Relevance of vasoactive intestinal peptide and total bronchial mucin in rat lung..
- Author:
Xiang LI
1
;
Xiao-Mei WANG
;
Jian-Song ZHANG
Author Information
1. Research Department of Applied Physiology, Medical College, Hunan Normal University, Changsha 410006, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Inflammation;
pathology;
Lung;
physiology;
physiopathology;
Mucins;
physiology;
Ozone;
adverse effects;
Rats, Sprague-Dawley;
Vasoactive Intestinal Peptide;
physiology
- From:
Acta Physiologica Sinica
2009;61(6):539-543
- CountryChina
- Language:Chinese
-
Abstract:
Vasoactive intestinal peptide (VIP) is a neuropeptide with potent bronchodilator, immunomodulator, and anti-inflammatory properties, and thus has biological properties capable of counteracting all major features of the asthmatic response. However, the effect of VIP on bronchial mucin secretion remains unclear. In order to observe the influence of VIP on bronchial mucin, the present study was designed to observe the correlation between VIP and total bronchial mucin changes under different time of ozone stress in rat lung. Sixty-four Sprague-Dawley rats were used in the experiment. Under different time of ozone stress, VIP content in lung homogenate was analyzed by radioimmunoassay, and changes in total bronchial mucin in the lung were analyzed by calculating the goblet cell hyperplasia ratio and the epithelial cell mucus occupying ratio from the periodic acid-Schiff reaction (PAS) staining. The results showed that, at early stage of respiratory tract injury, VIP did not change significantly, while the total bronchial mucin secretion increased; with the development of damage, the secretion of VIP increased by compensation, followed by a decrease in total bronchial mucin; with further injury, the numbers of pulmonary endocrine VIP positive nerve fibers and endocrine cells decreased, but bronchial mucin volume gradually increased. It is concluded that the secretion of VIP is negatively correlated with the secretion of bronchial mucin during the development of inflammation.
