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目的探讨脂溢性角化病(SK)发病过程中角质形成细胞增殖和凋亡的分子生物学机制。方法运用SP免疫组织化学染色方法,观察50例SK皮损组织及10例正常皮肤组织中CyclinE,Ki-67,EGFR和Bcl-2的水平。结果 CyclinE,Ki-67及EGFR在SK皮损中阳性率均明显高于正常皮肤,且平均积分光密度亦均高于正常皮肤组差异具有统计学意义(P<0.05);而Bcl-2的水平略高于正常组,平均积分光密度高于正常组,但两组间差异无统计学意义(P>0.05)。对50例SK免疫组织化学染色结果做Spearman相关系数分析显示,CyclinE和Ki-67,CyclinE和EGFR,EGFR和Bcl-2,各组相互间表达结果均具有明显的相关性(P<0.01)。结论 CyclinE,Ki-67,EGFR和Bcl-2分别或协同在SK增殖过度、凋亡受抑的发病机制中发挥作用。
Objective To explore the molecular mechanism of keratinocyte proliferation and apoptosis in the pathogenesis of seborrheic keratosis (SK). Methods The levels of CyclinE, Ki-67, EGFR and Bcl-2 in 50 cases of SK lesions and 10 cases of normal skin tissues were observed by SP immunohistochemical staining. Results The positive rates of CyclinE, Ki-67 and EGFR in SK lesions were significantly higher than those in normal skin (P <0.05), and the average integral optical density was also higher than that in normal skin (P <0.05) The level was slightly higher than the normal group, the average integral optical density was higher than the normal group, but there was no significant difference between the two groups (P> 0.05). Spearman correlation coefficient analysis of 50 cases of SK immunohistochemical staining results showed that the expressions of CyclinE, Ki-67, CyclinE, EGFR, EGFR and Bcl-2 were significantly correlated with each other (P <0.01). Conclusion CyclinE, Ki-67, EGFR and Bcl-2 play a role in the pathogenesis of SK hyperproliferation and apoptosis inhibition, respectively.