Dexamethasone Induces Apoptosis of Nasal Polyp-Derived Tissue Cultures Through JNK and p38 MAPK Activation

• DOI: 10.3342/ceo.2014.7.2.112
• Publication Date: 2014-06-02T07:42:09Z
• Authors: Tae-Hoon Lee; Jung Gwon Nam; Ho Min Lee; Bo-Young Kim; Myung-Koo Kang; Woo Yong Bae; Dae Young Hur; Seong Kook Park
• Keywords: Nasal Polyps

Glucocorticoids, such as dexamethasone (DEX), increase apoptosis in a variety of white cells nasal polyps and is an important factor the resolution inflammation. However, mechanism glucocorticoids induced polyp remains unclear. In this study authors evaluated which pathways were engaged by DEX ex vivo model polyps.Nasal tissues cultured using air-liquid interface method. Cultures maintained absence or presence (10 100 µM) for 24 hours. To investigate involvement apoptotic signaling polyp, caspase cascades, Fas-FasL pathway, mitochondrial pathway p38 mitogen-activated protein kinase (MAPK)/JNK performed reverse transcription-polymerase chain reaction Western blotting.The expression ratios FasL, activated form caspase-8, caspase-9, caspase-3 significantly higher DEX-treated (P<0.01). Bcl-2 family expression, anti-apoptotic molecules, Bcl-XL decreased, but pro-apoptotic Bax increased, Bid Bad activated. conventional MAPKs, JNK, phospho-p38 MAPK higher, phospho-extracellular signal-regulated (ERK)1/2 was lower (P<0.01).DEX induces via MAPK/JNK pathway.