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Safflower Yellow regulates microglial polarization and inhibits inflammatory response in LPS-stimulated Bv2 cells

机译:红花黄调节LPS刺激的Bv2细胞中的小胶质细胞极化和抑制炎症反应。

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Activated microglia, especially polarized M1 cells, produce pro-inflammatory cytokines and free radicals, thereby contributing directly to neuroinflammation and various brain disorders. Given that excessive or chronic neuroinflammation within the central nervous system (CNS) exacerbates neuronal damage, molecules that modulate neuroinflammation are candidates as neuroprotective agents. In this study, we provide evidence that Safflor yellow (SY), the main active component in the traditional Chinese medicine safflower, modulates inflammatory responses by acting directly on BV2 microglia. LPS stimulated BV2 cells to upregulate expression of TLR4-Myd88 and MAPK-NF-κB signaling pathways and to release IL-1β, IL-6, TNF-α, and COX-2. However, SY treatment inhibited expression of TLR4-Myd88 and p-38/p-JNK-NF-κB, downregulated expression of iNOS, CD16/32, and IL-12, and upregulated CD206 and IL-10. In conclusion, our results demonstrate that SY exerts an anti-inflammatory effect on BV2 microglia, possibly through TLR-4/p-38/p-JNK/NF-κB signaling pathways and the conversion of microglia from inflammatory M1 to an anti-inflammatory M2 phenotype.
机译:活化的小胶质细胞,尤其是极化的M1细胞,会产生促炎性细胞因子和自由基,从而直接导致神经炎症和各种脑部疾病。考虑到中枢神经系统(CNS)内过度或慢性神经炎症会加剧神经元损伤,因此调节神经炎症的分子可作为神经保护剂。在这项研究中,我们提供的证据表明,中药红花的主要活性成分番红花黄(SY)通过直接作用于BV2小胶质细胞来调节炎症反应。 LPS刺激BV2细胞上调TLR4-Myd88和MAPK-NF-κB信号通路的表达并释放IL-1β,IL-6,TNF-α和COX-2。但是,SY处理可抑制TLR4-Myd88和p-38 /p-JNK-NF-κB的表达,下调iNOS,CD16 / 32和IL-12的表达,并上调CD206和IL-10的表达。总之,我们的结果表明,SY对BV2小胶质细胞具有抗炎作用,可能是通过TLR-4 / p-38 / p-JNK /NF-κB信号通路以及小胶质细胞从炎症性M1转变为抗炎性M2表型。

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