수 종 대사증후군 개선약물이 포볼 에스터 및 상피세포 성장인자로 유발된 기도 MUC5AC 뮤신 유전자 발현 및 생성에 미치는 영향

약물 재창출 전략에 의한 기도점액 과분비 조절약물 탐색

We investigated whether rosiglitazone, metformin, thioctic acid, simvastatin, or glimepiride affects airway MUC5AC mucin gene transcription or protein expression induced by phorbol 12-myristate 13-acetate (PMA) or epidermal growth factor (EGF) in NCI-H292 cells. Cells were pretreated with each agent for 30 min, then stimulated with PMA or EGF for 24 h. Of the five agents, rosiglitazone inhibited PMA-induced gene transcription and production of MUC5AC mucin in NCI-H292 cells. This result suggests that rosiglitazone, an antidiabetic peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist, can inhibit PMA-induced mucin expression at mRNA and protein levels, through directly acting on airway epithelial cells.