实用医学杂志
實用醫學雜誌
실용의학잡지
THE JOURNAL OF PRACTICAL MEDICINE
2014年
20期
3210-3212,3213
,共4页
姜锋%王晓%李国军%朱书涛%郭阿雷%孟涛%宋仕永
薑鋒%王曉%李國軍%硃書濤%郭阿雷%孟濤%宋仕永
강봉%왕효%리국군%주서도%곽아뢰%맹도%송사영
激素性股骨头坏死%二甲双胍%小鼠
激素性股骨頭壞死%二甲雙胍%小鼠
격소성고골두배사%이갑쌍고%소서
Steroid-induced osteonecrosis of the femoral head%Metformin%Mice
目的:探讨二甲双胍对小鼠激素性股骨头坏死的防治效应。方法:昆明小鼠36只,随机分为3组(n=12):空白对照组A,模型组B,二甲双胍组C,B、C组按10 mL/kg腹腔注射马血清,间隔2周后按5 mL/kg再次腹腔注射马血清,第2次注射马血清同时肌肉注射醋酸泼尼松龙45 mL/(kg·d),共5 d,制备股骨头坏死模型。应用激素同时B组灌服生理盐水10 mL/(kg·d),C组按0.2 g/(kg·d)的剂量餐后灌服二甲双胍。A组不制备模型,于同时间点肌肉注射和灌服等量生理盐水。各组于造模前、造模后2、4、6周行血清总胆固醇(TC)、甘油三酯(TG)、血管性血友病因子(VWF)、纤溶酶原激活物抑制剂-1(PAI-1)含量检测,于造模后2、4、6周各组随机取4只小鼠处死,组织形态学观察股骨头情况。结果:3组各时间点股骨头外观、形态及关节软骨面均正常。B组较C组空骨陷窝率明显增高(P<0.05),A、C组间无明显差异(P>0.05)。TC、TG测定结果显示C组2、4、6周显著低于B组(P<0.05),但高于A组(P<0.05)。VWF、PAI-1测定结果显示C组2、4周明显低于B组(P<0.05),6周差异无统计学意义(P>0.05),A、C组间比较差异均无统计学意义。结论:二甲双胍可减轻激素所致的高脂、高凝、低纤状态,从而有效预防小鼠激素性股骨头缺血坏死。
目的:探討二甲雙胍對小鼠激素性股骨頭壞死的防治效應。方法:昆明小鼠36隻,隨機分為3組(n=12):空白對照組A,模型組B,二甲雙胍組C,B、C組按10 mL/kg腹腔註射馬血清,間隔2週後按5 mL/kg再次腹腔註射馬血清,第2次註射馬血清同時肌肉註射醋痠潑尼鬆龍45 mL/(kg·d),共5 d,製備股骨頭壞死模型。應用激素同時B組灌服生理鹽水10 mL/(kg·d),C組按0.2 g/(kg·d)的劑量餐後灌服二甲雙胍。A組不製備模型,于同時間點肌肉註射和灌服等量生理鹽水。各組于造模前、造模後2、4、6週行血清總膽固醇(TC)、甘油三酯(TG)、血管性血友病因子(VWF)、纖溶酶原激活物抑製劑-1(PAI-1)含量檢測,于造模後2、4、6週各組隨機取4隻小鼠處死,組織形態學觀察股骨頭情況。結果:3組各時間點股骨頭外觀、形態及關節軟骨麵均正常。B組較C組空骨陷窩率明顯增高(P<0.05),A、C組間無明顯差異(P>0.05)。TC、TG測定結果顯示C組2、4、6週顯著低于B組(P<0.05),但高于A組(P<0.05)。VWF、PAI-1測定結果顯示C組2、4週明顯低于B組(P<0.05),6週差異無統計學意義(P>0.05),A、C組間比較差異均無統計學意義。結論:二甲雙胍可減輕激素所緻的高脂、高凝、低纖狀態,從而有效預防小鼠激素性股骨頭缺血壞死。
목적:탐토이갑쌍고대소서격소성고골두배사적방치효응。방법:곤명소서36지,수궤분위3조(n=12):공백대조조A,모형조B,이갑쌍고조C,B、C조안10 mL/kg복강주사마혈청,간격2주후안5 mL/kg재차복강주사마혈청,제2차주사마혈청동시기육주사작산발니송룡45 mL/(kg·d),공5 d,제비고골두배사모형。응용격소동시B조관복생리염수10 mL/(kg·d),C조안0.2 g/(kg·d)적제량찬후관복이갑쌍고。A조불제비모형,우동시간점기육주사화관복등량생리염수。각조우조모전、조모후2、4、6주행혈청총담고순(TC)、감유삼지(TG)、혈관성혈우병인자(VWF)、섬용매원격활물억제제-1(PAI-1)함량검측,우조모후2、4、6주각조수궤취4지소서처사,조직형태학관찰고골두정황。결과:3조각시간점고골두외관、형태급관절연골면균정상。B조교C조공골함와솔명현증고(P<0.05),A、C조간무명현차이(P>0.05)。TC、TG측정결과현시C조2、4、6주현저저우B조(P<0.05),단고우A조(P<0.05)。VWF、PAI-1측정결과현시C조2、4주명현저우B조(P<0.05),6주차이무통계학의의(P>0.05),A、C조간비교차이균무통계학의의。결론:이갑쌍고가감경격소소치적고지、고응、저섬상태,종이유효예방소서격소성고골두결혈배사。
Objective To explore the effect of prevention and treatment on steroid-induced osteonecrosis of mice femoral head(ONFH) treated with metformin. Methods Thirty-six Kunming mice were randomly divided into three groups (n = 12):A (Control Group), B (Model Group)and C (Prevention Group). For producing ONFH mice models, did the intraperitoneal injection of horse serum (10 mL/kg) to B and C firstly. After two weeks, continuing the intraperitoneal injection of horse serum (5 mL/kg) again with the prednisolone intramuscularly [45 mL/(kg· day), totally for 5 days]. Meanwhile, feeding normal saline 10 mL/(kg·day) to B and feeding metformin hydrochloride [0.2 g/(kg·day)] to C. For A, mice were only given normal saline intramuscularly and intragastrically in equal quantity at the same time. The contents of serum cholesterol (TC), triglycerid (TG), plasma von willebrand factor (VWF) and plasminogen activator inhibitor 1 (PAI-1) were determined at the 2nd, 4th and 6th week after treatment. The micewere sacrificed at 2nd, 4th, and 6th weekafter treatment, and femoral heads were harvested to do histopathology analysis. Results The appearance and shape of the femoral head and the surface of cartilages were normal. The percentage of empty osteocyte lacunae in B was significantly higher than that in C (P < 0.05), there was no significant difference between A and C (P>0.05). TC and TG contents in C were significantly lower than that in B in 2th、4th、6th weeek(P<0.05), and higher than that in A(P<0.05). VWF and PAI-1 level in C were significantly lower than that in B at 2nd and 4th week (P<0.05), but there were no statistical significance at 6th week. there were no statistical significance for the comparison between A and C. Conclusion Metformin can prevent steroid-induced ONFH by improving hyperlipemia, hypercoagulability and hypofibrinolysis, then effectively prevent osteonecrosis.