CAJ | 학술논문

背景:雪腐镰刀菌烯醇和硒缺乏与大骨节病的发生有一定的联系.透明质酸的代谢直接影响着蛋白聚糖的聚合和软骨的正常结构与功能.透明质酸代谢的关键环节是与软骨细胞表面透明质酸受体的结合.软骨细胞膜上的CD44作为透明质酸的主要受体,其表达直接影响透明质酸的代谢,继而影响软骨基质代谢,对维持软骨基质的结构与功能具有极其重要的意义.目的:探讨大骨节病有关病因因素对靶组织细胞的损伤和保护作用以及引起软骨细胞变性坏死的机制.设计:随机对照观察.单位:西安交通大学医学院遗传学与分子生物学系.材料:实验于2002-10/2004-07在西安交通大学环境与疾病相关基因教育部重点实验室完成.选择30 d龄的新西兰纯种幼兔1只,手术截取兔肱骨、股骨和胫骨.方法:采用细胞培养法于体外再建软骨组织模型,并加入不同浓度的大骨节病可疑致病因子雪腐镰刀菌烯醇和保护因子硒,检测软骨细胞膜上透明质酸受体CD44和细胞培养液中可溶性CD44.主要观察指标: ①软骨细胞表面黏附分子CD44镜下观察. ②软骨细胞培养液中可溶性CD44浓度.结果: ①软骨细胞表面黏附分子CD44镜下观察:软骨细胞膜上CD44的表达随着雪腐镰刀菌烯醇浓度的增加而减少,加硒后有增加趋势. ②软骨细胞培养液中可溶性CD44浓度:细胞培养液中可溶性CD44浓度随雪腐镰刀菌烯醇浓度升高逐渐降低,但高浓度组出现了增高,加硒后趋势不变;除空白对照组与加硒对照组外,组间差异显著(P＜0.05).结论:雪腐镰刀菌烯醇能干扰软骨细胞表面黏附分子CD44表达,进而引起软骨细胞外基质代谢紊乱;补硒能够拮抗雪腐镰刀菌烯醇对软骨细胞的损伤,但作用有限.
배경:설부렴도균희순화서결핍여대골절병적발생유일정적련계.투명질산적대사직접영향착단백취당적취합화연골적정상결구여공능.투명질산대사적관건배절시여연골세포표면투명질산수체적결합.연골세포막상적CD44작위투명질산적주요수체,기표체직접영향투명질산적대사,계이영향연골기질대사,대유지연골기질적결구여공능구유겁기중요적의의.목적:탐토대골절병유관병인인소대파조직세포적손상화보호작용이급인기연골세포변성배사적궤제.설계:수궤대조관찰.단위:서안교통대학의학원유전학여분자생물학계.재료:실험우2002-10/2004-07재서안교통대학배경여질병상관기인교육부중점실험실완성.선택30 d령적신서란순충유토1지,수술절취토굉골、고골화경골.방법:채용세포배양법우체외재건연골조직모형,병가입불동농도적대골절병가의치병인자설부렴도균희순화보호인자서,검측연골세포막상투명질산수체CD44화세포배양액중가용성CD44.주요관찰지표: ①연골세포표면점부분자CD44경하관찰. ②연골세포배양액중가용성CD44농도.결과: ①연골세포표면점부분자CD44경하관찰:연골세포막상CD44적표체수착설부렴도균희순농도적증가이감소,가서후유증가추세. ②연골세포배양액중가용성CD44농도:세포배양액중가용성CD44농도수설부렴도균희순농도승고축점강저,단고농도조출현료증고,가서후추세불변;제공백대조조여가서대조조외,조간차이현저(P＜0.05).결론:설부렴도균희순능간우연골세포표면점부분자CD44표체,진이인기연골세포외기질대사문란;보서능구길항설부렴도균희순대연골세포적손상,단작용유한.
BACKGROUND: Deficit of nivalenol (NIV) and selenium (Se) is related with kashin-beck disease (KBD) to certain extent. Hyaluronic acid (HA) metabolism affects directly the polymerization of proteoglycans (PG) and normal structure and function of cartilage. The integration with HA receptor on surface of cartilage tissue is the key link in HA metabolism. Being the main receptor of HA on chondrocytic membrane, CD44 expression impacts directly HA metabolism, further affects cartilage matrix metabolism, which is extremely important to maintaining the structure and function of cartilage matrix.OBJECTIVE: To probe into the injury and protection of related etiology of KBD to target tissue cells and the mechanism on degenerative necrosis of chondrocytes.DESIGN: Randomized controlled observation was designed.SETTING: Department of Genetics and Molecular-Biology of Medical College of Xi' an Jiaotong University.MATERIALS: The experiment was performed in Key Laboratory Room on Ministry of Education associated with Environment and Disease of Xian Jiaotong University from October 2002 to July 2004. One New Zealand pedigree young rabbit aged 30 days was employed and its humerus, femurs and tibia were cut out in surgery.METHODS: With cell culture, the model of bone tissue was reconstructed in vitro, in which, NIV of various concentrations, KBD suspicious infectious agent and Se, the protective factor were added. HA receptor CD44 on chondrocytic membrane and soluble CD44 in cell culture solution were determined.MAIN OUTCOME MEASURES: ① Microscopic observation of adhesion molecule CD44 on chondrocytic surface. ② Soluble CD44 in chongrocytic culture solution.RESULTS: ① Microscopic observation of adhesion molecule CD44 on chondrocytic surface: CD expression in chondrocytic membrane was decreased with increasing of NIV concentration and it was in tendency of increasing with Se added. ② Soluble CD44 in chongrocytic culture solution:The concentration of soluble CD44 in cell culture solution was decreased gradually following the increased concentration of NIV, but it was increased in high concentration group and such tendency did not alter when Se added. Except blank control and Se control, significant difference was presented among groups (P ＜ 0.05).CONCLUSION: NIV disturbs adhesion molecule CD44 expression on chondrocytic surface and further induces metabolic disturbance of cartilage extracellular matrix. Se supplementation can resist the injury of NIV to chondrocytes, but its action is limited.