To Study The Role Of Fibroblasts And Chinese Intervention In COPD Airway Remodeling Into

Objective: To explore the regulative effects of tetrandrine on viabiling of HELF stimulated by the inflammation mediators or not, and to evaluate the role of tetrandrine in prevention and treatment of COPD.Method: The HELF in eight-ten era cultured in vitro was used in experiment. Lipopolysaccharide or tetrandrine was used at various concentration in culture medium. The quantity of HELF was measured with MTT and the cellular growth curve was mapped. The expression of TGF-β1 was deteced by ELISA in supernatant. Flow cytometr-ic analysis were performed to determine cellular DNA content.Result:(1) The quantity of HELF: Induced 24 hours, the control group is 0.344±0.004,. The groups of different concentration tetrandrine can quite depressed the growth of HELF(P＜0.05). Howerve, the groups of Lipopolysaccharide can’t influence the growth of HELF.(2) the cycle of HELF: Induced 24 hours, the "S" cycle of the control group is 43.87±1.324. The groups of tetrandrine can depressed the growth of HELF at the "S" cycle(P＜0.05). The group of Lipopolysaccharide can not effect any cy-cle of HELF.(3) Apoptosis of HELF: The groups of tetrandrine can induce the HE-LF’s apoptosis(P＜0.05).(4) the detection of TGF-β1: The groups of tetrandrine can depress the creation of TGF-β1(P＜0.05) Induced 1,2,3,4,5,6 days by higher concentr-ation tetrandrine, there is nodifference.Conclusion: (1) The proliferation of HELF in Tet group was reduced markedly in aconcentration d-ependent manner;(2) The cycle of HELF in Tet group was restrained markedly in aconcentration dependent manner;(3) Tetrandrine can promote the apoptosis of the HELF,, and when concentration is increasing, the apoptosis of HELF becomes more obvious;(4) The TGF-β1 of HELF in Tet group was reduced markedly in aconcentration dependent manner, but there is no regularity with the change of time.Therefore, Tetrandrine can quite depressed the growth of HELF. Tetrandrine can postponethe proceeding of the airway remodeling by depressing the proliferate, influencing thecycle, promoting the apoptosis and reducing the TGF-β1 in cell level.