激素性股骨头缺血性坏死模型兔股骨组织中间隙连接蛋白Cx43的表达

摘要

BACKGROUND:The mechanism of steroid-induced avascular necrosis of the femoral head is stil unclear, Cx43 protein as the main gap junction in bone tissue, through transmitting information between osteoblasts, regulates bone cel growth and differentiation, compensatory bone increase or decrease. The relationship between Cx43 protein and steroid-induced avascular necrosis of the femoral head is stil rarely reported. OBJECTIVE:To explore the changes in Cx43 expression in rabbit models of steroid-induced vascular necrosis of the femoral head. METHODS:Forty New Zealand rabbits were equal y and randomly divided into model group and control group. Rabbits in the model group were used to establish models of steroid-induced avascular necrosis of the femoral head using endotoxin and hormone. Rabbits in the control group were injected with the same volume of physiological saline at the same time points. RESULTS AND CONCLUSION:At 4 weeks after model establishment, hematoxylin-eosin staining results revealed that in the model group, the trabecula became thin and distributed disorderly in the femoral subchondral area. Empty lacuna increased significantly. Adipocytes increased. Hematopoietic cel s in medul ary cavity apparently diminished. In the control group, trabecula arranged orderly and empty lacuna could be seen. Bone marrow cel s were abundant, but adipocytes were less. Immunohistochemical method demonstrated that Cx43 protein expression was observed in osteoblasts of the edge of trabecula, cytoplasm of osteoblasts of trabecula, and bone marrow stromal cel s. Western blot assay results showed that alkaline phosphatase and Cx43 protein expression was lower in the model group than in the control group (P<0.05). Results indicated that Cx43 protein expression decreased in the model rabbits, which may be the key link of the occurrence and development of steroid-induced avascular necrosis of the femoral head.%背景：激素性股骨头缺血性坏死的发病机制至今尚未完全阐明，间隙连接蛋白 Cx43作为骨组织细胞间的主要间隙连接，通过介导骨细胞间信息、能力的正常传递参与调控骨组织细胞生长、分化，代偿性的骨增加或减少，间隙连接蛋白Cx43与激素性股骨头坏死发生发展的关系国内外尚少见报道。　　目的：通过建立兔激素性股骨头坏死模型，初步探讨间隙连接蛋白Cx43在激素性股骨头坏死中的表达变化。方法：将新西兰大白兔40只随机等分为两组，模型组采用内毒素+激素方法构建激素性股骨头坏死模型，对照组于相同时间点注射等量生理盐水。　　结果与结论：建模4周后，苏木精-伊红染色结果显示，模型组股骨头软骨下区骨小梁变细，结构紊乱，空骨陷窝明显增多，脂肪细胞增多，髓腔内造血细胞明显减少；对照组股骨头软骨下区骨小梁排列整齐、很少见空骨陷窝，骨髓造血细胞丰富，脂肪细胞较少；免疫组织化学检测显示：Cx43蛋白阳性表达于骨小梁边缘成骨细胞及骨小梁内骨细胞胞浆上及骨髓细胞间质。Western blot检测显示，碱性磷酸酶和Cx43蛋白的表达在模型组中低于对照组(P<0.05)。结果证实，在激素性股骨头坏死兔模型组织中Cx43蛋白表达下降，可能是激素性股骨头坏死发生发展的重要环节。