Effects Of Cyclooxygenase Inhibitor On Bleomycin-induced Pulmonary Fibrosis In Rats (Clinical Analysis Of Twenty IPF Patients Was Appended)

PART 1 Effects of cyclooxygenase inhibitor on bleomycin- induced pulmonary fibrosis in ratsObjective: To investigate the distribution of the cyclooxygenase (COX) in the lung tissues and effect of bleomycin (BLM) inhibitor induced pulmonary fibrosis in rats. Methods: 96 male SD rats were randomly divided into four groups: the control group, model group, aspirin group and celecoxib group. Immunohistochemical method was used to detect the distribution of COX-2 in the stage of acute pulmonary alveolitis. HE and Masson staining methods were used to evaculate the degree of alveolitis and pulmonary fibrosis. RIA was used to detect the levels of TNF-αin serum. The total numbers of white cells in BALF in four groups were counted to observe the relationship between alveolitis and pulmonary fibrosis. Results: (1) In early stage of pulmonary fibrosis, except the control group, COX-2 expression was found in small bronchial epithelial cells in the other three groups, especially in the model group. (2) Compared with the control group, the three other groups had alveolitis .The aspirin and BLM group peaked on 14th days and celecoxib on 7th day. Alveolitis in celecoxib group was lighter than BLM and aspirin group on 14th day (P <0.05). (3) On 14th day, compared with the control group, the three other groups have pulmonary fibrosis. On 42th day , the degree of pulmonary fibrosis in celecoxib group was obvious heavier than BLM and aspirin group. (4) Before 14th day, TNF-αexpression in BLM group was higher than the normal control group (P<0.05, seven days P <0.01).Before 28th day, the expression of TNF-αin aspirin group was significantly higher (P<0.01).The level of TNF-αin the serum in celecoxib group was higher than the control group and BLM group (P<0.01). Before 28th days, compared with the control group, the total number of leukocytes in BALF was higher than the three other groups (P<0.01, P<0.05). On 42th day there was no significant difference between them(P>0.05). Conclusion: (1) BLM can cause obvious alveolitis and pulmonary fibrosis . (2)COX-2 expression can be seen in small bronchial epithelial cells in BLM induced pulmonary fibrosis. (3) Compared with the control group , there were significant changes in pulmonary inflammation and fibrosis between selective COX-1 and COX-2 specific inhibitors group .Of the two COX, COX-2 has a closer relationship with pulmonary fibrosis . (4)When lack of COX-2 , TNF-αcan increase the susceptibility to pulmonary fibrosis BLM induced. 5PART 2 The analysis of clinical characteristics of twenty IPFObjective: To evaluate the clinical features ,diagnosis and treatment methods of patients with IPF. Methods: To have a retrospective study on clinical feathers,HRCT examination,pulmonary function tests of 20 cases of IPF, which were all pathologically confirmed in the Second Hospital of Jilin University between Jan.2006 and Dec. 2007. Results:Progressive dyspnea and dry cough were observed in all the patients. Velcro rales were heard in 65.0% of patients .15.0% of the patients have clubbed fingers . HRCT showed that the majority of patients with pleural lesions located, both new and old lesions could be seen in one patient. The lung function damage was limitation ventilation dysfunction and diffusion dysfunction. Arterial blood gas analysis indicated hypoxemia and I respiratory failure.With treatment of hormone, the majority of patients got recovered ,but prognosis was very poor. Conclusion: IPF diagnosis relies on clinical manifestations, imaging performance, pulmonary function and blood gas analysis. Early clinical diagnosis and treatment contribute to improve prognosis.