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1.
China Pharmacy ; (12)2005.
Article in Chinese | WPRIM | ID: wpr-532504

ABSTRACT

OBJECTIVE: To observe the regulatory effect of SNMC on the gene expression of the Smad family in pulmonary fibrosis model rats.METHODS: A total of 174 rats were assigned to 6 groups: normal group,model group,positive prednisolone acetate group,SNMC(20,15,10 mL?kg-1?d-1) groups,with the latter 5 groups treated with bleomycin injection to induce pulmonary fibrosis model.At 24 h after modeling,the rats in 6 groups were treated with corresponding drugs day by day before being sacrificed at 1,12,28 days after first-time treatment for extracting of RNA from pulmonary tissues.The expression levels of Smad3,Smad4 and Smad7 were assayed by RT-PCR respectively.RESULTS: As compared with model group,the expression levels of Smad4 and Smad7 genes were down-regulated but the expression level of Smad3 gene was up-regulated in SNMC groups,whereas the expression levels of 3 kinds of genes were all down-regulated in positive prednisolone acetate group.CONCLUSION: SNMC is more effective than prednisolone acetate in reversing the abnormal expression of Smad family in pulmonary fibrosis model rats.

2.
China Pharmacy ; (12)2001.
Article in Chinese | WPRIM | ID: wpr-527546

ABSTRACT

OBJECTIVE:To observe the antagonistic effect of compound glycyrrhizin on bleomycin A5-induced pul-monary fibrosis of rats.METHODS:Pulmonary fibrosis model was built by injecting bleomycin A5to tracheas of SD rats in one time,the next day,control groups were administered with compound glycyrrhizin and prednisolone acetate,21days after administration,organ coefficients,pathology,areas of alveolar septum,areas of the inflammatory cells and the integral pho-todensity of the pulmonary tissues were detected and analyzed.RESULTS:As compared with the model group,the compound glycyrrhizin group had a diminished organ coefficient,ameliorated pathological change for pulmonary tissues and reduced areas of alveolar septum(P0.05).CONCLUSION:Compound glycyrrhizin has antagonistic effect on pulmonary fibrosis of model rats.

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