Zhao Z Q, Bai R, Liu W L, Feng W, Zhao A Q, Wang Y, Wang W X, Sun L, Wu L S, Cui S X
Department of Pediatric Orthopedics, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Department of Orthopedics, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Genet Mol Res. 2016 Mar 24;15(1):gmr7706. doi: 10.4238/gmr.15017706.
An animal model of steroid-induced avascular necrosis of femoral head (SANFH) was established to investigate the role of oxidative DNA damage of bone marrow hematopoietic cells in SANFH. Forty-five-month-old Japanese white rabbits (male or female, 2.5 ± 0.5 kg) were randomly divided into groups A (methylprednisolone + Escherichia coli endotoxin), B (methylprednisolone alone), C (E. coli endotoxin alone), and D (blank control). The animals were sacrificed two and four weeks after administration of the last dose (N = 5 each group and each time). Left and right femoral heads were fixed and decalcified. Empty lacunae were counted by hematoxylin and eosin staining and oxidative DNA damage of bone marrow hematopoietic cells was detected by immunohistochemistry. At week 2, the rate of oxidative DNA damage in bone marrow hematopoietic cells was significantly higher in group A than in groups B, C, and D (P < 0.01), while there was no significant difference between groups B, C, and D. At week 4, the rate of oxidative DNA damage in bone marrow hematopoietic cells was significantly higher in group A than in groups B, C, and D (P < 0.01), while there was no significant difference among groups B, C, and D. Thus, oxidative DNA damage of bone marrow hematopoietic cells appears to play an important role in SANFH.
建立了类固醇诱导的股骨头缺血性坏死（SANFH）动物模型，以研究骨髓造血细胞氧化DNA损伤在SANFH中的作用。将45月龄的日本白兔（雄性或雌性，体重2.5±0.5kg）随机分为A组（甲基强的松龙+大肠杆菌内毒素）、B组（单独使用甲基强的松龙）、C组（单独使用大肠杆菌内毒素）和D组（空白对照）。在给予最后一剂药物后2周和4周处死动物（每组每次n=5）。取左右股骨头进行固定和脱钙。通过苏木精-伊红染色计数空骨陷窝，并通过免疫组织化学检测骨髓造血细胞的氧化DNA损伤。在第2周时，A组骨髓造血细胞氧化DNA损伤率显著高于B组、C组和D组（P<0.01），而B组、C组和D组之间无显著差异。在第4周时，A组骨髓造血细胞氧化DNA损伤率显著高于B组、C组和D组（P<0.01），而B组、C组和D组之间无显著差异。因此，骨髓造血细胞氧化DNA损伤似乎在SANFH中起重要作用。
