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首页> 外文期刊>Current therapeutic research, clinical and experimental. >Downregulation of Constitutive and Cytokine-Induced Complement 3 Expression by Morphine in Rat Astrocytes
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Downregulation of Constitutive and Cytokine-Induced Complement 3 Expression by Morphine in Rat Astrocytes

机译：吗啡在大鼠星形胶质细胞中下调组成型和细胞因子诱导的补体3表达。

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BACKGROUND: The effect of opioids on inflammation and immune responses is an important subject of investigation because immunoregulatory cytokines are produced in the central nervous system and opioid receptors are widespread in these cells.OBJECTIVES: The aim of this study was to evaluate the immunomodulatory effect of morphine on the C3 expression (both constitutive and proinflammatory cytokine-induced C3 expression) in primary rat astrocytes.METHODS: Primary rat astrocytes were untreated or treated with morphine in different concentrations (10~-6 to 10~-2 M) before incubation without or with 5 U/mL tumor necrosis factor-alpha (TNF-alpha), and C3 protein and mRNA expressions were measured. Similarly, astrocytes were treated with 10~-3 M morphine and stimulated with other proinflammatory cytokines, including 10 ng/mL interleukin-8 (IL-8) and 5 U/mL IL-lbeta. Astrocytes were exposed to 10~-5 M naloxone for 2 hours before adding morphine, and TNF-a and C3 protein was measured. Tumor growth factor-beta (TGF-bets) was measured from the supernatants of each proinflammatory cytokine.RESULTS: All results are expressed as mean percentages of C3 production by normalizing C3 without morphine or any cytokine treatment as 100%. Constitutive C3 protein production was decreased at morphine 10~-3 M (57.2%) and 10~-2 M (30.1%). Pretreatment with morphine suppressed induction of C3 expression at both the protein and mRNA levels in astrocytes stimulated with TNF-a, IL-8, and IL-1beta (P < 0.05) in a dose-dependent manner. The inhibition of C3 protein production by morphine (10~-3 M; 33%) was partially attenuated by naloxone (52.0%) (P < 0.05). The pretreatment of astrocytes with morphine (10~-3 M) before stimulation with TNF-a, IL-8, and IL-1/3 increased by 33% (P < 0.05), decreased by 15.2% (P < 0.05), and did not change the production of TGF-beta protein, respectively.CONCLUSIONS: Morphine downregulated both constitutive and proinflammatory cytokine-induced C3 expression of ast...
机译：背景：阿片类药物对炎症和免疫反应的影响是重要的研究课题，因为中枢神经系统中产生免疫调节细胞因子，且阿片类药物受体广泛分布于这些细胞中。目的：本研究的目的是评估阿片类药物的免疫调节作用。吗啡对原代大鼠星形胶质细胞C3表达的影响（组成型和促炎性细胞因子诱导的C3表达）方法：未经处理或未经孵育的原代大鼠星形胶质细胞以不同浓度（10〜-6至10〜-2 M）吗啡处理或使用5 U / mL肿瘤坏死因子-α（TNF-alpha），并测量C3蛋白和mRNA表达。同样，星形胶质细胞用10〜-3 M吗啡处理并用其他促炎细胞因子刺激，包括10 ng / mL白细胞介素8（IL-8）和5 U / mLIL-1β。在添加吗啡之前，将星形胶质细胞暴露于10〜-5 M纳洛酮中2小时，然后测量TNF-α和C3蛋白。从每种促炎细胞因子的上清液中测量肿瘤生长因子-β（TGF-bets）。结果：所有结果均表示为通过不使用吗啡或任何细胞因子处理将C3标准化为100％时C3产生的平均百分比。在吗啡10〜-3 M（57.2％）和10〜-2 M（30.1％）时，组成型C3蛋白产量降低。吗啡预处理可以抑制TNF-a，IL-8和IL-1beta刺激的星形胶质细胞中C3表达的蛋白和mRNA水平（P <0.05）。吗啡（10〜-3 M; 33％）对C3蛋白产生的抑制作用被纳洛酮（52.0％）部分减弱（P <0.05）。在用TNF-a，IL-8和IL-1 / 3刺激之前，用吗啡（10〜-3 M）预处理星形胶质细胞增加了33％（P <0.05），减少了15.2％（P <0.05），结论：吗啡下调了组成型和促炎性细胞因子诱导的Ast的C3表达，并下调了TGF-β的表达。

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