摘要
Background Recent studies have revealed that lung cell apoptosis plays an important role in pathogenesis of cigarette-induced chronic obstructive pulmonary disease （COPD）. Tumor necrosis factor alpha （TNF-α） is one of the most important cytokines which are involved in COPD. This study aimed at investigating the influence of its inhibitor, recombinant human necrosis factor-alpha receptor II：lgG Fc fusion protein （rhTNFR：Fc） on alveolar septal cell apoptosis in passive smoking rats. Methods Forty-eight rats were randomly divided into a normal control group, a passive smoking group, an rhTNFR：Fc intervention group and a sham intervention group. The passive smoking rats were treated by exposure to cigarette smoking daily for 80 days. After smoking for one month the rhTNFR：Fc intervention group was treated with rhTNFR：Fc by subcutaneous injection, the sham intervention group injected subcutaneously with a neutral preparation （normal saline 0.1 ml, manicol 0.8 ml, cane sugar 0.2 mg, Tris 0.024 mg as a control. Lung function was determined and the levels of TNF-a in serum and broncho-alveolar lavage fluid （BALF） were measured with enzyme-linked immunosorbnent assay （ELISA）. Lung tissue sections stained by hematoxylin and eosin （HE） were observed for study of morphological alternations. Mean linear intercept （MLI） and mean alveolar numbers （MAN） were measured and the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） method was carried out to determine the percentage of positive cells and distribution of apoptotic cells. Results Increased MLI and decreased MAN were found in the passive smoking group compared with both the normal control group and the rhTNFR：Fc intervention group （P〈0.05）. Forced expiratory volume in 0.3 second （FEVo.3）/forced vital capacity （FVC） and peak expiratory flow （PEF） were lower in the passive smoking group than that in the normal control group （P〈0.05）. Compared with the sham intervention group
Background Recent studies have revealed that lung cell apoptosis plays an important role in pathogenesis of cigarette-induced chronic obstructive pulmonary disease （COPD）. Tumor necrosis factor alpha （TNF-α） is one of the most important cytokines which are involved in COPD. This study aimed at investigating the influence of its inhibitor, recombinant human necrosis factor-alpha receptor II：lgG Fc fusion protein （rhTNFR：Fc） on alveolar septal cell apoptosis in passive smoking rats. Methods Forty-eight rats were randomly divided into a normal control group, a passive smoking group, an rhTNFR：Fc intervention group and a sham intervention group. The passive smoking rats were treated by exposure to cigarette smoking daily for 80 days. After smoking for one month the rhTNFR：Fc intervention group was treated with rhTNFR：Fc by subcutaneous injection, the sham intervention group injected subcutaneously with a neutral preparation （normal saline 0.1 ml, manicol 0.8 ml, cane sugar 0.2 mg, Tris 0.024 mg as a control. Lung function was determined and the levels of TNF-a in serum and broncho-alveolar lavage fluid （BALF） were measured with enzyme-linked immunosorbnent assay （ELISA）. Lung tissue sections stained by hematoxylin and eosin （HE） were observed for study of morphological alternations. Mean linear intercept （MLI） and mean alveolar numbers （MAN） were measured and the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） method was carried out to determine the percentage of positive cells and distribution of apoptotic cells. Results Increased MLI and decreased MAN were found in the passive smoking group compared with both the normal control group and the rhTNFR：Fc intervention group （P〈0.05）. Forced expiratory volume in 0.3 second （FEVo.3）/forced vital capacity （FVC） and peak expiratory flow （PEF） were lower in the passive smoking group than that in the normal control group （P〈0.05）. Compared with the sham intervention group
基金
This-study was supported by the grants from National Natural Science Foundation of China （No. 30770931）, Research Fund of National Education Ministry of China （No. 200050533023） and Research Fund for Reform of Postgraduate Education in Hunan Province （No. 06B07）.
