1.Role of mast cell and its subpopulations in simple and irradiated-wound of rats
Yufang CUI ; Guowei XIA ; Xiaobing FU ; Hong YANG ; Ruiyun PENG ; Yabing GAO ; Xuemei CUI ; Dewe WANG
Chinese Journal of Pathophysiology 1989;0(05):-
AIM:To examine the role and dynamic changes of mast cell(MC) and its subpopulations in simple and irradiated-wound of rats.METHODS:MC and its subpopulations were estimated using alcian blue-safranin (ABS)double staining RESULTS:(1)The total number of MC in two groups decreased coincidently on day 2 after wounding, and the total MC increased rapidly and reached maximal gradually on day 5 and 7 after wounding, the increment of MC remained consistently 28 day after wounding (2)Both mucosal MC( MMC) and Mix MC decreased obviously on day 2 after wounding, hereafter,they remained the low level all the time However, the CTMC kept in the high level after wounding (3)The Mix MC on day 5 and the total MC during day 5-15 after wounding were lower in irradiated group than in simple wound group CONCLUSION: MC and its subpopulations could delay the healing process of simple and irradiated wound
2.Establishment of chronic obstructive pulmonary disease rat models by passive cigarette smoking and intratracheal instillation of lipopolysaccharide
Hongmei LI ; Dejian CUI ; Xin TONG ; Baosen PANG ; Yabing GAO ; Dewe WANG
Chinese Journal of Pathophysiology 2000;0(07):-
AIM: To establish rat chronic obstructive pulmonary disease(COPD) models by passive cigarette smoking plus intratracheal instillation of lipopolysacchride(LPS) or passive cigarette smoking only, which would be similar to the pathogenesis of human COPD. METHODS: 48 Wistar rats were randomly divided into 4 groups.(1) Healthy control I group( n =12), rats were bred 4 weeks;healthy control II group( n =12), rats were bred for 3 months. (2) Model group I ( n =12), 200 ?g lipopolysaccharide(LPS) was instilled intratracheally once for every two weeks and the rats were exposured to 5% of cigarette smoke, 0.5 h/d for 4 weeks.(3) Model group II(n=12),rats were exposed to 5% of cigarette smoke, 0.5 h/d for 3 months. The pathologic changes of airways and lung tissues, pulmonary function and blood gas analysis were determined. The airway wall lymphocytes and alveolar macrophages were counted. The cross areas of epithelial layer, smooth muscle layer and lamina propria of bronchi were measured. The hydroxyproline of lung tissue homogenates was determined by biochemistry method. RESULTS: The pathologic changes of airways and lung tissue of two models were similar to but milder than those of COPD patients(biopsy data). The collagen deposition and the cross areas of epithelial layer and smooth muscle layer in airway walls of two model groups were significantly increased than those of control groups( P