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目的探讨泛酰巯基乙胺酶Vanin对胰岛NIT细胞的保护作用及机制。方法培养胰岛β细胞株NIT细胞,以5 ng/ml IFN-γ,50 pg/ml IL-1β,10 ng/ml Vanin处理细胞,分为IFN-γ+IL-1β+Vanin组、IFN-γ+IL-1β组、Vanin组、对照组(DMEM)。4组干预因素分别作用于对数生长期细胞24 h后采用MTT法检测各组NIT细胞的增殖抑制率,化学发光法检测上清液中胰岛素(Ins)水平,硝酸还原酶法检测上清液中一氧化氮(NO)水平。结果经IFN-γ+IL-1β处理的NIT-1细胞增殖受抑制,抑制率为60.11%;予Vanin预处理组细胞增殖抑制率为36.98%,较IFN-γ+IL-1β处理组降低(P<0.01)。经IFN-γ+IL-1β破坏的NIT-1细胞分泌胰岛素较其他3组减少(P<0.05,P<0.01),NO产生较其他3组增多(P<0.05,P<0.01)。而接受Vanin预处理组再予IL-1β+IFN-γ破坏的NIT-1细胞与IL-1β+IFN-γ组比较,分泌胰岛素增加(P<0.05)、NO水平降低(P<0.05)。结论 Vanin可减轻IFN-γ+IL-1β对NIT细胞的损伤作用,保护NIT细胞的胰岛素分泌功能。
Objective To investigate the protective effect and mechanism of pantetheine Vanarin on pancreatic islet NIT cells. Methods NIT cells were cultured and treated with 5 ng / ml IFN-γ, 50 pg / ml IL-1β and 10 ng / ml Vanin and divided into IFN-γ + IL-1β + + IL-1β group, Vanin group, control group (DMEM). Four groups of interventions were applied to the cells in logarithmic growth phase for 24 h. MTT assay was used to detect the proliferation inhibition rate of each group. Chemiluminescence was used to detect the level of insulin in the supernatant. Nitric acid reductase In the level of nitric oxide (NO). Results The proliferation of NIT-1 cells was inhibited by IFN-γ + IL-1β, the inhibition rate was 60.11%. The inhibition rate of cells pre-treated with Vanin was 36.98%, which was lower than that of IFN-γ + IL- P <0.01). NIT-1 cells secreted by IFN-γ + IL-1β reduced insulin production compared with the other three groups (P <0.05, P <0.01), NO production increased more than the other three groups (P <0.05, P <0.01). Compared with IL-1β + IFN-γ group, NIT-1 cells treated with Vanin pretreatment and then treated with IL-1β + IFN-γ increased insulin secretion (P <0.05) and NO level decreased (P <0.05). Conclusion Vanin can reduce the injury of NIT cells induced by IFN-γ + IL-1β and protect the insulin secretion of NIT cells.