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FasL在家兔退变髓核组织中的表达及其与白细胞介素-6和肿瘤坏死因子-α的相关性 被引量:5

The expression of Fas ligand in stabbed disc cells of rabbit IDD model and its correlation with interleakin-6,and turner necrosis factor-α
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摘要 目的 观察生理解剖学屏障与FasL的分子生物学效应之间的关系,探讨椎间盘退变的发病机制.方法 采用18规格的皮肤穿刺针穿刺家兔纤维环,在术后的3、6、10周收集正常及穿刺后的椎间盘组织,免疫组织化学染色观察FasL及白细胞介素(IL)-6和肿瘤坏死因子(TNF)-α等炎性因子的表达.结果 正常髓核组织中可见少许髓核细胞质中FasL呈弱阳性染色(8.7%),实验组髓核细胞质则呈强阳性染色(41.6%、48.8%、46.4%).FasL阳性细胞百分比在正常组与各实验组之间的两两比较,差异有统计学意义(P〈0.01).实验组髓核细胞FasL阳性表达百分比与IL-6及TNF-α阳性表达百分比之间显著相关(r=0.424,P〈0.05及r=0.527,P〈0.01).结论 FasL与理解剖学屏障的共同作用,可能是使髓核组织产生免免效应的重要因素.当生理解剖学屏障受到损伤后(如穿刺纤维环),FasL、IL-6及TNF-α的表达程度增强,FasL所介导的免疫炎性反应是引起椎间盘退变的重要机制之一. Objective To clarify the relation between physiologic barrier and the role of Fas ligand,and investigate a possible pathogenesis of IDD.Methods The anular puncture model of rabbit was established using defined needle gauges and depths.The normal and the stabbed discs were harvested at each time point of 3,6,and 10 weeks after surgery.Immunohistochemical staining of these discs for Fas ligand and interleakin-6(IL-6),TNF-α was performed by standard procedures.Results The normal discs cells exhibited relatively weak immunopositivity(8.7%),and the stabbed disc cells intense immunopositivity(41.6%,48.8%,46.4%on the postoperative week 3,6,and 10,respectively).There was significant difference in the percentage of FasL-positive disc cells between the normal discs and the stabbed discs(P〈0.01).There was a significant correlation between the positive expression rate of FasL and that of IL-6,TNF-α in the disc cells post stab(r=0.424,P〈0.05 andr=0.527,P〈0.01).Conclusion The nucleus pulposus is an"immune-privileged"site.The immune privilege is maintained by FasL and the physiologic barrier together.When the physiologic barrier was damaged,the expression of FasL,IL-6,and TNF-α was increased.FasL-mediated inflammatory reaction may be one of the important mechanisms inducing disc degeneration.
出处 《中华实验外科杂志》 CAS CSCD 北大核心 2010年第1期114-115,共2页 Chinese Journal of Experimental Surgery
关键词 椎间盘 生理屏障 FAS配体 炎性因子 Intervertebral disk Physiologic barrier Fas ligand Inflammatory factor
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