Hypoxia is one of the main reasons for islet apoptosis after transplantation as well as during isolation. In this study, we attempted to determine the potential usefulness of NF-${kappa}B$ inhibitor for suppression of hypoxia-induced ${eta}$-cell apoptosis as well as the relationship between IP-10 induction and ${eta}$-cell apoptosis in hypoxia. To accomplish this, we cultured the mouse pancreatic ${eta}$-cell line MIN6 in hypoxia (1% $O_2$). Among several examined chemokines, only IP-10 mRNA expression was induced under hypoxia, and this induced IP-10 expression was due to NF-${kappa}B$ activity. Since a previous study suggested that IP-10 mediates ${eta}$-cell apoptosis, we measured hypoxia-induced IP-10 protein and examined the effect of anti-IP-10 neutralizing Ab on hypoxia-induced ${eta}$-cell apoptosis. However, IP-10 protein was not detected, and anti-IP-10 neutralizing Ab did not rescue hypoxia-induced MIN6 apoptosis, indicating that there is no relationship between hypoxia-induced IP-10 mRNA expression and hypoxia-induced ${eta}$-cell apoptosis. Since it was still not clear if NF-${kappa}B$ functions as an apoptotic or anti-apoptotic mediator in hypoxia-induced ${eta}$-cell apoptosis, we examined possible involvement of NF-${kappa}B$ in hypoxia-induced ${eta}$-cell apoptosis. Treatment with 1 ${mu}M$ NF-${kappa}B$ inhibitor suppressed hypoxiainduced apoptosis by more than 50%, while 10 ${mu}M$ AP-1 or 4 ${mu}M$ NF-AT inhibitor did not, indicating involvement of NF-${kappa}B$ in hypoxia-induced ${eta}$-cell apoptosis. Overall, these results suggest that IP-10 is not involved in hypoxia-induced ${eta}$-cell apoptosis, and that NF-${kappa}B$ inhibitor can be useful for ameliorating hypoxia-induced ${eta}$-cell apoptosis.