-beta1 and IFN-gamma imbalance.
