ABSTRACT
AIM: To investigate the effect of exercise stress on chronic cigarette smoking-induced downregulation of expression of large-conductance calcium-activated potassium channel (BK_(Ca)) and voltage-dependent delayed rectifier potassium channel (Kv1.5) in rat bronchial smooth muscle cells. METHODS: Rats were divided into 3 groups: normal control, smoking control and smoking plus exercise training group. The alteration of airway responsiveness and plasma cortisol level were detected, and potassium channel expression and pathological changes in lung tissue were determined with HE staining, immunohistochemistry, in situ hybridization and Western blot techniques. RESULTS: (1) Cigarette smoking induced an increase in airway responsiveness, smoking plus exercise lead to a decrease in airway responsiveness in contrast to smoking control group; (2) Plasma level of cortisol determined immediately after exercise was higher than that determined before exercise; (3) HE staining showed that there was severe chronic pulmonary inflammatory response in smoking control group, which was slight in the smoking plus exercise group; (4) The protein and mRNA expression of BK_(Ca) in cigarette smoking group were less than that in control group in BSMC, the mRNA expression of BK_(Ca) in exercise group were higher than that in smoking group; (5) The protein and mRNA expression of Kv1.5 in smoking group were less than that in control group in BSMC, and expression of Kv1.5 in exercise group was higher than that in smoking group in bronchioli. CONCLUSION: Proper exercise training can increase the expression of potassium channel BK_(Ca) and Kv1.5, and increase the cortisol secretion, which may contribute to the decreasing of airway hyperresponsiveness induced by cigarette smoking. [
ABSTRACT
AIM: To investigate the expression of FIZZ1/RELM? in lung tissue of chronic cigarette smoking rat,and to determine the relationship between airway inflammation and airway hyperresponsiveness.METHODS: Made rat model of chronic cigarette smoking was used.The expression of FIZZ1/RELM? in lung tissue was determined by immuno-histochemistry and in situ hybridization.RESULTS: In control rats,FIZZ1/RELM? protein and mRNA expressions were observed at low levels.In cigarette smoking rats,FIZZ1/RELM? expression increased in all the cells especially in bronchial smooth muscle cells,vascular wall cells and alveolar epithelial cells.CONCLUSION: FIZZ1/RELM? is a secreted peptide specifically expressed in lung.Cigarette smoking induces its upregulation,which possibly contributes to cigarette smoking-induced airway hyperresponsiveness.