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首页> 外文期刊>Journal of neuroinflammation >Interleukin-1 beta-induced up-regulation of opioid receptors in the untreated and morphine-desensitized U87 MG human astrocytoma cells
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Interleukin-1 beta-induced up-regulation of opioid receptors in the untreated and morphine-desensitized U87 MG human astrocytoma cells

机译：白细胞介素1β诱导的未经治疗和吗啡脱敏的U87 MG人星形细胞瘤细胞中阿片受体的上调

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Background Interleukin-1beta (IL-1β) is a pro-inflammatory cytokine that can be produced in the central nervous system during inflammatory conditions. We have previously shown that IL-1β expression is altered in the rat brain during a morphine tolerant state, indicating that this cytokine may serve as a convergent point between the immune challenge and opiate mediated biological pathways. We hypothesized that IL-1β up-regulates opioid receptors in human astrocytes in both untreated and morphine-desensitized states. Methods To test this hypothesis, we compared the basal expression of the mu (MOR), delta (DOR), and kappa (KOR) opioid receptors in the human U87 MG astrocytic cell line to SH-SY5Y neuronal and HL-60 immune cells using absolute quantitative real time RT-PCR (AQ-rt-RT-PCR). To demonstrate that IL-1β induced up-regulation of the MOR, DOR and KOR, U87 MG cells (2 x 105 cells/well) were treated with IL-1β (20 ng/mL or 40 ng/mL), followed by co-treatment with interleukin-1 receptor antagonist protein (IL-1RAP) (400 ng/mL or 400 ng/mL). The above experiment was repeated in the cells desensitized with morphine, where U87 MG cells were pre-treated with 100 nM morphine. The functionality of the MOR in U87 MG cells was then demonstrated using morphine inhibition of forksolin-induced intracellular cAMP, as determined by radioimmunoassay. Results U87 MG cells treated with IL-1β for 12 h showed a significant up-regulation of MOR and KOR. DOR expression was also elevated, although not significantly. Treatment with IL-1β also showed a significant up-regulation of the MOR in U87 MG cells desensitized with morphine. Co-treatment with IL-1β and interleukin-1 receptor antagonist protein (IL-1RAP) resulted in a significant decrease in IL-1β-mediated MOR up-regulation. Conclusion Our results indicate that the pro-inflammatory cytokine, IL-1β, affects opiate-dependent pathways by up-regulating the expression of the MOR in both untreated and morphine-desensitized U87 MG.
机译：背景白介素-1β（IL-1β）是一种促炎性细胞因子，可在发炎期间在中枢神经系统中产生。先前我们已经证明，吗啡耐受状态期间大鼠脑中IL-1β表达发生变化，表明该细胞因子可能充当免疫挑战和鸦片介导的生物途径之间的汇合点。我们假设IL-1β在未治疗和吗啡脱敏状态下均上调人类星形胶质细胞中的阿片受体。方法为了验证这一假设，我们使用以下方法比较了人U87 MG星形细胞系mu（MOR），δ（DOR）和kappa（KOR）阿片受体与SH-SY5Y神经元和HL-60免疫细胞的基础表达绝对定量实时RT-PCR（AQ-rt-RT-PCR）。为了证明IL-1β诱导MOR，DOR和KOR的上调，先用IL-1β（20 ng / mL或40 ng / mL）处理U87 MG细胞（2 x 105细胞/孔），然后进行-白介素-1受体拮抗剂蛋白（IL-1RAP）（400 ng / mL或400 ng / mL）治疗。在用吗啡脱敏的细胞中重复上述实验，其中U87 MG细胞用100 nM吗啡预处理。然后，使用吗啡抑制苦参素诱导的细胞内cAMP，通过放射免疫测定法证实了U87 MG细胞中MOR的功能。结果用IL-1β处理12小时的U87 MG细胞显示出明显的MOR和KOR上调。 DOR表达也升高，尽管不明显。 IL-1β处理还显示了吗啡脱敏的U87 MG细胞中MOR的显着上调。与IL-1β和白介素1受体拮抗剂蛋白（IL-1RAP）共同治疗导致IL-1β介导的MOR上调显着降低。结论我们的结果表明，促炎细胞因子IL-1β通过上调未治疗和吗啡脱敏的U87 MG中MOR的表达来影响鸦片依赖性途径。

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