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地黄醇提物含药血清调控BV2小胶质细胞极化干预神经炎症的机制
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| 篇名： | 地黄醇提物含药血清调控BV2小胶质细胞极化干预神经炎症的机制 |
| TITLE： | Mechanism of Rehmannia glutinosa-medicated serum regulating BV2 microglia polarization to interfere with neuroinflammation |
| 摘要： | 目的 研究地黄醇提物含药血清（RG）调控脂多糖（LPS）诱导的BV2小胶质细胞极化干预神经炎症的作用机制。方法采用LPS诱导BV2细胞建立体外神经炎症模型。将细胞分为对照组、LPS组、10%RG组、20%RG组、BAY11-7082[核因子κB（NF-κB）抑制剂]组、20%RG+BAY11-7082组，除control组外，其余各组细胞先加入相应药液预处理12h，再加入LPS刺激24h。观察各组细胞形态，检测离子钙结合适配分子1（Iba-1）、诱导型一氧化氮合酶（iNOS）、分化簇206（CD206）荧光强度，肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）、IL-1β、iNOS、IL-4、IL-10、转化生长因子β（TGF-β）、精氨酸酶1（Arg-1）mRNA表达以及Toll样受体4（TLR4）/NF-κB/NOD样受体热蛋白结构域相关蛋白3（NLRP3）信号通路相关蛋白表达。结果与对照组比较，LPS组细胞形态发生明显改变，呈典型M1型活化形态；Iba-1、iNOS荧光强度，TNF-α、IL-6、IL-1β、iNOSmRNA相对表达量，TLR4、NLRP3、胱天蛋白酶1p20、IL-1βp17蛋白相对表达量及NF-κBp65、NF-κB抑制蛋白α磷酸化水平均显著升高（P＜0.05）；CD206荧光强度和IL-4、IL-10、TGF-β、Arg-1mRNA相对表达量均显著降低（P＜0.05）。与LPS组比较，10%RG组、20%RG组、BAY11-7082组和20%RG+BAY11-7082组细胞中上述指标变化均显著逆转（P＜0.05），且后3组比较差异均无统计学意义（P＞0.05）。结论RG可有效抑制小胶质细胞的整体活化并纠正其M1/M2极化失衡，其机制可能与抑制TLR4/NF-κB/NLRP3信号通路的过度激活相关。 |
| ABSTRACT： | Abstract OBJECTIVE To study the mechanism of action of Rehmannia glutinosa-medicated serum （RG） in regulating lipopolysaccharide （LPS）-induced polarization of BV2 microglia to interfere with neuroinflammation. METHODS An in vitro neuroinflammation model of BV2 cells induced by LPS was established. Cells were divided into control group， LPS group， 10%RG group， 20%RG group， BAY 11-7082 [nuclear factor kappa B （NF-κB） inhibitor] group， and 20%RG+BAY 11-7082 group. Except for the control group， cells in all other groups were pretreated with corresponding drugs for 12 h and then stimulated with LPS for 24 h. The morphology of cells in each group was observed， and the fluorescence intensity of ionized calcium binding adaptor molecule 1 （Iba-1）， inducible nitric oxide synthase （iNOS）， CD206， the mRNA expression of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， IL-1β， iNOS， IL-4， IL-10， transforming growth factor-β （TGF-β）， arginase-1 （Arg-1）， and the Toll-like receptor 4 （TLR4）/NF-κB/NOD-like receptor thermal protein domain associated protein 3 （NLRP3） signaling pathway-related protein expression were detected. RESULTS Compared with the control group， the LPS group showed significant changes in cell morphology， exhibiting a typical M1 activated morphology. The fluorescence intensity of Iba-1 and iNOS， the relative expression levels of TNF-α， IL-6， IL-1β， iNOS mRNA， the relative expression levels of TLR4， NLRP3， caspase-1 p20， IL-1β p17 protein， and the phosphorylation levels of NF-κB p65 and inhibitor of nuclear factor kappa B α were significantly increased （P＜0.05）. The fluorescence intensity of CD206 and the relative expression levels of IL-4， IL-10， TGF-β， and Arg-1 mRNA were significantly reduced （P＜0.05）. Compared with the LPS group， the changes in the above indicators in the cells of the 10%RG group， 20%RG group， BAY 11-7082 group， and 20%RG+BAY 11-7082 group were significantly reversed （P＜0.05）， and there was no statistically significant difference in the comparison of the last three groups （P＞0.05）. CONCLUSIONS RG can effectively inhibit the overall activation of microglia and correct their M1/M2 polarization imbalance， and its mechanism may be closely related to the inhibition of excessive activation of the TLR4/NF-κB/NLRP3 signaling pathway. |
| 期刊： | 2026年第37卷第15期 |
| 作者： | 田萍；安鸿志；费千；梁瑞峰；杨丹；张雪侠；葛文静；刘一菲；李红伟；韩德恩 |
| AUTHORS： | TIAN Ping，AN Hongzhi， FEI Qian，LIANG Ruifeng，YANG Dan，ZHANG Xuexia，GE Wenjing，LIU Yifei，LI Hongwei，HAN Deen |
| 关键字： | 地黄醇提物；含药血清；小胶质细胞；神经炎症；TLR4/NF-κB/NLRP3信号通路；抑郁症 |
| KEYWORDS： | Rehmannia glutinosa； medicated serum； microglia； neuroinflammation； TLR4/NF-κB/NLRP3 signaling pathway； depression |
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