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首页> 外文期刊>Journal of biomaterials and tissue engineering >The Cannabinoid 2 Receptor (CB2R) Alleviates Inflammatory and Oxidative Stress in Lipopolysaccharide-Induced BV-2 Cells and Regulates M1/M2 Polarization
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The Cannabinoid 2 Receptor (CB2R) Alleviates Inflammatory and Oxidative Stress in Lipopolysaccharide-Induced BV-2 Cells and Regulates M1/M2 Polarization

机译：大麻素2受体（CB2R）减轻了脂多糖诱导的BV-2细胞中的炎症和氧化应激，并调节M1 / M2极化

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Background : Microglia, which participates in the inflammatory responses in the CNS, can be polarized into M1 and M2 phenotypes, showing many functional properties such as the production of inflammation association molecules. The main aim of this study is to explore whether CB2R is involved in the transformation of BV-2 cells from M1 to M2 to reduce inflammation and oxidative stress, thus promoting the repair of damaged nerves. Material and Methods: The viability of BV-2 cells was detected by CCK-8 assay. For the analysis of the phenotypic properties of BV-2 cells, we further detected the expression of M1 markers (CD32, iNOS), M2 marker (Arg1) and CB2R using western blot or immunofluorescence. After transfection into cells, the overexpressed CB2R was treated with CB2R inhibitor (AM630), then the functional properties of BV-2 cell types regarding cytokine expression profiles were assessed by measuring the production of IL-6, IL-1 beta, TNF-alpha, and ROS with ELISA assay. In addition, the neurotrophic factors, including NRF-2, HO-1 and NGF, were detected by western blot. Results : Under M1 conditions, BV-2 cells were overexpressed with CD32 and iNOS, and M1-polarizing conditions induced the production of pro-inflammatory cytokines and ROS. The overexpression of CB2R promotes the transformation from M1 into M2 phenotype in BV-2 cells, following with the upregulation of Arg-1. Meanwhile, the neurotrophic factors were increased in LPS-induced BV-2 cells after CB2R transfection. All these effects were attenuated by AM630. Conclusion : Targeting CB2R might be a new therapeutic option for the treatment of nerve injury and neurological diseases associated with neuroinflammation.
机译：背景：参与CNS中的炎症反应的小胶质细胞可以被偏振成M1和M2表型，呈现许多功能性质，例如炎症结合分子的产生。本研究的主要目的是探讨CB2R是否参与来自M1至M2的BV-2细胞的转化，以降低炎症和氧化应激，从而促进受损神经的修复。材料和方法：通过CCK-8测定检测BV-2细胞的活力。为了分析BV-2细胞的表型特性，我们进一步使用蛋白质印迹或免疫荧光进一步检测了M1标记（CD32，InOS），M2标记（Arc1）和CB2R的表达。在转染后，用CB2R抑制剂（AM630）处理过表达的CB2R，然后通过测量IL-6，IL-1β，TNF-α的产生来评估关于细胞因子表达谱的BV-2细胞类型的功能性质和ros有elisa测定。此外，通过Western印迹检测包括NRF-2，HO-1和NGF，包括NRF-2，HO-1和NGF的神经营养因子。结果：根据M1条件，用CD32和InOS过表达BV-2细胞，M1偏振条件诱导促炎细胞因子和ROS的产生。 CB2R的过度表达促进在BV-2细胞中的M1转化为M2表型，随后用ARG-1的上调。同时，在CB2R转染后LPS诱导的BV-2细胞中，神经营养因子增加。所有这些效果都在AM630衰减。结论：靶向CB2R可能是治疗神经损伤和与神经炎症相关的神经疾病的新治疗选择。

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