Study On The Pulmonary Pathomorphology And Effects Of CNS On Animal Model With Pulmonary Fibrosis Induced By Bleomycin

Objective:To study the pulmonary pathomorphology and effects of CNS on bleomycin-induced pulmonary fibrosis and explore its mechanisms.Methods:Mice were randomly divided into 5 groups : normal group,model group,prednisolone group and two CNS-treated groups(360mg/kg,180mg/kg ). Rats were randomly divided into 5 groups : normal group,model group,prednisolone group and two CNS-treated groups(180mg/kg,90 mg/kg). And all the animals except those in normal control group were given bleomycin endotracheally. On day 2, each bleomycin group was given CNS, prednisolone and normal sodium respectively. On days 7,14,28 after drugs administration, the animals in each group were killed. The pulmonary index,the pathomor- phology,the ultrastructure,GSH,T-AOC and HYP were measured and compared with that of the control group. The expression of TGF-β1,α-SMA were analyzed by means of immunohistochemistry. Further more, the mRNA expression of TGF–β1 was determined by RT-PCR.Results: (1)The pulmonary index was significantly decreased in CNS groups compared with that of model group(P<0.01,P<0.05); (2)CNS could obviously reduce alveolitis and pulmonary fibrosis and improve the pathomorphology and ultrastructure of pulmonary fibrosis animal model; (3)CNS could enhance the activity of GSH and improve the level of T-AOC in lung tissue(P<0.01,P<0.05); (4)CNS could inhibit the expression of TGF-β1andα-SMA(P<0.01,P<0.05); (5)The amount of HYP was significantly lower than that of model group(P<0.01,P<0.05);(6) The mRNA expression of TGF–β1 was downregulated in lung tissue of CNS groups compared with that of model group. Conclusion:CNS inhibits the collagen deposition and decrease the express of TGF-β1 in lung tissue of pulmonary fibrosis of mice and rats; CNS possesses a high inhibiting action on oxygen free radicals and lessen pulmonary pathological damage.