凋亡蛋白Bcl-2、Bax在白斑、口腔扁平苔藓中的表达

目的:观察凋亡蛋白Bcl-2、Bax在白斑、口腔扁平苔藓上皮细胞中的表达,探讨其在口腔白斑、口腔扁平苔藓癌变过程中的作用机制。方法:采用免疫组化法检测10例正常口腔黏膜上皮、18例口腔扁平苔藓、23例白斑、22例口腔鳞癌上皮组织中凋亡相关蛋白Bcl-2、Bax的表达水平。结果:Bcl-2在白斑、口腔扁平苔藓上皮细胞层无异常表达,但在口腔扁平苔藓淋巴细胞浸润带过度表达。Bcl-2在鳞癌组织中呈高表达,与正常黏膜相比有显著性差异(P<0.05)。Bax在上皮单纯增生、轻度、中度不典型增生和低分化鳞癌及糜烂型口腔扁平苔藓组织中呈过度表达,与正常黏膜相比有显著性差异(P<0.05)。结论:Bax参与了口腔白斑癌变的早期事件,而Bcl-2在不典型增生转化为鳞癌的阶段并未发生作用。口腔扁平苔藓的发病机制可能与Bcl-2抑制淋巴细胞凋亡,使细胞免疫亢进,从而刺激上皮细胞Bax过度表达,诱导角朊细胞凋亡有关。

The expression of apoptosis-associated proteins Bcl-2,Bax in oral leukoplakia and lichen planus

PURPOSE: The purpose of this study was to explore the pathogenesis and carcinogenesis of oral leukoplakia (LK) and oral lichen planus (OLP) by examining the expression of apoptosis-associated proteins Bcl-2,Bax in LK and OLP. METHODS: The expression of Bcl-2 and Bax were measured in 10 cases of normal oral mucosa,18 cases of OLP, 23 cases of LK and 22 cases of oral squamous cell carcinoma (SCC) by immunohistochemical assays. RESULTS: In the epithelial cell layer of LK and OLP, the positive Bcl-2 expression was similar to oral normal mucosa,but in the part of the lymphocytic infiltration of OLP, overexpression of Bcl-2 was observed. In the SCC, the Bcl-2 expression was significantly higher than that in normal oral mucosa(P<0.05). In the tissue of simple hyperplasia, mild dysplasia, moderate dysplasia, poorly differentiated SCC and erosive OLP, the expression of Bax was significantly higher than that in normal oral mucosa(P<0.05). CONCLUSIONS: Bax was closely related to the early event of LK carcinogenesis. Bcl-2 may not play a role in LK carcinogenesis. Bcl-2 and Bax play an important role in pathogenesis of OLP. We postulate that the Bcl-2 inhibits the apoptosis of lymphocytes that strengthen the cell-mediated immune process and the overexpression of Bax was related to the apoptosis of epithelial cells in OLP.