中医正骨
中醫正骨
중의정골
THE JOURNAL OF TRADITIONAL CHINESE ORTHOPEDICS AND TRAUMATOLOGY
2015年
8期
1-6
,共6页
徐西林%赵永兰%张晓峰%王智%韩雪松%吕航
徐西林%趙永蘭%張曉峰%王智%韓雪鬆%呂航
서서림%조영란%장효봉%왕지%한설송%려항
股骨头坏死%血管内皮生长因子类%活骨注射液%模型,动物%动物实验
股骨頭壞死%血管內皮生長因子類%活骨註射液%模型,動物%動物實驗
고골두배사%혈관내피생장인자류%활골주사액%모형,동물%동물실험
femur head necrosis%vascular endothelial growth factors%Huogu injection%models,animal%animal experimentation
目的:观察活骨注射液髋关节腔灌注对兔股骨头坏死模型血管内皮生长因子(vascular endothelial growth factor,VEGF)表达的动态影响。方法:将90只新西兰大白兔随机分为对照组、模型组和实验组,每组30只。对模型组和实验组动物采用液氮冷冻法进行股骨头坏死造模;造模成功后,分别以生理盐水和活骨注射液进行髋关节腔灌注。对照组不进行任何干预。药物干预开始后1、3、6、9、12周时,分别从各组随机选取6只动物处死后取出股骨头,采用免疫组化法和实时定量 PCR 法检测 VEGF 表达情况。结果:药物干预后各时点,3组动物股骨头 VEGF 蛋白表达量比较,组间差异均有统计学意义(490.56±60.62,661.99±64.51,796.09±86.17,F =27.670,P =0.000;501.41±58.85,781.71±87.32,854.71±76.97,F =36.810,P =0.000;489.33±53.19,592.42±117.35,905.51±107.95,F =29.930,P =0.000;498.96±40.37,571.31±111.38,1158.20±147.35,F =65.820, P =0.000;500.47±33.67,508.01±138.76,1528.20±146.09,F =150.770,P =0.000)。对照组各时点股骨头 VEGF 蛋白表达量均低于实验组(P =0.000,P =0.000,P =0.000,P =0.000,P =0.000);药物干预后1、3周时对照组股骨头 VEGF 蛋白表达量均低于模型组(P =0.001,P =0.000);药物干预后1、6、9、12周时模型组股骨头 VEGF 蛋白表达量均低于实验组(P =0.005,P =0.000,P =0.000,P =0.000);其余各时点组间两两比较,差异均无统计学意义。药物干预后各时点,3组动物股骨头 VEGF mRNA表达量比较,组间差异均有统计学意义(1.000±0.000,1.313±0.380,1.546±0.204,F =9.650,P =0.001;1.000±0.000,1.412±0.345,1.750±0.236,F =19.361,P =0.000;1.000±0.000,1.235±0.095,1.807±0.211,F =35.216,P =0.000;1.000±0.000,1.234±0.250,2.691±0.289,F =137.743,P =0.000;1.000±0.000,1.113±0.180,3.106±0.287,F =293.245,P =0.000)。对照组各时点股骨头 VEGF mRNA 表达量均低于实验组(P =0.000,P =0.000,P =0.000,P =0.000,P =0.000);药物干预后1、3、6、9周时对照组股骨头 VEGF mRNA 表达量均低于模型组(P =0.020,P =0.003,P =0.027,P =0.046);药物干预后3、6、9、12周时模型组股骨头 VEGF mRNA 表达量均低于实验组(P =0.011,P =0.000,P =0.000,P =0.000);其余各时点组间两两比较,差异均无统计学意义。结论:活骨注射液髋关节腔灌注可持续促进兔股骨头坏死模型坏死股骨头局部 VEGF 表达,这可能是其治疗股骨头坏死的主要作用机制之一。
目的:觀察活骨註射液髖關節腔灌註對兔股骨頭壞死模型血管內皮生長因子(vascular endothelial growth factor,VEGF)錶達的動態影響。方法:將90隻新西蘭大白兔隨機分為對照組、模型組和實驗組,每組30隻。對模型組和實驗組動物採用液氮冷凍法進行股骨頭壞死造模;造模成功後,分彆以生理鹽水和活骨註射液進行髖關節腔灌註。對照組不進行任何榦預。藥物榦預開始後1、3、6、9、12週時,分彆從各組隨機選取6隻動物處死後取齣股骨頭,採用免疫組化法和實時定量 PCR 法檢測 VEGF 錶達情況。