目的 探讨马鞭草苷对口腔扁平苔藓（OLP）免疫反应的抑制作用及机制。方法 用脂多糖（LPS）体外刺激角质形成细胞系HaCaT细胞构建OLP炎症模型，CCK-8法检测细胞活力；实时荧光定量聚合酶链式反应（PCR）法检测细胞中肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）的基因表达变化；蛋白质印迹法检测细胞中核因子-κB p65（NF-κB p65）和p-NF-κB p65蛋白的表达变化。结果 在HaCaT细胞中，LPS刺激抑制细胞活力，并诱导TNF-α、IL-1β和IL-6基因的表达上调，以及NF-κB p65和p-NF-κB p65蛋白的表达上调；20 mg/L马鞭草苷作用24 h可减轻LPS诱导的HaCaT细胞损伤、抑制炎症因子的表达和NF-κB p65信号通路的活化；同时，经G蛋白偶联受体18（GRP18）抑制剂O1918预处理后，马鞭草苷的保护作用显著减弱。结论 马鞭草苷可以通过激活GPR18受体抑制NF-κB信号通路的活化，进而降低炎症因子的表达和减轻OLP口腔黏膜炎症反应。

Objective To investigate the inhibitory effect and its mechanism of verbenalin on immune response of oral lichen planus (O LP). Methods OLP inflammatory model was established by stimulating Keratinocyte cells (HaCaT cells) with lipopolysaccharide (LPS) in vitro. CCK-8 was adopted to detect the cell viability. The expression changes of tumor necrosis factor-α (TNF-α), interleukin-1 β (IL-1β) and interleukin-6 (IL-6) were detected by the real-time fluorescence quantitative PCR. The protein expression changes of NF-κB p65 and p-NF -κB p65 were detected by Western blotting. Results In HaCaT cells, LPS inhibited the cell viability, and up-regulated the expression of TNF-α, IL-1β and IL-6, as well as the proteins of NF-κB p65 and p-NF-κB p65. The introduction of 20 mg/L verbenalin with the duration of 24 h reduced LPS-induced HaCaT cell damages and inhibited the expression of inflammatory factors as well as the activation of NF-κB p65 signal pathway. Meanwhile, after pre-treatment with G protein-coupled receptor 18 (GRP18) inhibitor O1918, the protective effect of verbenalin was significantly reduced. Conclusion Verbenalin can inhibit the activation of NF-κB signal pathway by activating GPR18 receptor, thereby reducing the expression of inflammatory factors and alleviating the oral inflammatory response of OLP.

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