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新生Wistar大鼠离体胰岛与细胞因子孵育后 ,观测胰岛素释放和一氧化氮 (NO )生成的变化 ,并用逆转录 聚合酶链反应 (RT PCR )观察IL 18受体信号链 (IL 18Rβ )mRNA的表达水平。结果表明 :(1) 0 6 2 5～ 10nmol/L基因重组小鼠 (rm )IL 18孵育胰岛 2 4h后 ,对累积的和葡萄糖刺激的胰岛素释放以及NO生成均无显著效应 ;(2 ) 2 0 0U/ml基因重组大鼠 (rr)γ干扰素 (IFN γ )或 2 5 0U/ml基因重组人 (rh )肿瘤坏死因子 α (TNF α)单独存在对胰岛素释放和NO生成均无明显效应 ,也不能促使 10nmol/LrmIL 18对胰岛素释放和NO生成产生影响 ;(3) 2 0 0U/mlrrIFN γ +2 5 0U/mlrhTNF α或 15pg/mlrhIL 1β均明显促进NO生成和抑制胰岛素释放 ,而 10nmol/LrmIL 18则不影响IFN γ +TNF α或IL 1β的上述效应 ;(4 )即使经IL 1β和 (或 )IFN γ +TNF α或IL 12孵育后 ,大鼠胰岛素瘤 (RIN )细胞或离体大鼠胰岛仍未见IL 18RβmRNA的表达。提示IL 18在细胞因子所致胰岛β细胞损伤中不发挥直接作用 ,原因是IL 18受体在胰岛 β细胞中不表达。
The changes of insulin release and nitric oxide (NO) production were observed after incubation of isolated islets and cytokines in neonatal Wistar rats. IL 18 receptor mRNA (IL 18Rβ) mRNA was detected by reverse transcriptase-polymerase chain reaction (RT PCR) The level of expression. The results showed that: (1) There was no significant effect on cumulative and glucose-stimulated insulin release and NO production when incubated with 0 6 2 5 ~ 10 nmol / L recombinant mouse (rm) IL 18 for 24 hours; (2) 2 0 0U / ml gene recombinant IFNγ (IFNγ) or 250U / ml recombinant human rh TNF TNFα alone had no effect on insulin release and NO production (3) 200uL / ml rhIFNγ + 250U / ml rhTNFα or 15pg / mlrhIL 1β significantly promoted the production of NO and inhibited the release of NO, while 10nmol / LrmIL 18 had no effect on insulin release and NO production. / LrmIL 18 did not affect the above effects of IFNγ + TNFα or IL₁β; (4) even after incubation with ILβ and / or IFNγ + TNFα or IL 12, rat Insulinoma (RIN) The expression of IL 18RβmRNA in rat islet has not been found in vivo. Suggesting that IL 18 does not play a direct role in cytokine-induced islet beta cell injury due to the fact that IL 18 receptor is not expressed in pancreatic beta cells.