Protective and therapeutic effect of pulmonary surfactant on the experimental chronic obstructive pulmonary disease in hamsters.
- Author:
Li LI
1
;
Ying-mao RUAN
;
Ying MENG
;
Ying CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cricetinae; Male; Mesocricetus; Pancreatic Elastase; Pulmonary Alveoli; ultrastructure; Pulmonary Disease, Chronic Obstructive; metabolism; prevention & control; Pulmonary Surfactant-Associated Protein A; metabolism; Pulmonary Surfactants; therapeutic use; Smoking
- From: Acta Academiae Medicinae Sinicae 2004;26(3):279-284
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the protective and therapeutic effects of pulmonary surfactant in the pathogenesis of chronic obstructive pulmonary disease (COPD) in hamsters.
METHODSCOPD 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.
RESULTSSmoking 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.
CONCLUSIONPulmonary surfactant may have a long-term protective effect on chronic smoking and elastase-induced COPD.
