LncRNA NKILA/NF-κB信号通路在口腔扁平苔藓角质形成细胞损伤中的作用研究  

The role of LncRNA NKILA/NF-κB signal pathway in the injury of keratinocytes in oral lichen planus

作　　者：南丽君 王静[1] 李博亚 孟伟涛 张筱娅 NAN Lijun;WANG Jing;LI Boya;MENG Weitao;ZHANG Xiaoya(Department of Stomatology,The First Affiliated Hospital of Zhengzhou University,450000,China)

机构地区：[1]郑州大学第一附属医院口腔科,450000

出　　处：《实用口腔医学杂志》2025年第2期227-234,共8页Journal of Practical Stomatology

基　　金：河南省科技攻关项目(编号:222102310207)。

摘　　要：目的:探究LncRNA NKILA/NF-κB信号通路在口腔扁平苔藓角质形成细胞损伤中的作用。方法:细菌脂多糖(LPS)诱导人类永生化表皮细胞(HaCaTs)构建口腔扁平苔藓(OLP)体外细胞模型,通过慢病毒法构建稳定过表达NKILA的HaCaTs细胞株,将HaCaTs分为4组:Control组、Control+LPS组、感染慢病毒空载体(NC)+LPS组、过表达NKILA(OE)+LPS组,分别检测细胞活性、细胞凋亡、总超氧化物歧化酶(SOD)活性、脂质氧化丙二醛(MDA)、活性氧(ROS)、相关炎症因子水平、p65(核、质)等NF-κB信号通路相关蛋白表达及p65的表达和定位。结果:与Control组相比,Control+LPS组NKILA表达、细胞活性、SOD酶活性显著下降,细胞凋亡率、MDA、ROS、IL-6、IL-1β、TNF-α、p65(核、质)表达水平显著上调(P<0.05);与Control+LPS组相比,OE+LPS组细胞活性、SOD酶活性升高,细胞凋亡率、MDA、ROS、IL-6、IL-1β、TNF-α、p65(核、质)表达水平明显降低(P<0.05),p65蛋白在细胞核中的定位(亮度)明显降低。结论:LncRNA NKILA通过抑制NF-κB信号通路减轻口腔扁平苔藓角质形成细胞损伤。Objective:To explore the role of LncRNA NKILA/NF-κB signal pathway in the injury of keratinocytes in oral lichen planus(OLP).Methods:Immortalized human epidermal cells(HaCaTs)were induced by bacterial lipopolysaccharide(LPS)to establish an in vitro cell model of OLP.HaCaTs stably overexpressing NKILA were constructed by lentivirus method.HaCaTs were divided into 4 groups:Control group,Control+LPS group,empty vector infected with lentivirus(NC)+LPS group,overexpressed NKILA(OE)+LPS group.Cell proliferation,apoptosis,total superoxide dismutase(SOD)activity,lipid malondialdehyde oxide(MDA),reactive oxygen species(ROS),expression of related inflammatory factors,p65(nuclear,mass)and NF-κB signaling pathway related protein expression and p65 expression and localization were respectively detected.Results:Compared with Control group,the expression of NKILA,cell proliferation activity and SOD enzyme activity in Control+LPS group were significantly decreased,while the apoptosis rate,MDA,ROS,IL-6,IL-1β,TNF-αand p65(nuclear and plasma)expression levels were significantly up-regulated(P<0.05).Compared with Control+LPS group,the cell proliferation activity and SOD activity were increased in OE+LPS group,and the expression levels of cell apoptosis,MDA,ROS,IL-6,IL-1β,TNF-αand p65(nuclear and plasma)were significantly decreased(P<0.05),and the localization of p65 protein in the nucleus was significantly decreased in OE+LPS group.Conclusion:LncRNA NKILA may reduce the damage of keratinocytes in oral lichen planus by inhibiting NF-κB signal pathway.

关 键 词：LncRNA NKILA NF-ΚB 口腔扁平苔藓 角质形成细胞 

分 类 号：R781.5[医药卫生—口腔医学]