CAJ | 학술논문

背景：激素导致股骨头缺血坏死是一个复杂的生物学过程，其发病机制仍不清楚，探明其病因学机制，仍然是该领域研究的重点。目的：观察骨髓造血细胞DNA氧化损伤与骨细胞凋亡在早期激素性股骨头缺血坏死中的病理改变。方法：4月龄日本大耳白兔40只，随机数字表法分为4组，每组10只。其中3组兔分别给予激素联合内毒素、单纯激素、单纯内毒素处理，另1组做空白对照。分别于最后一次给药后第2，4周处死实验动物，每次每组5只。光镜下计数各组兔股骨头空缺骨陷窝、电镜观察骨细胞形态变化、TUNEL法检测骨细胞凋亡、免疫组织化学法检测骨髓造血细胞DNA氧化损伤。结果与结论：与其他3组比较，激素联合内毒素组第2，4周空缺骨陷窝率、骨髓造血细胞DNA氧化损伤率及第4周骨细胞凋亡率均显著增高(P <0.01)；其他3组之间空缺骨陷窝率、骨髓造血细胞DNA氧化损伤率及骨细胞凋亡率各指标比较差异无显著性意义。激素联合内毒素组空缺骨陷窝率与细胞凋亡率呈正相关(r=0.793)。结果提示在激素性股骨头缺血坏死早期，骨髓造血细胞DNA氧化损伤与骨细胞凋亡参与了激素性股骨头缺血坏死的病理变化过程，前者先于后者发生，骨细胞的死亡方式为凋亡。
배경：격소도치고골두결혈배사시일개복잡적생물학과정，기발병궤제잉불청초，탐명기병인학궤제，잉연시해영역연구적중점。목적：관찰골수조혈세포DNA양화손상여골세포조망재조기격소성고골두결혈배사중적병리개변。방법：4월령일본대이백토40지，수궤수자표법분위4조，매조10지。기중3조토분별급여격소연합내독소、단순격소、단순내독소처리，령1조주공백대조。분별우최후일차급약후제2，4주처사실험동물，매차매조5지。광경하계수각조토고골두공결골함와、전경관찰골세포형태변화、TUNEL법검측골세포조망、면역조직화학법검측골수조혈세포DNA양화손상。결과여결론：여기타3조비교，격소연합내독소조제2，4주공결골함와솔、골수조혈세포DNA양화손상솔급제4주골세포조망솔균현저증고(P <0.01)；기타3조지간공결골함와솔、골수조혈세포DNA양화손상솔급골세포조망솔각지표비교차이무현저성의의。격소연합내독소조공결골함와솔여세포조망솔정정상관(r=0.793)。결과제시재격소성고골두결혈배사조기，골수조혈세포DNA양화손상여골세포조망삼여료격소성고골두결혈배사적병리변화과정，전자선우후자발생，골세포적사망방식위조망。
BACKGROUND:Hormones-induced avascular necrosis of the femoral head is a complex biological process, and its pathogenesis remains unclear. To prove its etiologic mechanism is stil the focus of research in this field. OBJECTIVE:To discuss the pathological changes of hematopoietic cels and osteocytes in early avascular necrosis of the femoral head induced by glucocorticoids . METHODS: Forty Japanese white rabbits, 4 months old, were randomly divided into glucocorticoids+ lipopolysaccharide group (combination group), glucocorticoids group, lipopolysaccharide group and blank control group, with 10 rabbits in each group. Five animals from each group were sacrificed at 2 and 4 weeks after the last dosing, respectively. Vacant bone lacunae were counted under optical microscope, morphology of osteocytes was observed under electron microscope, osteocyte apoptosis was assay by TUNEL, and DNA oxidative damage to hematopoietic cels was detected by immunohistochemistry. <br> RESULTS AND CONCLUSION:Compared with the other three groups, the rates of vacant lacunae and DNA oxidative damage to hematopoietic cels in the combination group were significantly higher at 2 and 4 weeks after treatment as wel as the apoptosis rate of osteocytes at 4 weeks after treatment (P < 0.01); while there were no statistical differences between the other three groups. In the combination group, the vacant rate of bone lacunae and apoptosis rate of osteocytes were positively correlated (r=0.793). These findings indicate that DNA oxidative damage to hematopoietic cels and apoptosis of osteocytes participate in the pathological changes of early avascular necrosis of the femoral head induced by glucocorticoids. The former is prior to the latter, and the death manner of osteocytes is apoptosis.