The role of LncRNA NKILA/NF-κB signal pathway in the injury of keratinocytes in oral lichen planus
10.3969/j.issn.1001-3733.2025.02.014
- VernacularTitle: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
- Author:
Lijun NAN
1
;
Jing WANG
1
;
Boya LI
1
;
Weitao MENG
1
;
Xiaoya ZHANG
1
Author Information
1. 450000,郑州大学第一附属医院口腔科
- Publication Type:Journal Article
- Keywords:
LncRNA NKILA;
NF-κB;
Oral lichen planus;
Keratinocytes
- From:
Journal of Practical Stomatology
2025;41(2):227-234
- CountryChina
- Language:Chinese
-
Abstract:
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 de-creased,while the apoptosis rate,MDA,ROS,IL-6,IL-1β,TNF-α and p65(nuclear and plasma)expression levels were signifi-cantly 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-α and 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.
