| 雷凤萍,胡 斌,王 晨,郭 琪,胡 渤,高淑兰.SOCS1在氯胺酮减轻小胶质细胞活化中的机制研究[J].,2018,(22):4219-4223 |
| SOCS1在氯胺酮减轻小胶质细胞活化中的机制研究 |
| Role of SOCS1 in Ketamine-Induced Inhibition of Microglial Activation |
| 投稿时间：2018-03-08 修订日期：2018-03-31 |
| DOI：10.13241/j.cnki.pmb.2018.22.004 |
| 中文关键词: 氯胺酮 炎症 脂多糖 小胶质细胞 细胞因子信号转导抑制因子1 |
| 英文关键词: Ketamine Inflammation Lipopolysaccharide Microglia Suppressor of cytokine signaling 1 |
| 基金项目:广东省医学科研基金项目(A2017526) |
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| 中文摘要: |
| 摘要 目的：探讨麻醉药氯胺酮(Ketamine, KET)对暴露于脂多糖(Lipopolysaccharide, LPS)中的小胶质细胞活化水平的影响，并观察细胞因子信号转导抑制因子1(Suppressor of Cytokine Signaling 1, SOCS1)在其中的作用。方法：本研究选用N9小胶质细胞系，将其暴露于浓度为10 ng/mL的LPS中，模拟炎症反应，同时给与浓度为1 mM的KET，采用Western blot、酶联免疫吸附检测（En- zyme-Linked Immunosorbent Assay, ELISA）小RNA干扰和免疫细胞染色等方法，观察KET对暴露于LPS中的小胶质细胞活化水平的影响，及SOCS1分子在其中的作用。结果：将细胞分为3组，分别为正常培养的Control组、LPS组和KET+LPS组，研究发现，将N9小胶质细胞暴露于含10 ng/mL的细胞培养基中24 h后，细胞诱导型一氧化氮合酶（Inducible Nitric Oxide Synthase, iNOS）表达和培养基肿瘤坏死因子α（Tumor Necrosis Factor α, TNF-α）含量显著增加（P<0.05），而KET可显著降iNOS蛋白表达和培养基TNF-α含量（P<0.05）。随后，将细胞分为5组，分别为Control组、LPS组、KET+LPS组、SOCS1-siRNA+KET+LPS组和乱序siRNA(SC-siRNA)+KET+LPS组，我们发现，LPS可显著增加小胶质细胞TNF-α和白细胞介素1β（Interleukin-1β, IL-1β）的释放、增加SOCS1和核因子κB（Neuclear Factor κB, NF-κB）表达（P<0.05），而KET可显著逆转LPS对炎症因子释放和NF-κB表达的影响，并进一步增加SOCS1表达（P<0.05），而SOCS1-siRNA显著逆转了KET的上述作用（P<0.05），SC-siRNA未对KET产生的上述作用造成显著影响（P>0.05）。结论：KET可降低LPS对小胶质细胞的活化作用，上述作用可能通过SOCS1分子介导。 |
| 英文摘要: |
| ABSTRACT Objective: To explore ketamine (KET)-induced effects on the microglial activation caused by lipopolysaccharide (LPS), and to investigate the role of Suppressor of Cytokine Signaling 1 (SOCS1) in the process. Methods: We took N9 microglial cells, and the cells were exposed to the medium containing LPS of 10 ng/mL to mimic inflammation, meanwhile, 1mM of KET was added into the medium. After the treatments of 24 h, western blot, enzyme-linked immunosorbent assay (ELISA), siRNA interfering and immunocy- tochemistry were taken to assess the activation of microglia and the role of SOCS1 in the process. Results: The cells were divided into three groups, including control group, LPS group and KET+LPS group, after the treatments, we found that LPS increased the inducible nitric oxide synthase (iNOS) protein expression and Tumor Necrosis Factor α (TNF-α) concentration in the medium (P<0.05), and KET reduced the iNOS expression and TNF-α concentration significantly (P<0.05). Then, the cells were divided into five groups, including control group, LPS group, KET+LPS group, SOCS1-siRNA+KET+LPS group and SC-siRNA+KET+LPS group, after 24-h treatments, we found that LPS increased TNF-α and Interleukin-1β (IL-1β) releases and the protein expressions of SOCS1 and nuclear factor-κB (NF-κB), and KET significantly reversed the effects induced by LPS, and increased SOCS1 expression (P<0.05). However, SOCS1-siRNA, not the SC-siRNA, significantly reversed the KET-induced effects above (P<0.05). Conclusion: KET can reduce LPS-induced microglial activation, and SOCS1 protein may mediate the process. |
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