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Ⅰ diabetes is a serious threat to human health, a common and frequently-occurring disease , because of its wide source of islet transplantation , easy to store , safe and repeatable transplantation and other advantages, to become the most potential Ⅰ diabetes treatment. But all along , no primary islet graft function (primary islet graftnonfunction, PINF) the existence , limiting the development of islet transplantation . The current study suggests that the main mechanism leading PINF There are two kinds, namely anoikis and islet β cell factor-related apoptosis . Inhibition of apoptosis triggered by the above mechanism is to reduce PINF, improve the success rate of islet transplantation effective way . DcR3/TR6 1998 a newly discovered inhibitor of apoptosis , which through competitive binding FasL and LIGHT, LIGHT -dependent blocking FasL and apoptosis signal transduction pathway , thereby inhibiting both mediated apoptosis. This experiment through DcR3/TR6 islet donor mice pretreated in vitro study of protection against apoptosis in pancreatic islet blow , keeping the role and mechanism of islet viability . It was found that , DcR3/TR6 treated islets in vitro by IFN-γ/IL-2 incubated for 20 hours, the survival , vitality and secretion were significantly higher than the positive control (82.0 ± 9.9% vs57.4 ± 9,9% , P <0.002; 67.3 ± 8.3% vs 34.9 ± 14.6%, P <0.002; 195.7 ± 10.8μIU/Lv.s.158.3 ± 8.5μIU / L, P <0.0001). Because the existing research in 2001 , Zhejiang University master's degree thesis research has proven applications , Fa s-FasL system is involved in islet p cells in vitro and in vivo apoptosis , DCR3/TR6 may inhibit this pathway mediated islet cell apoptosis , achieve the islet protection. We think: this experiment shows DCRVTR6 enhancements , Jl rat islets in vitro against resistance on the role of cytokines , which may block the cytokine stimulated Fa s fighting a sL dependent pathway in pancreatic islet cell apoptosis are closely related.
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