Effects of bilirubin on alveolar macrophages in rats with emphysema and expression of iNOS and NO in them.
- Author:
Jianqiang LI
1
;
Hui ZHAO
;
Manjing SONG
;
Yongjian XU
;
Zhenxiang ZHANG
Author Information
1. Department of Respiratory Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Antioxidants;
pharmacology;
Bilirubin;
pharmacology;
Cells, Cultured;
Emphysema;
metabolism;
pathology;
Female;
Macrophages, Alveolar;
drug effects;
metabolism;
pathology;
Male;
Nitric Oxide;
biosynthesis;
Nitric Oxide Synthase;
biosynthesis;
Nitric Oxide Synthase Type II;
Rats;
Rats, Wistar
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2004;24(4):322-341
- CountryChina
- Language:English
-
Abstract:
To explore the effects of bilirubin on alveolar macrophages (AM) and expression of iNOS and NO in them in emphysema model, the rats were pretreated with bilirubin before exposed to smoke. AM were isolated from bronchoalveolar lavage fluid (BALF) and cultured. Pathological microscopic examination of AM and immunohistochemical analysis of iNOS were performed. Nitric oxide (NO) content in the samples was determined by nitrate reductase technique. The results showed both alveoli and alveolar septum appeared normal in size and shape in normal group. AM showed kidney-shaped nucleus and were rich in Golgi complexes and primary lysosomes in the cytoplasm. The inner membrane of mitochondrion was continuous. Most cristae of the mitochondria were intact. In model group, the alveoli were expanded, ruptured and bullaes were formed. Both the population and sizes of AM increased significantly. Secondary lysosomes were rich in the cytoplasm. Deformation and pyknosis of the nucleus, swelling of the mitochondrions and rupture of the inner mitochondrial membrane could also be seen. At high magnification, most of the mitochondrial cristae were broken, or completely lost at certain points. In bilirubin group, alveoli partly expanded and the population of AM also increased, with morphological changes being slighter than that in model group. Both NO contents and expression of iNOS in model group were higher than those in normal group (P<0.05). In bilirubin group the two indice were lower than those in model group (P<0.05). Our findings suggested that high expression of iNOS and high NO content in AM accelerate the development of emphysema associated with smoking in rats. Bilirubin may exert protective effects on AM and retards the development of emphysema in rats.
