Effect Of Nicorandil On The Airway Inflammation Of Rats With Chronic Obstructive Pulmonary Disease

Objective To evaluate the protective and therapeutic effect of potassium channel opener nicorandil(NCR) on the expression of interleukin-6(IL-6), tumor necrosis factorα(TNF-α) in the bronchoalveolar lavage fluid(BALF)and the adhesion molecule CD11b on the inflammation cells in the BALF of rats with chronic obstructive pulmonary disease(COPD).Methods 18 Wistar rats were randomly divided into 3 groups, the control group, the model group and the treatment group. The model of COPD was established by intratrachel instillation of lipopolysaccharide(LPS) and daily exposure to cigarette smog. From the second day the rats in treatment group accepted intragastric administration of NCR with dose of 3mg/kg before smog exposure. The control group was established by intratrachel instillation of normal saline without cigarette exposure. After four weeks, total and differential cell counts in bronchoalveolar lavage fluid (BALF) were observed, and the pathomorphological changes in the lung were analyzed. The expressions of CD11b on inflammatory cells were observed by immunocytochemistry. The expression of IL-6 and TNF-αin the BALF was evaluated by ELISA.Results Compared with the control group, the total cell counts was significantly higher in the model group(P<0.05), the percentages of neutrophilic granulocytes and macrophages were much higher in the model group(P<0.05), the expression of IL-6, TNF-αand CD11b in the BALF was significantly higher than those in the control group(P<0.05). Compared with the model group, the total cell counts was significantly lower in the treatment group(P<0.05), the percentages of neutrophilic granulocytes and macrophages were lower in the treatment group(P<0.05), and the expression of IL-6, TNF-αand CD11b in the BALF was significantly lower than those in the treatment group(P<0.05).Conclusion The expression of IL-6,TNF-αand CD11b was much higher in the COPD group than the control group. Nicorandil presents a preventive and therapeutic effect on the airway inflammation of COPD by decreasing the expression of CD11b on inflammation cells and IL-6, TNF-αin the BALF.