中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2013年
7期
1162-1167
,共6页
洪汉刚%张耀武%牛清海%方锐%孟庆才
洪漢剛%張耀武%牛清海%方銳%孟慶纔
홍한강%장요무%우청해%방예%맹경재
组织构建%软骨组织构建%骨关节炎%关节炎%膝关节%关节软骨%前炎性因子%白细胞介素 1β%白细胞介素 1%维药买朱尼%Mankin 评分%软骨细胞%省级基金%组织构建图片文章
組織構建%軟骨組織構建%骨關節炎%關節炎%膝關節%關節軟骨%前炎性因子%白細胞介素 1β%白細胞介素 1%維藥買硃尼%Mankin 評分%軟骨細胞%省級基金%組織構建圖片文章
조직구건%연골조직구건%골관절염%관절염%슬관절%관절연골%전염성인자%백세포개소 1β%백세포개소 1%유약매주니%Mankin 평분%연골세포%성급기금%조직구건도편문장
背景:骨关节炎病理过程中,白细胞介素1β被认为是促进软骨基质降解和关节软骨破坏的最重要的细胞因之一.目的:观察白细胞介素1β在关节软骨中的表达,并观察维药买朱尼对其的影响.方法:将40只 SD 大鼠随机数字表法随机等分为模型对照组、维药买朱尼组、假手术组、正常对照组.模型对照组和维药买朱尼组采用改良 Hulth 造模法建立大鼠膝骨关节炎模型,假手术组仅显露膝关节,不切断韧带,不切除内侧半月板.维药买朱尼组建模第2周开始灌胃维药买朱尼10.31 mg/(kg?d),模型组及假手术组大鼠均灌服等量生理盐水,连续4周.结果与结论:模型组软骨退变程度明显重于维药买朱尼组,模型组软骨大体评分及 Mankin 评分均明显高于维药买朱尼组(P <0.05),模型组软骨细胞白细胞介素1β的表达强度亦明显高于维药买朱尼组(P <0.05).与正常对照组比较,假手术组软骨大体评分、Mankin 评分及软骨细胞白细胞介素1β差异无显著性意义(P >0.05).结果说明,维药买朱尼可以抑制关节软骨前炎性因子白细胞介素1β的表达.
揹景:骨關節炎病理過程中,白細胞介素1β被認為是促進軟骨基質降解和關節軟骨破壞的最重要的細胞因之一.目的:觀察白細胞介素1β在關節軟骨中的錶達,併觀察維藥買硃尼對其的影響.方法:將40隻 SD 大鼠隨機數字錶法隨機等分為模型對照組、維藥買硃尼組、假手術組、正常對照組.模型對照組和維藥買硃尼組採用改良 Hulth 造模法建立大鼠膝骨關節炎模型,假手術組僅顯露膝關節,不切斷韌帶,不切除內側半月闆.維藥買硃尼組建模第2週開始灌胃維藥買硃尼10.31 mg/(kg?d),模型組及假手術組大鼠均灌服等量生理鹽水,連續4週.結果與結論:模型組軟骨退變程度明顯重于維藥買硃尼組,模型組軟骨大體評分及 Mankin 評分均明顯高于維藥買硃尼組(P <0.05),模型組軟骨細胞白細胞介素1β的錶達彊度亦明顯高于維藥買硃尼組(P <0.05).與正常對照組比較,假手術組軟骨大體評分、Mankin 評分及軟骨細胞白細胞介素1β差異無顯著性意義(P >0.05).結果說明,維藥買硃尼可以抑製關節軟骨前炎性因子白細胞介素1β的錶達.
배경:골관절염병리과정중,백세포개소1β피인위시촉진연골기질강해화관절연골파배적최중요적세포인지일.목적:관찰백세포개소1β재관절연골중적표체,병관찰유약매주니대기적영향.방법:장40지 SD 대서수궤수자표법수궤등분위모형대조조、유약매주니조、가수술조、정상대조조.모형대조조화유약매주니조채용개량 Hulth 조모법건립대서슬골관절염모형,가수술조부현로슬관절,불절단인대,불절제내측반월판.유약매주니조건모제2주개시관위유약매주니10.31 mg/(kg?d),모형조급가수술조대서균관복등량생리염수,련속4주.결과여결론:모형조연골퇴변정도명현중우유약매주니조,모형조연골대체평분급 Mankin 평분균명현고우유약매주니조(P <0.05),모형조연골세포백세포개소1β적표체강도역명현고우유약매주니조(P <0.05).여정상대조조비교,가수술조연골대체평분、Mankin 평분급연골세포백세포개소1β차이무현저성의의(P >0.05).결과설명,유약매주니가이억제관절연골전염성인자백세포개소1β적표체.
@@@@BACKGROUND: Interleukin-1β is considered as an important cytokine for improvement of cartilage matrix degradation and destruction of articular cartilage during the pathological process of osteoarthritis. OBJECTIVE: To establish the expression of interleukin-1β in the articular cartilage of osteoarthritis rats and to study the effect of Uygur Medicine Maizhuni. METHODS: Forty healthy Sprague Dawley rats were randomly assigned into four groups: Maizhuni intervention group, model control group, shame operation group, and normal control group. Knee osteoarthritis models were established in the model control and Maizhuni intervention groups using modified Hulth method. In the sham operation group, only the knee was exposed with no ligament resection and medial meniscectomy. Rats in the Maizhuni intervention group were treated with Uygur Medicine Maizhuni (10.31 mg/(kg?d)) and those in the model control and sham operation groups were administrated with saline by gavage at week 2 after model establishment. The treatment was continued for 4 weeks. RESULTS AND CONCLUSION: The degree of cartilage degeneration in the model control group was higher than that in the Maizhuni intervention group as observed by naked eye. General score and Mankin score in the model group were significantly higher than those in the Maizhuni intervention group (P < 0.05). There was significantly greater expression of interleukin-1β in the chondrocytes of the model control group (P < 0.05). Sham operation group did not differ from the normal control group in general score, Mankin score and interleukin-1β expression in the chondrocytes (P > 0.05). These findings indicate that Uyghur Medicine Maizhuni may protect the articular cartilage by inhibiting the expression of interleukin-1β.