1.Mometasone Furoate Suppresses PMA-Induced MUC-5AC and MUC-2 Production in Human Airway Epithelial Cells.
Orapan POACHANUKOON ; Sittichai KOONTONGKAEW ; Paopanga MONTHANAPISUT ; Napaporn PATTANACHAROENCHAI
Tuberculosis and Respiratory Diseases 2017;80(1):60-68
BACKGROUND: Mucus hypersecretion from airway epithelium is a characteristic feature of airway inflammatory diseases. Tumor necrosis factor α (TNF-α) regulates mucin synthesis. Glucocorticoids including mometasone fuorate (MF) have been used to attenuate airway inflammation. However, effects of MF on mucin production have not been reported. METHODS: Effects of MF and budesonide (BUD) on the phorbol-12-myristate-13-acetate (PMA)–induction of mucin and TNF-α in human airway epithelial cells (NCI-H292) were investigated in the present study. Confluent NCI-H292 cells were pretreated with PMA (200 nM) for 2 hours. Subsequently, the cells were stimulated with MF (1–500 ng/mL) or BUD (21.5 ng/mL) for 8 hours. Dexamethasone (1 µg/mL) was used as the positive control. Real-time polymerase chain reaction was used to determine MUC2 and MUC5AC mRNA levels. The level of total mucin, MUC2, MUC5AC, and TNF-α in culture supernatants were measured using enzyme-linked immunosorbent assay. RESULTS: MF and BUD significantly suppressed MUC2 and MUC5AC gene expression in PMA-stimulated NCI-H292 cells. The inhibitory effects of the two steroid drugs were also observed in the production of total mucin, MUC2 and MUC5AC proteins, and TNF-α. CONCLUSION: Our findings demonstrated that MF and BUD attenuated mucin and TNF-α production in PMA-induced human airway epithelial cells.
Budesonide
;
Dexamethasone
;
Enzyme-Linked Immunosorbent Assay
;
Epithelial Cells*
;
Epithelium
;
Gene Expression
;
Glucocorticoids
;
Humans*
;
Inflammation
;
Mometasone Furoate*
;
Mucins
;
Mucus
;
Real-Time Polymerase Chain Reaction
;
RNA, Messenger
;
Tumor Necrosis Factor-alpha
2.Inhibitory effect of Phlai capsules on skin test responses among allergic rhinitis patients: a randomized, three-way crossover study.
Pattara TANTICHAROENWIWAT ; Prapasri KULALERT ; ; Sittichai KOONTONGKAEW ; Weena JIRATCHARIYAKUL ; Ruedee SOAWAKONTHA ; Prakongsiri BOONCONG ; Orapan POACHANUKOON
Journal of Integrative Medicine 2017;15(6):462-468
BACKGROUNDZingiber cassumunar Roxb., commonly known as Phlai in Thai, has been used as a traditional medicine in Thailand for the treatment of various diseases, including inflammation and chronic airway disease.
OBJECTIVEThe purpose of this study was to assess the antihistaminic effect of Phlai on skin testing.
DESIGN, SETTING, PARTICIPANTS AND INTERVENTIONThis was a randomized, open-label, three-way crossover study. Twenty allergic rhinitis (AR) patients were enrolled. In randomized sequence, patients received a single dose of Phlai capsules (100 or 200 mg) or loratadine (10 mg) with a washout period of 1 week between each treatment.
MAIN OUTCOME MEASURESSkin prick testing for histamine and common aeroallergen (house dust mite) were performed before treatment and after 1, 2, 3, 4, 6, 8, 12 and 24 hours of treatment. The main treatment outcomes were the mean wheal and flare responses to the skin prick test after treatment.
RESULTSBoth 100 mg and 200 mg Phlai doses suppressed wheal and flare responses to house dust mite allergen, but only 200 mg of Phlai capsules significantly suppressed wheal and flare responses to histamine. Repeated measures analysis of variance showed that loratadine caused more wheal and flare suppression than Phlai capsules in responses to the histamine skin prick test. However, there were no significant differences among the effects of 100 mg Phlai capsules, 200 mg Phlai capsules and loratadine in suppression of wheal and flare induced by the mite skin prick test. Both doses of Phlai were well-tolerated with no adverse events.
CONCLUSIONBoth 100 mg (compound D 4 mg) and 200 mg (compound D 8 mg) Phlai capsules, when taken as a single therapeutic dose, inhibited skin reactivity to histamine and mite skin prick tests in AR patients.
TRIAL REGISTRATIONThai clinical trial registry (TCTR20160510001).