목적: Salivary gland (SG) dysfunction arises from various conditions, including salivary obstruction-induced inflammation. Dexamethasone, a potent corticosteroid, is a common prescription in clinics, renowned for its anti- inflammatory and immunomodulatory properties. This study aims to investigate the therapeutic implications and potential side effects of dexamethasone on the recovery from obstructive sialadenitis using in vivo duct ligation mice and in vitro SG organoid models. 방법:The functional and pathological changes were assessed after administering dexamethasone into the duct following de-ligation after maintaining ligation of mice submandibular duct for 2 weeks. Additionally, lipopolysaccharide (LPS) and tumor necrosis factor (TNF)-induced SG organoid inflammation model was established, and the effects and underlying mechanisms of dexamethasone were investigated through quantitative reverse transcription-polymerase chain reaction and cytokine assays. 결과:Dexamethasone administration facilitated the restoration of SG function, as evidenced by increased SG weight and saliva volume and decreased salivary lag time. Histological evaluations demonstrated that dexamethasone ameliorated acinar cell atrophy and fibrosis compared to PBS injection as a control group. Moreover, dexamethasone suppressed the expression levels of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and TNF. In the LPS and TNF-induced SG organoid inflammation model, dexamethasone restored the reduced gene expression levels of acinar markers, AQP5 and STATH and inhibited the induction of pro-inflammatory cytokines, TNF and IL6, and chemokines, CCL2, CXCL5 and CXCL12 compared to the untreated control group. In addition, experiments testing for side effects in both in vivo and in vitro models showed that high-dose or prolonged dexamethasone treatment induced acino-ductal metaplasia. 결론:Our findings indicate the effectiveness of corticosteroids in treating SG dysfunction induced by obstructive sialadenitis by regulating pro- inflammatory cytokines.