CAJ | 학술논문

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%国家自然科学基金實驗動物%骨及關節損傷模型%股骨頭壞死%激素誘導%動物模型%間隙連接蛋白Cx43%堿性燐痠酶%免疫組化%免疫印跡實驗%囌木精-伊紅染色%骨細胞調亡%髮病機製%國傢自然科學基金
실험동물%골급관절손상모형%고골두배사%격소유도%동물모형%간극련접단백Cx43%감성린산매%면역조화%면역인적실험%소목정-이홍염색%골세포조망%발병궤제%국가자연과학기금
Tissue Engineering%Femur Head Necrosis%Hormones%Alkaline Phosphatase

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。
배경：격소성고골두결혈성배사적발병궤제지금상미완전천명，간극련접단백 Cx43작위골조직세포간적주요간극련접，통과개도골세포간신식、능력적정상전체삼여조공골조직세포생장、분화，대상성적골증가혹감소，간극련접단백Cx43여격소성고골두배사발생발전적관계국내외상소견보도。 　　목적：통과건립토격소성고골두배사모형，초보탐토간극련접단백Cx43재격소성고골두배사중적표체변화。방법：장신서란대백토40지수궤등분위량조，모형조채용내독소+격소방법구건격소성고골두배사모형，대조조우상동시간점주사등량생리염수。 　　결과여결론：건모4주후，소목정-이홍염색결과현시，모형조고골두연골하구골소량변세，결구문란，공골함와명현증다，지방세포증다，수강내조혈세포명현감소；대조조고골두연골하구골소량배렬정제、흔소견공골함와，골수조혈세포봉부，지방세포교소；면역조직화학검측현시：Cx43단백양성표체우골소량변연성골세포급골소량내골세포포장상급골수세포간질。Western blot검측현시，감성린산매화Cx43단백적표체재모형조중저우대조조(P<0.05)。결과증실，재격소성고골두배사토모형조직중Cx43단백표체하강，가능시격소성고골두배사발생발전적중요배절。
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.