effects of mitochondrial atp-sensitive potassium channels on the proliferation and secretion of human airway smooth muscle cells.

bronchial asthma is the common chronic inflammatory disease and is characterized by chronic airway inflammation, airway remodeling, and airway hyperreactivity (ahr). aim of this study was to investigate the effects of mitochondrial atp-sensitive potassium channels (mitokatp) on the proliferation and secretion of human airway smooth muscle cells (hasmcs). hasmcs were treated with the serum from asthmatic patients to establish hasmcs asthma model of passive sensitization. rhodamine 123 (r-123) and 2,7-dichloro-dihydrofluorescein diacetate (dcfh-da) fluorescence staining were used to detect mitochondrial membrane potential (δψm) and the content of reactive oxygen species (ros) in the cells, respectively. the cell counting was used to detect cell proliferation, and rt-pcr was used to detect the expression of tgf-β1 mrna. in the normal + diazoxide group, the fluorescence intensity of r-123, ros content, cell proliferation and tgf-β1 expression were enhanced, compared with the normal control group (p<0.05). there were no significant differences between the normal + 5-hydroxydecanoate (5-hd) group and the normal control group. in the asthma model control group, the fluorescence intensity of r-123, ros content, cell proliferation and tgf-β1 expression were enhanced, compared with normal control group, (p<0.05). the aforementioned indices were enhanced in the asthma model + diazoxide group, when compared with the asthma model control group, whereas these indices were attenuated in the asthma model + 5-hd group, when compared with the asthma model control group (p<0.05). in conclusion, asthma could activate mitokatp channels in hasmcs, promote hasmc proliferation and tgf-β1 expression.