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Objective This paper aims to investigate the apoptotic effect of inactivated Sendai virus(hemagglutinating virus of Japan-enveloped,HVJ-E) on murine melanoma cells(B16F10) and the possible mechanisms involved in the putative apoptotic reactions.Methods B16F10 cells were treated with HVJ-E at various multiplicities of infection(MOI),and the reactive oxygen species(ROS),cell viability,and apoptosis were measured.Next,the roles of ROS in the regulation of Bcl-2/Bax and the activation of mitogen-activated protein kinase(MAPK) pathways in HVJ-E-treated B16F10 cells were analyzed.To further evaluate the cytotoxic effect of HVJ-E-generated ROS on B16F10 cells,HVJ-E was intratumorally injected,both with and without N-acetyl-L-cysteine(NAC),into melanoma tumors on BALB/c mice.Tumor volume was then monitored for 3 weeks,and the tumor proteins were separated for immunoblot assay.Results Treatment of B16F10 cells with HVJ-E resulted in a dose-dependent inhibition of cell-viability and an induction of apoptosis.The latter effect was associated with the generation of ROS.Inhibition of ROS generation by NAC resulted in a significant reduction of HVJ-E-induced Erk1/2,JNK,and p38 MAPK activation.Additionally,ROS inhibition caused a decrease in the Bcl-2/Bax ratio as well as promoting activation of apoptosis both in vitro and in vivo.Conclusion These results suggest that HVJ-E possesses potential anticancer activity in B16F10 cells through ROS-mediated mitochondrial dysfunction involving the MAPK pathway.
Objective This paper aims to investigate the apoptotic effect of inactivated Sendai virus (hemagglutinating virus of Japan-enveloped, HVJ-E) on murine melanoma cells (B16F10) and the possible mechanisms involved in the putative apoptotic reactions. Methods B16F10 cells were treated with HVJ -E at various multiplicities of infection (MOI), and the reactive oxygen species (ROS), cell viability, and apoptosis were measured .Next, the roles of ROS in the regulation of Bcl-2 / Bax and the activation of mitogen- activated further evaluated the cytotoxic effect of HVJ-E-generated ROS on B16F10 cells, HVJ-E was intratumorally injected, both with and without N-acetyl-L -cysteine (NAC), into melanoma tumors on BALB / c mice. Volume volume was then monitored for 3 weeks, and the tumor proteins were separated for immunoblot assay. Results Treatment of B16F10 cells with HVJ-E resulted in a dose-dependent inhibition of cell-viability and an induction of apoptosis. The latter effect was associated with the generation of ROS. Inhibition of ROS generation by NAC induced in a significant reduction of HVJ-E-induced Erkl / 2, JNK, and p38 MAPK activation. Adpendent, ROS inhibition caused a decrease in the Bcl-2 / Bax ratio as well as promoting activation of apoptosis both in vitro and in vivo. Conclusions These results suggest that HVJ-E possesses potential anticancer activity in B16F10 cells through ROS-mediated mitochondrial dysfunction in the MAPK pathway.