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目的观察大骨节病软骨组织中Fas相关死亡结构域蛋白(FADD)和细胞FLICE抑制蛋白(c-FLIP)表达的变化,明确其在大骨节病软骨损伤中的作用。方法将依据大骨节病和骨关节病诊断标准收集的软骨分为大骨节病组(KBD)、骨关节病组(OA)和正常对照组。采用免疫组化染色法检测3组关节软骨的死亡受体调节因子FADD和c-FLIP表达变化,并在显微镜下计数和比较3组关节软骨不同层间阳性表达率的显著性差异。结果(1)KBD和OA组软骨[分别为(28.68±2.19)%和(35.40±2.34)%]中层FADD表达显著较正常组增高(F=16.245,P=0.000),而在表、深层3组间均无显著差异(P=0.206,P=0.761);(2)FADD在KBD软骨中表达以中层最高,为(28.68±5.38)%,其次为深层的(17.94±8.38)%;(3)KBD和OA软骨表层FLIP表达均显著低于正常组(F=5.929,P=0.018),而中层和深层与正常组间均无显著差异。结论 KBD软骨中层FADD显著上调,而软骨表层FLIP表达显著下调,表明死亡受体途径及其调节因子在大骨节病软骨损伤中具有重要作用。
Objective To observe the changes of Fas-related death domain protein (FADD) and cellular FLICE inhibitory protein (c-FLIP) expression in KKD cartilage, and to clarify its role in cartilage damage in Kashin-Beck disease. Methods The cartilage collected according to diagnostic criteria of Kashin-Beck disease and osteoarthrosis were divided into KBD (KBD) group, osteoarthrosis group (OA) and normal control group. The expression of death receptor regulators FADD and c-FLIP in the three groups of articular cartilage were detected by immunohistochemical staining. The significant difference in the positive expression rates of different layers of articular cartilage was counted and compared under the microscope. Results (1) The expression of FADD in middle layer of KBD and OA cartilage [(28.68 ± 2.19)% and (35.40 ± 2.34)% respectively) was significantly higher than that of the normal group (F = 16.245, P = 0.000) (P = 0.206, P = 0.761). (2) The expression of FADD in KBD cartilage was highest (28.68 ± 5.38)%, followed by deep (17.94 ± 8.38)%; (3) ) The expression of FLIP in KBD and OA cartilage surface were significantly lower than those in normal group (F = 5.929, P = 0.018), but there was no significant difference between middle and deep layers and normal group. Conclusions FADD in KBD cartilage middle layer is significantly up-regulated, while the expression of FLIP in cartilage surface is significantly down-regulated, indicating that death receptor pathway and its regulatory factors play an important role in cartilage damage of KDAs.