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作 者:林心强[1] 王挥戈[1] 沈志忠[1] 杨丹娜[1] 郑朝生[1]
机构地区:[1]汕头大学医学院第一附属医院耳鼻咽喉-头颈外科,广东汕头515041
出 处:《汕头大学医学院学报》2007年第4期200-202,F0002,共4页Journal of Shantou University Medical College
基 金:广东省医学科研基金资助项目(A1997321)
摘 要:其其发病学意义。方法:用免疫组化染色法检测鼻息肉组(29例)和下鼻甲组(11例)上皮细胞Fas、FasL、Bcl-2基因蛋白的表达。结果:鼻息肉组上皮细胞Fas、FasL和Bcl-2阳性细胞指数(PIFas、PIFasL、PIBcl-2)均大于下鼻甲组(P<0.01),PIBcl-2/PIFas也大于下鼻甲组(P<0.01),但鼻息肉组PIFasL/PIFas与下鼻甲组比无统计学意义;鼻息肉组PIFasL/PIFas和PIBcl-2/PIFas均大于1(理论值,P<0.05)。结论:Bcl-2介导的抑制细胞凋亡机制和FasL介导的细胞免疫逃逸机制可能对Fas/FasL系统介导的细胞凋亡产生部分抑制作用,有可能是鼻息肉上皮细胞增殖和细胞凋亡平衡失调的根本原因。Objectiv: To explore the expression and its pathogenic significance of apoptosis-associated proteins(Fas, FasL and Bcl-2)in epithelial cells of nasal polyps. Methods: The protein expressions of Fas, FasL and Bcl-2 of epithelial cells in the nasal polyps group(29 cases)and in the inferior turbinate group( 11 cases)were detected by immunohistochemical staining. Results: PIFas, PIFasL and PIBcl-2 of epithelial cells in the nasal polyps group were higher than those of epithelial cells in the inferior turbinate group( P 〈 0.01). PIBcl-2/PIFas of epithelial cells in the nasal polyps group was higher than that of epithelial cells in the inferior turbinate group( P 〈 0.01), however, PIFasL/PIFas in the nasal polyps group was no significant difference compared with the inferior turbinate. PIFasL/PIBcl-2 of epithelial cells in the nasal polyps group was higher than PIFas ( P 〈 0.05). Conclusion: Both Bcl-2 mediated apoptosis inhibition mechanism and FasL mediated cell immune escape mechanism may partly inhibite Fas/FasL system mediated cell apoptosis in epithelia of nasal polyps. This might be the ultimate cause leading to imbalance between proliferation and apoptosis on epithelia in nasal polyps.
分 类 号:R765.2[医药卫生—耳鼻咽喉科] R363.2[医药卫生—临床医学]
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