2004Yiyao daobaoRequires access

Anti-pulmonary Fibrosis Effect of Captopril in Rats

Xu Qiyong

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Abstract

Objective:To study the anti-pulmonary fibrosis effect of captopril (CPT) and its mechanism. Methods:Thirty SD rats were randomized into three groups: CPT-treated group, model group and control group evenly. The treatment group and the model group were intratracheally instilled with bleomycin (5 mg·kg -1, 0.2-0.3 mL), and the control group received sodium chloride injection. Then the treatment group fed with CPT, and the control fed with sodium chloride injection until they were killed. Five rats in each group were separately killed 7 d later and 28 d later for experimental check. Lung weights, ACE activity were tested. The degrees of lung alveolitis and pulmonary fibrosis were checked by hemotoxylin and eosin colouration, and by HPIAS image analysis. Transforming growth factor (TGF-β 1) was assessed by immunohistochemical technique. Results:The lung alveolitis and pulmonary fibrosis in the treatment group were significantly relieved by comparison to the model group. ACE activities in the treatment group were lower than in model group significantly 7 d later(P0.01), and in model group, ACE activities still higher 28 d later. TGF-β 1 level in CPT-treated group was lower than model group 7 later, but there were no significant difference among the three groups 28 d later. Conclusion:Captopril has the effect of anti-pulmonary fibrosis in experimental rats by reducing ACE activity and inhibit expression of TGF-β 1.

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Objective:To study the anti-pulmonary fibrosis effect of captopril (CPT) and its mechanism. Methods:Thirty SD rats were randomized into three groups: CPT-treated group, model group and control group evenly. The treatment group and the model group were intratracheally instilled with bleomycin (5 mg·kg -1, 0.2-0.3 mL), and the control group received sodium chloride injection. Then the treatment group fed with CPT, and the control fed with sodium chloride injection until they were killed. Five rats in each group were separately killed 7 d later and 28 d later for experimental check. Lung weights, ACE activity were tested. The degrees of lung alveolitis and pulmonary fibrosis were checked by hemotoxylin and eosin colouration, and by HPIAS image analysis. Transforming growth factor (TGF-β 1) was assessed by immunohistochemical technique. Results:The lung alveolitis and pulmonary fibrosis in the treatment group were significantly relieved by comparison to the model group. ACE activities in the treatment group were lower than in model group significantly 7 d later(P0.01), and in model group, ACE activities still higher 28 d later. TGF-β 1 level in CPT-treated group was lower than model group 7 later, but there were no significant difference among the three groups 28 d later. Conclusion:Captopril has the effect of anti-pulmonary fibrosis in experimental rats by reducing ACE activity and inhibit expression of TGF-β 1.

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Available abstract

Objective:To study the anti-pulmonary fibrosis effect of captopril (CPT) and its mechanism. Methods:Thirty SD rats were randomized into three groups: CPT-treated group, model group and control group evenly. The treatment group and the model group were intratracheally instilled with bleomycin (5 mg·kg -1, 0.2-0.3 mL), and the control group received sodium chloride injection. Then the treatment group fed with CPT, and the control fed with sodium chloride injection until they were killed. Five rats in each group were separately killed 7 d later and 28 d later for experimental check. Lung weights, ACE activity were tested. The degrees of lung alveolitis and pulmonary fibrosis were checked by hemotoxylin and eosin colouration, and by HPIAS image analysis. Transforming growth factor (TGF-β 1) was assessed by immunohistochemical technique. Results:The lung alveolitis and pulmonary fibrosis in the treatment group were significantly relieved by comparison to the model group. ACE activities in the treatment group were lower than in model group significantly 7 d later(P0.01), and in model group, ACE activities still higher 28 d later. TGF-β 1 level in CPT-treated group was lower than model group 7 later, but there were no significant difference among the three groups 28 d later. Conclusion:Captopril has the effect of anti-pulmonary fibrosis in experimental rats by reducing ACE activity and inhibit expression of TGF-β 1.

Key concepts: Captopril, Pulmonary fibrosis, Bleomycin, Medicine, Lung, Lung fibrosis, Fibrosis, Internal medicine

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