Tacking troublesome tinnitus in Lothian children

Abstract

Methods: HEI-OC1 and KELLY neuroblastoma cells were treated with CDDP (100μM), capsaicin(5μM) and capsaicin (5μM)-CDDP (100μM) at 24 h. Cell viability and apoptotic cell death evaluated by WST-1 and annexin-V/PI flow cytometric analysis. DNA-damage related gene expressions were evaluated by Real-time PCR array (Bio-Rad) in cochlear cells.Results: Capsaicin did not alter cell viability of HEI-OC1 and KELLY. CDDP reduced the viability of HEI-OC1 (46%) and KELLY cells (74%). Combined treatment of capsaicin (5μM)-CDDP (100μM) resulted in a marked decrease in KELLY (16%) cells. Moreover cell viability in HEI-OC1 (80%) cells were increased. Capsaicin alone induced apoptotic cell death of KELLY cells while it did not induce apoptosis in HEI-OC1 cells. CDDP alone and capsaicin-CDDP combinations increased the apoptotic cell death at same ratios in HEI-OC1 cells. In KELLY cells, capsaicin-CDDP combinations induced apoptotic cell death more than CDDP alone. Capsaicin-CDDP induced Fancg, Mif, Mlh3 DNA repair related gene expressions in cochlear cells when compared to CDDP. Bax, Parp2, Pms2, Rad51, Sumo1 and Trp53 (apoptotic and DNA repair) gene expressions were decreased with capsaicin-CDDP combinations while increased in CDDP alone. Expression of Cdc25c was increased with capsaicin-CDDP while decreased with CDDP alone.Conclusion: This study showed that capsaicin increased CDDP induced neuroblastoma cell death while cochlear cells viability was increased. Capsaicin might be nontumor interfering protective agent and the effects must be shown by further studies.Learning Objectives: Congenital cholesteatoma surgical technique preserving intact tympanic structures.