![Sample our Medicine, Dentistry, Nursing & Allied Health journals, sign in here to start your FREE access for 14 days]({"type":"image" , "src" : "/sda/5944/TOC-Subject-Sample-2021-Medicine-Dentistry-Nursing-Allied-Health.jpg"})
Abstract
Conclusion: Glucocorticoid (GC) administration enhanced apoptotic changes in mature olfactory receptor neurons (ORNs). GC administration may enhance regeneration of olfactory epithelium (OE). Objectives: The mechanism underlying olfactory epithelial cells turnover involves apoptosis replaced by new ORNs. On regeneration of OE, we evaluated the apoptotic changes in OE. Our aim was to corroborate the enhancement of apoptosis of ORNs induced by GCs that are generally administered locally or systemically to patients with olfactory dysfunction. Materials and methods: For the in vitro study, we established cultured murine ORNs. Triamcinolone acetonide was added to culture supernatants. ORNs were then cultured for another 2 weeks. In the in vivo study, triamcinolone acetonide was administered to mice 5 or 10 times. The mice were dissected 3 days after the final injection, and the olfactory regions were removed and embedded in paraffin. All samples were examined by immunohistochemical staining and the TdT-mediated dUTP-biotin nick-end labeling (TUNEL) method. Results: Glucocorticoid receptor (GR) expression of cultured murine ORNs was observed among ORNs at the mature stage. Expression of GRs by murine OE was localized on mature ORNs and supporting cells. Administration of GC to both cultured ORNs and mice resulted in proportions of apoptotic cells that were significantly higher than those in the control groups.