Melatonin partially protects 661W cells from H2O2-induced death by inhibiting Fas/FasL-caspase-3.

摘要: Purpose Previous studies have shown that melatonin (MEL) signaling is involved in the modulation of photoreceptor viability during aging. Recent work by our laboratory suggested MEL may protect cones modulating Fas/FasL-caspase-3 pathway. In this study, we first investigated presence receptors (MT1 and MT2) 661W cells, then whether can prevent H2O2-induced cell death, last, through which pathway confers protection. Methods The mRNA proteins were detected with quantitative PCR (q-PCR) immunocytochemistry, respectively. To test protective effect MEL, cells treated H2O2 for 2 h or absence a agonist, an antagonist. study pathways H2O2-mediated Fas/FasL antagonist was used before exposure to H2O2. Finally, caspase-3 analyzed q-PCR immunocytochemistry and/or MEL. Cell using Trypan Blue. Results Both at protein levels cells. partially prevented death (20-25%). This replicated IIK7 (a receptor agonist) when concentration 1 µM. Preincubation luzindole antagonist) blocked Kp7-6, Fas/FasL, caused similarly what observed Fas, FasL, expression increased H2O2, treatment activation Conclusions results demonstrate are present functional induced via inhibition proapoptotic Fas/FasL-caspase-3.