Effect of ginkgo biloba extract against pulmonary fibrosis and its mechanisms.
- Author:
Jie QI
1
;
Yanchao LIU
;
Qingjun LI
;
Xiaoling CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Bleomycin; adverse effects; analogs & derivatives; Bronchoalveolar Lavage Fluid; chemistry; Disease Models, Animal; Drugs, Chinese Herbal; administration & dosage; Ginkgo biloba; chemistry; Humans; Macrophages, Alveolar; drug effects; metabolism; Male; Malondialdehyde; metabolism; Pulmonary Fibrosis; chemically induced; drug therapy; genetics; metabolism; Random Allocation; Rats; Rats, Sprague-Dawley; Transforming Growth Factor beta1; genetics; metabolism
- From: China Journal of Chinese Materia Medica 2010;35(22):3043-3047
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of Ginkgo biloba extract (GbE) against the bleomycin induced pulmonary fibrosis and to investigate its mechanisms.
METHODSD rats were randomly divided into 3 groups: Control group, BLM + NS group and BLM + GbE group (n = 6 in each time point of each group). Rats in each group were sacrificed on the 14th and 30th day after endotracheal injection of bleomycin A5. Lung injury through HE stain and pulmonary fibrosis through Masson stain were observed by light microscope. The content of collagen protein in lung tissue and malondialdehyde (MDA) in plasma were assayed by biochemical methods. The expressions of TGF-beta1 in tissue and bronchoalveolar lavage fluid (BALF) were detected by immunohistochemistry and immunocytochemistry respectively.
RESULTCompared with control group, every datum in each time point in BLM + NS group showed significant changes which indicated the success of the model. Compared with BLM + NS (14 d) group, MDA in serum and TGF-beta1 in alveolar macrophage were significantly reduced in BLM + GbE (14 d) group. The data in BLM + GbE (30 d) group were compared with those in BLM + NS (30 d) group as follows. The lung injury and fibrosis were significantly ameliorated, the content of collagen in lung tissue and MDA in plasma were significantly reduced, the expression of TGF-beta1 in lung tissue was significantly reduced, however the expression of TGF-beta1 in BALF cells was not significantly changed.
CONCLUSIONGbE inhibited bleomycin induced lung injury and fibrosis in rats. The possible mechanisms were that GbE could inhibit the expression of TGF-beta1 in alveolar macrophage in early stage of fibrosis (14 d) and in noninflammatory cells in proliferative stage (30 d), and GbE could also attenuate the oxidative stress induced by bleomycin.
