半胱氨酸天冬氨酸蛋白酶8、受体作用蛋白及核因子-κBp65在口腔扁平苔藓中的表达及意义

目的 探讨口腔扁平苔藓(oral lichen planus,OLP)中半胱氨酸天冬氨酸蛋白酶8(caspase-8)、受体作用蛋白(receptor interacting protein,RIP)、核因子-KB(nuclear factor-kB,NF-kB)p65的表达及其与细胞凋亡的关系.方法 采用脱氧核糖核苷酸末端转移酶介导的原位缺口末端标记法(TUNEL)、SP免疫组化法检测30例OLP及15例正常口腔黏膜(正常黏膜组)中caspase-8、RIP、NF-kBp65的表达及细胞凋亡情况.结果 OLP中上皮细胞凋亡指数(6.76±2.32)明显高于正常对照组(2.10±0.42),而固有层的凋亡指数(1.75±0.74)明显低于正常对照组(6.10±0.96),差异均有统计学意义(P<0.05).OLP的上皮层角质细胞caspase-8、RIP、NF-kBp65的阳性率分别为97%(29/30)、87%(26/30)及93%(28/30),均显著高于正常黏膜组(P<0.01).固有层淋巴细胞caspase-8、RIP、NF-p65的阳性率分别为100%(30/30)、90%(27/30)及80%(24/30),均明显高于正常黏膜组(P<0.01).OLP的上皮角质细胞和固有层淋巴细胞caspase-8、RIP、NF-kB065表达水平分别与其自身凋亡指数(apototic index,AI)正相关.OLP上皮层中RIP、NF-kBp65和caspase-8的表达均互为正相关关系,三者在固有层的表达亦互为正相关关系,固有层淋巴细胞NF-kB阳性表达强弱与上皮细胞AJ呈正相关.结论 OLP中同时存在角质细胞凋亡亢进及固有层淋巴细胞凋亡的减少,这种凋亡的异常可能与OLP的发生、发展密切相关.OLP中caspase-8、RIP和NF-kBp65高表达,提示caspase-8、RIP和NF-kB065在口腔扁平苔藓的发病中起一定作用.

Expression of caspase-8,receptor interacting protein and nuclear factor-kBp65 in oral lichen planus

Objective To investigate the expressions of caspase-8,receptor interacting protein (RIP) and nuclear factor(NF)-kBp65 in oral lichen planus(OLP)and their relationship with cell apoptosis.Methods Immunohistochemical technique with SP method was used to detect the expressions of caspase-8,RIP and NF-kBp65 in 30 OLP cases and 15 normal oral mucosa specimens.Terminal deoxynucleotidyl transferase-mediated nucleotide shift enzyme(TdT)mediated d-UTP end labeling(TUNEL)was used for detecting the cell apoptotic index(AI)in 15 OLP cases and 5 nomal oral mucosa specimens.Results Compared with the control group,the AI of epithelial cells(6.76±2.32)increased and the AI of lymphocytes(1.75±0.74)decreased in OLP(P<0.01).The positive rate of caspase-8,RIP and NF-kBp65 OLP than in normal control(P<0.05).The positive rate of caspase-8,RIP and NF-kBp65 of lymphocytes control(P<0.01).A positive correlation was also observed between NF-kBp65 expression of lymphocytes and AI of epithelial cells.Conclusions Accelerated apoptosis of the keratinocytes and inhibition of lymphocyte apoptosis may coexist and contribute to the formation and progression of OLP.The over expression of caspase-8,RIP and NF-kBp65 in OLP may play a role in the pathogenesis of OLP.