核因子Kappa B与肿瘤坏死因子α在口腔扁平苔藓中的相关性

Activation of Nuclear Factor-kappa B Correlates with Tumor Necrosis Factor-alpha in Oral Lichen Planus.

目的:研究核因子Kappa B(NF-κB)和肿瘤坏死因子α(TNF-α)在口腔扁平苔藓(OLP)中的相关性,及其两种因子的表达与OLP临床特征之间的联系。方法:30例OLP患者根据其临床表现分为萎缩-糜烂型及斑纹型,采用免疫组化方法研究OLP两种临床类型NF-κB p65及TNF-α的表达,并计算阳性细胞百分率。选取10例正常组织作为对照。结果:NF-κB p65阳性表达位于OLP上皮基底层及临近细胞的胞核内,而正常组织未见胞核着色。TNF-α阳性表达位于OLP上皮基底层细胞的胞质内,正常组织中仅有散在阳性表达。NF-κB p65和TNF-α的表达在不同临床类型、年龄及病损部位中有显著性差异(P<0.05),但与性别无关(P>0.05)。NF-κB p65的胞核着色与TNF-α的高表达呈正相关(r=0.676,P<0.01)。结论:OLP中NF-κB被激活与TNF-α的高表达密切相关。在NF-κB和TNF-α之间可能存在一个正反馈调节环,这种正反馈的机制可能加重了OLP的炎性反应,同时也可能保护了上皮细胞,避免了过多的凋亡。

Objective： To investigate the possible relationship between NF - KB activation and expression of TNF - α in oral lichen planus （OLP）, and their expression pattern in relation to several clinical features. Methods： Thirty OLP cases were divided into atrophic -erosive form （14 cases ） and reticular form （16 cases） according to their clinical manifestations. The expression of NF - KB p65 and TNF - α of both groups were investigated by immunohistochemical staining, and the percentage of positive cells was calculated in each case. Biopsies of 10 normal oral mucosa （NOM） were also underwent the same procedure as control. Results： NF - KB p65 nuclear staining was found in the nucleus of basal and supra- basal epithelial keratinocytes in OLP, however, no positive staining was found in NOM. Positive TNF -α staining was detected in cytoplasm of basal epithelial keratinocytes in OLP, and only scattered staining was detected in NOM. Expression of NF - KB p65 and TNF - ct was significantly different clinical forms, ages and lesion sites （ P 〈 0.05 ） , except for genders （ P 〉 0.05 ） in 30 OLP cases. NF - KB nuclear staining positively correlated （ r = O. 676, P 〈 0.01 ） with TNF - α overexpression in OLP. Conclusion： NF - KB activation and its correlation with overexpressions of TNF - α may play an important role in pathogenesis of OLP. There might be a positive regulatory loop between NF - KB and TNF - α, which may contribute to inflammation in OLP, but may also protect epithelial keratinocytes from excessive apoptosis.