脂多糖对人牙龈上皮细胞β-防御素表达的影响及其机制研究  

Effect of lipopolysaccharide on the expression of β-defensin in human gingival epithelial cells and its mechanism

作　　者：罗琴[1] 方梅飞 刘贞敏[1] 林小洁[1] 曾启新[1] 陶人川[1] Luo Qin Fang Meifei Liu Zhenmin Lin Xiaojie Zeng Qixin Tao Renchuan.(Department of Periodontics and Oral Medicine, College of Stomatology, Guangxi Medical University, Nanning 530021, China)

机构地区：[1]广西医科大学附属口腔医院牙周黏膜科,南宁530021

出　　处：《广西医科大学学报》2017年第2期173-177,共5页Journal of Guangxi Medical University

基　　金：国家自然科学基金资助项目(No.8126017);广西科技厅重点课题基金资助项目(No.2015GXNSFDA139018)

摘　　要：目的:研究脂多糖(LPS)对人牙龈上皮细胞(HGECs)β-防御素(hBD)-1、hBD-2、hBD-3表达的影响及其分子机制。方法:采用实时荧光定量PCR(FQ-PCR)检测不同浓度(0.1mg/L、1mg/L、10mg/L)LPS作用后HGECs hBD-1、hBD-2、hBD-3mRNA的相对表达量。选用10mg/L LPS诱导p38MAPK抑制剂SB203580或NF-κB抑制剂PDTC孵育2h后的细胞,24h后再次检测hBD-2mRNA的表达量。结果:不同浓度LPS作用下的HGECs hBD-1mRNA相对表达量比较,差异均无统计学意义(均P>0.05)。hBD-2mRNA相对表达量随LPS浓度升高而增加,10mg/L LPS作用下细胞hBD-3mRNA相对表达量显著升高(P<0.001)。在p38MAPK或NF-κB抑制剂存在的情况下,LPS诱导的HGECs hBD-2mRNA相对表达量明显降低(P<0.001)。结论:LPS可能通过激活p38MAPK和NF-κB信号通路诱导HGECs hBD-2的表达。Objective： To investigate the effect and mechanism of lipopolysaccharide （LPS） on the expression of human β-defensins （hBD） -1, hBD-2 and hBD-3 in human gingival epithelial cells （HGECs）. Methods： HGECs were incubated with 0.1 mg/L, 1 mg/L and 10 mg/L of LPS for 24 h, respectively. Subsequently, the hBD-1, hBD-2 and hBD-3 mRNA levels in HGECs were determined by fluorescence quantitative polymerase chain reaction （FQ-PCR）. The cells were treated with SB203580 （an p38MAPK pathway inhibitor） or PDTC （an NFmB pathway inhibitor） for 2 h, and cultured with 10 mg/L LPS for 24 h, then the mRNA expression of hBD-2 in HGECs was detected by FQ-PCR. Results： The hBD-1 mRNA level were not significant different in cells cultured with different concentrations of LPS （ P 〈0.05）. The mRNA expression of hBD-2 was increased along with the dosage of LPS. In cells cultured with 10 mg/L of LPS, the hBD-3 mRNA expression was significantly up-regulated （ P 〈0. 001）. However, the LPS-induced up-regulation of hBD-2 mRNA expression was blocked in the presence of p38MAPK or NF-κB inhibitor （ P 〈0. 001）. Conclusion： These findings suggested that LPS induces the up-regulation of hBD-2 expression in HGECs via the p38MAPK and NF-κB signaling pathway.

关 键 词：人牙龈上皮细胞 脂多糖 Β-防御素 P38MAPK NF-ΚB 

分 类 号：R781.42[医药卫生—口腔医学]