CAJ | 학술논문

目的：观察大骨节病软骨组织中程序化细胞死亡分子5（programmed cell death 5, PDCD5）和早期生长反应蛋白1（early growth response protein-1, EGR-1）表达的变化及其在大骨节病软骨损伤中的作用。方法收集来自大骨节病患者关节软骨（KBD组）10例，同时收集15例骨关节炎病人关节软骨（OA组）作为疾病对照，收集6例正常软骨作为健康对照（正常组）。采用免疫组化染色法检测3组关节软骨组织中死亡受体调节因子PDCD5和EGR-1表达变化，并在显微镜下计数和分析3组关节软骨不同分层间阳性表达率的显著性差异。结果（1）KBD软骨中层PDCD5阳性细胞表达率（41.35±2.97）%显著高于OA组（26.48±2.04）%和正常组（19.02±1.88）%（P=0.001和P=0.000），KBD软骨深层显著高于正常组和OA组（P=0.000和P=0.029），OA组也高于正常组（P=0.038），而3组间的表层软骨细胞PDCD5阳性率无差异（P>0.05）；（2）在KBD软骨表层，EGR-1表达显著高于OA软骨和正常软骨表层（P=0.000和P=0.000），3组软骨的阳性表达率分别为（27.94±3.09）%、（3.20±1.49）%和（12.66±1.06）%，KBD软骨中层EGR-1阳性细胞表达率显著低于OA组软骨（P=0.002），而高于正常软骨（P=0.017），KBD软骨和OA软骨深层阳性率均明显高于正常组（P=0.000和P=0.001），而KBD组和OA组的平均阳性率无统计学差异（P=0.187）；（3）KBD组与正常组的PDCD5和EGR-1分别在3个软骨细胞层的表达均无相关性，而PDCD5和EGR-1在OA关节软骨表层呈强正相关。结论 KBD软骨深层PDCD5显著上调，而软骨表层和深层EGR-1显著高表达，提示这两种重要的细胞死亡相关因子在大骨节病软骨破坏过程中发挥重要作用。
목적：관찰대골절병연골조직중정서화세포사망분자5（programmed cell death 5, PDCD5）화조기생장반응단백1（early growth response protein-1, EGR-1）표체적변화급기재대골절병연골손상중적작용。방법수집래자대골절병환자관절연골（KBD조）10례，동시수집15례골관절염병인관절연골（OA조）작위질병대조，수집6례정상연골작위건강대조（정상조）。채용면역조화염색법검측3조관절연골조직중사망수체조절인자PDCD5화EGR-1표체변화，병재현미경하계수화분석3조관절연골불동분층간양성표체솔적현저성차이。결과（1）KBD연골중층PDCD5양성세포표체솔（41.35±2.97）%현저고우OA조（26.48±2.04）%화정상조（19.02±1.88）%（P=0.001화P=0.000），KBD연골심층현저고우정상조화OA조（P=0.000화P=0.029），OA조야고우정상조（P=0.038），이3조간적표층연골세포PDCD5양성솔무차이（P>0.05）；（2）재KBD연골표층，EGR-1표체현저고우OA연골화정상연골표층（P=0.000화P=0.000），3조연골적양성표체솔분별위（27.94±3.09）%、（3.20±1.49）%화（12.66±1.06）%，KBD연골중층EGR-1양성세포표체솔현저저우OA조연골（P=0.002），이고우정상연골（P=0.017），KBD연골화OA연골심층양성솔균명현고우정상조（P=0.000화P=0.001），이KBD조화OA조적평균양성솔무통계학차이（P=0.187）；（3）KBD조여정상조적PDCD5화EGR-1분별재3개연골세포층적표체균무상관성，이PDCD5화EGR-1재OA관절연골표층정강정상관。결론 KBD연골심층PDCD5현저상조，이연골표층화심층EGR-1현저고표체，제시저량충중요적세포사망상관인자재대골절병연골파배과정중발휘중요작용。
Objective To compare the expressions of programmed cell death 5 (PDCD5) and early growth response protein-1 (EGR-1) in the articular cartilage between Kashin-Beck disease (KBD) and primary osteoarthritis and the roles of these factors in KBD cartilage. Methods Cartilage specimens were collected from 10 confirmed KBD patients, 15 osteoarthritic patients and 6 healthy subjects. The expression levels of PDCD5 and EGR-1 in the cartilage were detected by immunohistochemistry staining, and the positive chondrocyte counts were recorded in the different layers of KBD and OA cartilages. Results The KBD cartilages contained a significantly higher percentage of PDCD5-positive chondrocytes in the middle layer [(41.35 ± 2.97)%] than OA cartilages [(26.48 ± 2.04)%, P=0.001] and normal cartilages [(19.02 ± 1.88)%, P=0.000] with also obvious PDCD5 over-expression in the deeper layer compared to OA (P=0.000) and normal cartilages (P=0.029), but PDCD5 expression in the superficial layer of the cartilages showed no significant difference among the 3 groups(P>0.05). The average EGR-1 positivity rate in the superficial layer of the cartilage was significantly higher in KBD patients than in OA patients (P=0.000) and healthy controls (P=0.000), but in the middle layer, its positivity rate in KBD patients was higher than that in the normal control (P=0.017) but lower than that of OA cartilage (P=0.002); EGR-1 expression in the deeper layer was comparable in KBD and OA cartilages but both was higher than that in normal cartilages. PDCD5 and EGR-1 expressions were not correlated in either KBD or normal cartilages, but were positively correlated in the superficial layer of OA cartilages. Conclusions KBD cartilages show a significantly increased PDCD5 expression in the deeper layer and enhanced EGR-1 expression in both superficial and deeper layers, suggesting the involvement of PDCD5 and EGR-1 in the pathogenesis of KBD.