陈颖
中国医学科学院阜外医院 手术室
OBJECTIVE:To investigate the protective and therapeutic effects of pulmonary surfactant in the pathogenesis of chronic obstructive pulmonary disease (COPD) in hamsters.METHODS:COPD animal model was established by smoke inhalations and intratracheal instillations of pancreatic elastase in hamsters. Ninty hamsters were divided into 9 groups as follows: normal group (N), two groups received smoke inhalations for 1 and 3 months (S1 and S3), one group received intratracheal instillation of surfactant (10 mg/100 g BW) for once after 1 month smoking (SP1), one group was treated with surfactant after 1.5, 2 and 2.5 months of smoking (SP3), and two groups received intratracheal administration of elastase (40 U/100 g BW) and were killed after 1 month and 3 months, respectively (E1 and E3). The surfactant was injected intratracheally after 1 week, 0.5, 1.0, 1.5, 2.0, and 2.5 months, followed by administration with elastase (EP1 and EP3). EP1 group were killed at the first month, and EP3 at the third month. Light microscopy and electromicroscopy observations were performed in each group. Pulmonary mean linear intercept (MLI), mean alveolar numbers (MAN), and pulmonary alveolar area (PAA) was measured by image analysis. The expression of surfactant protein A (SP-A) were observed by immunohistochemistry.RESULTS:Smoking for 3 months and instillations of elastase resulted in chronic bronchitis and emphysema. MLI and PAA increased and MAN decreased in all the experimental groups compared with in the normal group (P < 0.05 or P < 0.01). Administration of surfactant for 3 months resulted in statistically significant inhibition of pulmonary injury. MLI and PAA decreased and MAN increased in SP3 compared with in S3. Only MLI decreased in EP3 compared with E3. The expressions of SP-A in the type II alveolar epithelia decreased in S3 and E3 (compared with the normal group P < 0.01). After pulmonary surfactant intervention, the expression of SP-A increased significantly.CONCLUSION:Pulmonary surfactant may have a long-term protective effect on chronic smoking and elastase-induced COPD.
Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae 2004
OBJECTIVE:To investigate the effects of Salvia miltiorrhiza (SM) extracts on the expression of heme oxygenase-1 (HO-1) and nitric oxide synthase (NOS) in small pulmonary arteries (SPAs) of rats with chronic hypoxia.METHODS:After two weeks of hypoxia, rats were treated with diltiazem, and small, median, and large doses of SM extracts. The lungs were tested for the expression and distribution of HO-1, endothelial NOS (eNOS) and inducible NOS (iNOS) by using immunohistochemistry and Western blot method.RESULTS:Median and large doses of SM extracts significantly reduced hypoxia-induced media thickening in the SPAs (similar with diltiazem), recovered repaired ultrastructure injury, decreased HO-1 and iNOS levels, and increased eNOS expression in the SPAs.CONCLUSIONS:Median and large doses of SM extracts play significant roles in inhibiting structural remodeling in rats with hypoxic pulmonary hypertension. These effects might attribute to the suppression of HO-1 and iNOS, and the promotion of eNOS expression under the conditions of hypoxia.
Chinese medical journal 2003
OBJECTIVE:To study the role of transforming growth factor-beta(1) (TGF-beta(1)) in the pathogenesis of chronic bronchitis and emphysema.METHODS:An animal model of chronic bronchitis and emphysema was developed in hamsters by chronic smoke inhalation. The expression of TGF-beta(1) mRNA and protein in the pulmonary tissue was observed. The bronchial epithelia was stimulated with cigarette smoke extract (CSE) in vitro and the expression of TGF-beta(1) was measured.RESULTS:3 months after smoking, the animals developed chronic bronchitis and emphysema. TGF-beta(1) immunoreactivity in the pulmonary tissue and cultured bronchial epithelia increased significantly as compared to the normal control (2.75 +/- 0.23 vs 0.84 +/- 0.39, P = 0.001 and 2.67 +/- 0.16 vs 0.85 +/- 0.54, P = 0.001). The expression of TGF-beta(1) mRNA was also increased in the animal model (1.28 vs 0.98).CONCLUSIONS:Smoking can induce over-expression of TGF-beta(1) in bronchial epithelia, which may be one of the mechanisms for smoking-induced chronic bronchitis and emphysema.
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 2002
