摘要
目的 探讨凋亡相关基因P5 3、Bcl- 2、Fas、Fas-L的表达在口腔扁平苔藓 (OralLichenPlanus,OLP)病变形成及发展中的作用。方法 采用免疫组化SABC法对 2 8例OLP病损中凋亡调节蛋白P5 3、Bcl- 2、Fas、Fas-L进行检测 ;并与正常口腔粘膜比较。结果 ①P5 3蛋白在正常口腔粘膜中表达阴性 ,但可在OLP上皮基底细胞及部分棘细胞中表达。②Bcl- 2蛋白在正常口腔粘膜及OLP病损上皮中表达很弱或阴性 ,但在OLP固有层浸润的淋巴细胞呈强阳性表达。③Fas和Fas -L在正常口腔粘膜及OLP病损上皮中表达差异不显著 (P >0 .0 5 )。结论 口腔扁平苔藓病变的形成及发展部分归因于凋亡。P5 3和Bcl- 2蛋白对OLP局部上皮病变及炎性细胞浸润的存在可能有一定作用。而Fas和Fas-L系统在OLP病变形成及发展中可能不起主要作用。
Objective To clarify the relationship between the expression of apoptosis-associated genes and the development of OLP. Methods Specimens of 28 cases of OLP were immunostained with monoclonal anti-p53, anti-Bcl-2, polyclonal anti-Fas, anti-Fas-ligand by SABC method. Normal buccal mucosa was used as the controls.Results ①Prominent p53 protein expression was seen in 46.43% of OLP, but negative in normal buccal mucosa.②Bcl-2 protein was generally negative in the Keratinocytes of normal buccal mucosa and OLP, but strongly positive in the infiltrating lymphoid cells in case of OLP.③No definite difference in Fas and Fas-ligand staining was noted between normal buccal mucosa and OLP.Conclusion ①The occurrence and development of OLP are in part due to apoptosis. Mutated p53 protein expressed by the basal and a portion of the prickle keratinocytes in cases of OLP may lead to spinal layer hyperplasia in OLP by anti-apoptotic mechanism. Bcl-2 protein expressed by the infiltrating lymphocytes and macrophages in cases of OLP may contribute to the prolonged life span of these inflammatory cells, and therefore to chronicity of the lesion in OLP.②The measurable alteration in the phenotypic expression of Fas and Fas-ligand proteins provided no apparent suggestion that Fas and Fas-ligand play important roles in the death of basal cell that typifies OLP.
出处
《现代口腔医学杂志》
CAS
CSCD
2002年第2期124-126,I000,共4页
Journal of Modern Stomatology
