目的 探討馬鞭草苷對口腔扁平苔蘚（OLP）免疫反應(yīng)的抑制作用及機(jī)制。方法 用脂多糖（LPS）體外刺激角質(zhì)形成細(xì)胞系HaCaT細(xì)胞構(gòu)建OLP炎癥模型，CCK-8法檢測細(xì)胞活力；實(shí)時(shí)熒光定量聚合酶鏈?zhǔn)椒磻?yīng)（PCR）法檢測細(xì)胞中腫瘤壞死因子-α（TNF-α）、白細(xì)胞介素-1β（IL-1β）和白細(xì)胞介素-6（IL-6）的基因表達(dá)變化；蛋白質(zhì)印跡法檢測細(xì)胞中核因子-κB p65（NF-κB p65）和p-NF-κB p65蛋白的表達(dá)變化。結(jié)果 在HaCaT細(xì)胞中，LPS刺激抑制細(xì)胞活力，并誘導(dǎo)TNF-α、IL-1β和IL-6基因的表達(dá)上調(diào)，以及NF-κB p65和p-NF-κB p65蛋白的表達(dá)上調(diào)；20 mg/L馬鞭草苷作用24 h可減輕LPS誘導(dǎo)的HaCaT細(xì)胞損傷、抑制炎癥因子的表達(dá)和NF-κB p65信號通路的活化；同時(shí)，經(jīng)G蛋白偶聯(lián)受體18（GRP18）抑制劑O1918預(yù)處理后，馬鞭草苷的保護(hù)作用顯著減弱。結(jié)論 馬鞭草苷可以通過激活GPR18受體抑制NF-κB信號通路的活化，進(jìn)而降低炎癥因子的表達(dá)和減輕OLP口腔黏膜炎癥反應(yīng)。

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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