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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
引用本文:韦 露,罗高斌,李 巍,林义才,阮中坚,周志广,薄占东. 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[J]. 中国组织工程研究, 2015, 19(18): 2814-2819. DOI: 10.3969/j.issn.2095-4344.2015.18.005
作者姓名:韦 露  罗高斌  李 巍  林义才  阮中坚  周志广  薄占东
作者单位:广西医科大学第一附属医院骨关节外科,广西壮族自治区南宁市 530021
基金项目:国家自然科学基金(81460348);广西教育厅一般项目(2013YB314)
摘    要: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。中国组织工程研究杂志出版内容重点:肾移植;肝移植;移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植;组织工程全文链接:

关 键 词:实验动物  骨及关节损伤模型  股骨头坏死  激素诱导  动物模型  间隙连接蛋白Cx43  碱性磷酸酶  免疫组化  免疫印迹实验  苏木精-伊红染色  骨细胞调亡  发病机制  国家自然科学基金  
收稿时间:2015-02-13

Cx43 expression in the femur of rabbit models of steroid-induced vascular necrosis of the femoral head
Wei Lu,Luo Gao-bin,Li Wei,Lin Yi-cai,Ruan Zhong-jian,Zhou Zhi-guang,Bo Zhan-dong. Cx43 expression in the femur of rabbit models of steroid-induced vascular necrosis of the femoral head[J]. Chinese Journal of Tissue Engineering Research, 2015, 19(18): 2814-2819. DOI: 10.3969/j.issn.2095-4344.2015.18.005
Authors:Wei Lu  Luo Gao-bin  Li Wei  Lin Yi-cai  Ruan Zhong-jian  Zhou Zhi-guang  Bo Zhan-dong
Affiliation:Department of Bone and Joint Surgery, First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Zhuang Autonomous Region, China
Abstract:BACKGROUND: The mechanism of steroid-induced avascular necrosis of the femoral head is still unclear, Cx43 protein as the main gap junction in bone tissue, through transmitting information between osteoblasts, regulates bone cell growth and differentiation, compensatory bone increase or decrease. The relationship between Cx43 protein and steroid-induced avascular necrosis of the femoral head is still 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 equally 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 cells in medullary cavity apparently diminished. In the control group, trabecula arranged orderly and empty lacuna could be seen. Bone marrow cells 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 cells. 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.
Keywords:Tissue Engineering  Femur Head Necrosis  Hormones  Alkaline Phosphatase  
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