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1.
Acta Physiologica Sinica ; (6): 539-543, 2009.
Article in Chinese | WPRIM | ID: wpr-302416

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.


Subject(s)
Animals , Inflammation , Pathology , Lung , Physiology , Mucins , Physiology , Ozone , Rats, Sprague-Dawley , Vasoactive Intestinal Peptide , Physiology
2.
Journal of Central South University(Medical Sciences) ; (12): 772-781, 2006.
Article in Chinese | WPRIM | ID: wpr-813601

ABSTRACT

OBJECTIVE@#To investigate the effect of intrapulmonary regulatory peptides on adhesion of eosinophils (EOS) to bronchial epithelial cells (BECs).@*METHODS@#Two regulatory peptides, namely vasoactive intestinal peptide (VIP) and epidermal growth factor (EGF) were investigated. VIP and EGF were observed on the secretion of ILs and expression of intercellular adhesion molecule-1 (ICAM-1).@*RESULTS@#VIP and EGF could decrease ILs secretion and ICAM-1 expression.@*CONCLUSION@#VIP and EGF inhibited the adhesion of EOS to BEC in the inflammatory process to lighten the airway inflammation.


Subject(s)
Animals , Female , Male , Rabbits , Bronchi , Cell Biology , Cell Adhesion , Cells, Cultured , Eosinophils , Cell Biology , Epidermal Growth Factor , Physiology , Epithelial Cells , Cell Biology , Intercellular Adhesion Molecule-1 , Interleukin-5 , Vasoactive Intestinal Peptide , Physiology
3.
Acta Physiologica Sinica ; (6): 225-228, 2002.
Article in Chinese | WPRIM | ID: wpr-279307

ABSTRACT

The effect of alveolar macrophages (AM) harvested from Wistar rats by lung lavage on proliferation of human embryo pulmonary fibroblasts in culture was investigated. It was observed that supernatants of AM decreased the uptake of (3)H TdR by the pulmonary fibroblasts. The AM activated with opsonized zymosan (OPZ) showed a stronger inhibitory effect on fibroblast proliferation compared with inactivated AM. Following pretreatment with indomethacin, the inhibitory effect of AM was abolished and reversed to stimulatory effect on pulmonary fibroblast proliferation. The PGE content in AM supernatant was measured with radioimmunoassay. It was observed that the inhibitory effect of AM was highly correlated to prostaglandin (PGE) content in the supernatant of AM. The results suggest that AM has both inhibitory and stimulatory effects on the proliferation of pulmonary fibroblast; the inhibitory effect is primary under normal conditions. This inhibitory action is mainly due to PGE secreted from AM. It is, therefore, suggested that AM plays an important role in suppressing pulmonary fibrosis under normal conditions.


Subject(s)
Animals , Female , Humans , Male , Rats , Cell Division , Physiology , Cells, Cultured , Fibroblasts , Cell Biology , Lung , Cell Biology , Embryology , Macrophages, Alveolar , Physiology , Prostaglandins E , Physiology , Pulmonary Fibrosis , Pathology
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