中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2015年
42期
6735-6739
,共5页
组织构建%软骨组织工程%降钙素%骨关节炎模型%骨关节炎%骨组织形态%蛋白多糖
組織構建%軟骨組織工程%降鈣素%骨關節炎模型%骨關節炎%骨組織形態%蛋白多糖
조직구건%연골조직공정%강개소%골관절염모형%골관절염%골조직형태%단백다당
背景：近年来有报道指出降钙素在临床上治疗骨关节炎有较好的临床疗效，但关于其对骨关节炎的作用机制却少有报道。目的：观察降钙素对实验性骨关节炎模型大鼠软骨组织形态及蛋白多糖的影响。方法：将30只SD大鼠随机均分为3组，模型组与给药组均切断右肢前交叉韧带制作骨关节炎模型，假手术组仅打开关节腔，不做韧带切断，给药组于造模后成功后第2天开始皮下注射降钙素15 IU/(kg?d)，模型组与假手术组均皮下注射等量生理盐水，连续给药6周。造模后10周，观察各组大鼠胫骨关节面，X射线检查股骨远端和内外侧踝软骨下骨骨密度，苏木精-伊红染色观察骨组织形态，甲胺苯蓝染色观察软骨组织中蛋白多糖含量。结果与结论：假手术组大鼠胫骨关节面光滑，有光泽；模型组大鼠胫骨关节面无光泽，关节软骨暗红色，有较大溃疡面形成；给药组大鼠软骨面无光泽，局部溃疡，表面粗糙不平。与假手术组比较，模型组内外侧踝软骨下骨骨密度、骨体积、骨小梁数目升高(P <0.05)，骨小梁分离度及蛋白多糖含量降低(P <0.05)；给药组内外侧踝软骨下骨骨密度、骨体积、骨小梁数目低于模型组(P <0.05)，骨小梁分离度及蛋白多糖含量高于模型组(P <0.05)。表明降钙素对骨关节炎大鼠软骨有较好的保护作用，并能促进骨组织分泌蛋白多糖。
揹景：近年來有報道指齣降鈣素在臨床上治療骨關節炎有較好的臨床療效，但關于其對骨關節炎的作用機製卻少有報道。目的：觀察降鈣素對實驗性骨關節炎模型大鼠軟骨組織形態及蛋白多糖的影響。方法：將30隻SD大鼠隨機均分為3組，模型組與給藥組均切斷右肢前交扠韌帶製作骨關節炎模型，假手術組僅打開關節腔，不做韌帶切斷，給藥組于造模後成功後第2天開始皮下註射降鈣素15 IU/(kg?d)，模型組與假手術組均皮下註射等量生理鹽水，連續給藥6週。造模後10週，觀察各組大鼠脛骨關節麵，X射線檢查股骨遠耑和內外側踝軟骨下骨骨密度，囌木精-伊紅染色觀察骨組織形態，甲胺苯藍染色觀察軟骨組織中蛋白多糖含量。結果與結論：假手術組大鼠脛骨關節麵光滑，有光澤；模型組大鼠脛骨關節麵無光澤，關節軟骨暗紅色，有較大潰瘍麵形成；給藥組大鼠軟骨麵無光澤，跼部潰瘍，錶麵粗糙不平。與假手術組比較，模型組內外側踝軟骨下骨骨密度、骨體積、骨小樑數目升高(P <0.05)，骨小樑分離度及蛋白多糖含量降低(P <0.05)；給藥組內外側踝軟骨下骨骨密度、骨體積、骨小樑數目低于模型組(P <0.05)，骨小樑分離度及蛋白多糖含量高于模型組(P <0.05)。錶明降鈣素對骨關節炎大鼠軟骨有較好的保護作用，併能促進骨組織分泌蛋白多糖。
배경：근년래유보도지출강개소재림상상치료골관절염유교호적림상료효，단관우기대골관절염적작용궤제각소유보도。목적：관찰강개소대실험성골관절염모형대서연골조직형태급단백다당적영향。방법：장30지SD대서수궤균분위3조，모형조여급약조균절단우지전교차인대제작골관절염모형，가수술조부타개관절강，불주인대절단，급약조우조모후성공후제2천개시피하주사강개소15 IU/(kg?d)，모형조여가수술조균피하주사등량생리염수，련속급약6주。조모후10주，관찰각조대서경골관절면，X사선검사고골원단화내외측과연골하골골밀도，소목정-이홍염색관찰골조직형태，갑알분람염색관찰연골조직중단백다당함량。결과여결론：가수술조대서경골관절면광활，유광택；모형조대서경골관절면무광택，관절연골암홍색，유교대궤양면형성；급약조대서연골면무광택，국부궤양，표면조조불평。여가수술조비교，모형조내외측과연골하골골밀도、골체적、골소량수목승고(P <0.05)，골소량분리도급단백다당함량강저(P <0.05)；급약조내외측과연골하골골밀도、골체적、골소량수목저우모형조(P <0.05)，골소량분리도급단백다당함량고우모형조(P <0.05)。표명강개소대골관절염대서연골유교호적보호작용，병능촉진골조직분비단백다당。
BACKGROUND:In recent years, calcitonin has been reported to have better clinical efficacy in the treatment of osteoarthritis, but its mechanism of action for osteoarthritis is rarely reported. OBJECTIVE:To investigate the effect of calcitonin on the cartilage morphology and proteoglycan expression in rats with osteoarthritis. METHODS:Thirty Sprague Dawley rats were randomly divided into three groups: model group, treatment group, and sham group. Anterior cruciate ligament transaction of the right limbs was implemented in the model and treatment groups, and only the joint cavity was exposed in the sham group. At 2 days after modeling, the treatment group received a daily subcutaneous injection of salmon calcitonin, 15 IU/(kg?d), and the model group and sham group were administered with normal saline at the same dose. The injection lasted for 6 weeks. At 10 weeks after modeling, the articular surface of the tibia of rats in each group was generaly observed; bone mineral density of the distal femoral bone and subchondral bone of the lateral and medial ankle were detected using X-ray test; bone morphology and proteoglycan secretion were measured by hematoxylin-eosin staining and toluidine blue staining, respectively. RESULTS AND CONCLUSION:The tibial articular surface was smooth and glossy in the sham group, but oxblood in the model group with large-area ulcers; the treatment group showed rough and local ulceration. Compared with the sham group, the bone mineral density of the subchondral bone of medial and lateral ankle were increased significantly in the model group (P < 0.05), but trabecular separation and proteoglycan content were decreased (P < 0.05). Compared with the model group, the bone mineral density of the subchondral bone of medial and lateral ankle were decreased significantly in the treatment group (P < 0.05), while the trabecular separation and proteoglycan content were increased (P < 0.05). These findings indicate that calcitonin has better protection on the cartilage of rats with osteoarthritis, and can promote bone the secretion of proteoglycan.
