Apoptosis Of Mycosis Fungoides Hut-102 Cells Induced By Triptolide In Combination With Dexamethasone And Its Mechanism

Mycosis fungoides is the most common cutaneous T-cell lymphomas, a group of rare cancers that grow in the skin with high recurrence rate and poor prognosis. Treatments such as steroid creams during the early stage of mycosis fungoides concern the clinical prognosis of the patients. Triptolide and dexamethasone are common drugs for treatment of skin diseases, with anti-inflammation and immunosuppression activities. Combination of triptolide and dexamethasone has apparent curative effect on treatment for inflammatory diseases such as severe dermatitis, eczema and psoriasis.The cellular responses of glucocorticoids are achieved by specifically binding to its ligands. Glucocorticoids mainly regulates the biological effect of cellular metabolism by its ligands, and affects the expression of tumor related genes in the transcription and translation level. Caspase enzyme, especially Caspase-3, plays an important role in the cell apoptosisIn this study, we aimed to investigate the effect of triptolide combined with dexamethasone on proliferation and apoptosis of the mycosis fungoides hut-102 cells and the possible mechanisms.The viability of hut-102 cells was measured by MTT assay; the apoptotic rate of hut-102 cells was detected by flow cytometry. The expression levels of Glucocorticoid receptor (GR) and apoptosis-related protein Caspase-3 were determined by Western Blot analysis.MTT assays showed that different concentrations of triptolide or dexamethasone can effectively inhibit the proliferation of hut-102 cells in a dose and time-dependent manner. When triptolide (12.5 nm/L) was co-administered with dexamethasone, the inhibition rate increased along with the concentration of dexamethasone. And we observed positive cooperative inhibitory effects of triptolide and dexamethasone on the proliferation of hut-102 cells. Both triptolide and dexamethasone can independently promote apoptosis of the hut-102 cell. And the apoptotic rate in the combination group was higher than single group(P﹤0.05). Compared with the significantly decreased expression of Glucocorticoid receptor (GR) in hut-102 cells in dexamethasone group, the expression of GR and activated Caspase-3 increased in the combination group(P<0.05).The apoptosis of hut-102 cells induced by dexamethasone was enhanced by triptolide, which maybe connected with the increased expression of GR and activated Caspase-3 in hut-102 cells.