一氧化氮和Ca^(2+)介导的细胞因子损伤大鼠胰岛细胞的研究  

A study on nitric oxide and Ca^(2+) mediated rat islet cells of Langerhans injury induced by cytokine

作　　者：余华荣[1] 张能[1] 方海立[1] 郑倩[2] 

机构地区：[1]重庆医科大学基础医学院生理教研室,重庆400016 [2]川北医学院生理教研室,四川南充637007

出　　处：《中国现代医学杂志》2006年第1期60-63,共4页China Journal of Modern Medicine

摘　　要：目的观察一氧化氮和Ca2+在白细胞介素-1β(IL-1β)、肿瘤坏死因子(TNF)和γ-干扰素(IFN-γ)诱导的胰岛细胞凋亡中的作用。方法应用体外单层培养的3￣5d的Wistar大鼠胰岛细胞,分别检测IL-1β、TNF和IFN-γ对胰岛细胞凋亡细胞百分率、[Ca2+]i含量以及培养液中基础和高糖刺激下胰岛素分泌量、NO含量及NOS活性以及DNA片段的影响。结果IL-1β、TNF和IFN-γ联合可诱导胰岛细胞凋亡率明显增加及DNA片段化,基础和高糖刺激下胰岛素分泌量降低,同时胰岛细胞[Ca2+]i、NO含量和NOS活性亦明显升高(P<0.01),且有时间和剂量依赖性。结论NO和Ca2+可能是介导上述细胞因子引起胰岛细胞凋亡的重要途径。[Objective] To observe the role of nitric oxide and Ca^2＋ on injury of isolated pancreatic islet ceils induced by combination of IL-1β, TNF and IFN-γ. [Methods] Isolated pancreatic islet cells from Wistar rats of 3-5 days were incubated in monolayer in vitro. Intracellular Ca^2＋, insulin secretion, NO production, NOS activity, apoptotic percentage of islet cells and DNA fragmentation in pancreatic islet cells incubated with combination of IL-1β, TNF and IFN-γ were measured. [Results] Combination of IL-1β, TNF and IFN-γ induced a significant increase of apoptotic percentage of pancreatic islet cells and DNA ladder appearance and decrease of the medium insulin accumulation and the glucosestimulated insulin release. Intracellular Ca^2＋, NO production and NOS activity also remarkably increased （P 〈0.01）. These effects bear the characters of time and dose dependence. [Conclusion] NO and Ca^2＋ might be important ways of inducing apoptotis of pancreatic islet cells by combination of IL-1β, TNF and IFN-γ.

关 键 词：白细胞介素-1 β 细胞凋亡 一氧化氮 CA^2+ 胰岛细胞 

分 类 号：R335[医药卫生—人体生理学]