結果:藥物榦預後各時點,3組動物股骨頭 VEGF 蛋白錶達量比較,組間差異均有統計學意義(490.56±60.62,661.99±64.51,796.09±86.17,F =27.670,P =0.000;501.41±58.85,781.71±87.32,854.71±76.97,F =36.810,P =0.000;489.33±53.19,592.42±117.35,905.51±107.95,F =29.930,P =0.000;498.96±40.37,571.31±111.38,1158.20±147.35,F =65.820, P =0.000;500.47±33.67,508.01±138.76,1528.20±146.09,F =150.770,P =0.000)。對照組各時點股骨頭 VEGF 蛋白錶達量均低于實驗組(P =0.000,P =0.000,P =0.000,P =0.000,P =0.000);藥物榦預後1、3週時對照組股骨頭 VEGF 蛋白錶達量均低于模型組(P =0.001,P =0.000);藥物榦預後1、6、9、12週時模型組股骨頭 VEGF 蛋白錶達量均低于實驗組(P =0.005,P =0.000,P =0.000,P =0.000);其餘各時點組間兩兩比較,差異均無統計學意義。藥物榦預後各時點,3組動物股骨頭 VEGF mRNA錶達量比較,組間差異均有統計學意義(1.000±0.000,1.313±0.380,1.546±0.204,F =9.650,P =0.001;1.000±0.000,1.412±0.345,1.750±0.236,F =19.361,P =0.000;1.000±0.000,1.235±0.095,1.807±0.211,F =35.216,P =0.000;1.000±0.000,1.234±0.250,2.691±0.289,F =137.743,P =0.000;1.000±0.000,1.113±0.180,3.106±0.287,F =293.245,P =0.000)。對照組各時點股骨頭 VEGF mRNA 錶達量均低于實驗組(P =0.000,P =0.000,P =0.000,P =0.000,P =0.000);藥物榦預後1、3、6、9週時對照組股骨頭 VEGF mRNA 錶達量均低于模型組(P =0.020,P =0.003,P =0.027,P =0.046);藥物榦預後3、6、9、12週時模型組股骨頭 VEGF mRNA 錶達量均低于實驗組(P =0.011,P =0.000,P =0.000,P =0.000);其餘各時點組間兩兩比較,差異均無統計學意義。結論:活骨註射液髖關節腔灌註可持續促進兔股骨頭壞死模型壞死股骨頭跼部 VEGF 錶達,這可能是其治療股骨頭壞死的主要作用機製之一。
목적:관찰활골주사액관관절강관주대토고골두배사모형혈관내피생장인자(vascular endothelial growth factor,VEGF)표체적동태영향。방법:장90지신서란대백토수궤분위대조조、모형조화실험조,매조30지。대모형조화실험조동물채용액담냉동법진행고골두배사조모;조모성공후,분별이생리염수화활골주사액진행관관절강관주。대조조불진행임하간예。약물간예개시후1、3、6、9、12주시,분별종각조수궤선취6지동물처사후취출고골두,채용면역조화법화실시정량 PCR 법검측 VEGF 표체정황。결과:약물간예후각시점,3조동물고골두 VEGF 단백표체량비교,조간차이균유통계학의의(490.56±60.62,661.99±64.51,796.09±86.17,F =27.670,P =0.000;501.41±58.85,781.71±87.32,854.71±76.97,F =36.810,P =0.000;489.33±53.19,592.42±117.35,905.51±107.95,F =29.930,P =0.000;498.96±40.37,571.31±111.38,1158.20±147.35,F =65.820, P =0.000;500.47±33.67,508.01±138.76,1528.20±146.09,F =150.770,P =0.000)。대조조각시점고골두 VEGF 단백표체량균저우실험조(P =0.000,P =0.000,P =0.000,P =0.000,P =0.000);약물간예후1、3주시대조조고골두 VEGF 단백표체량균저우모형조(P =0.001,P =0.000);약물간예후1、6、9、12주시모형조고골두 VEGF 단백표체량균저우실험조(P =0.005,P =0.000,P =0.000,P =0.000);기여각시점조간량량비교,차이균무통계학의의。약물간예후각시점,3조동물고골두 VEGF mRNA표체량비교,조간차이균유통계학의의(1.000±0.000,1.313±0.380,1.546±0.204,F =9.650,P =0.001;1.000±0.000,1.412±0.345,1.750±0.236,F =19.361,P =0.000;1.000±0.000,1.235±0.095,1.807±0.211,F =35.216,P =0.000;1.000±0.000,1.234±0.250,2.691±0.289,F =137.743,P =0.000;1.000±0.000,1.113±0.180,3.106±0.287,F =293.245,P =0.000)。대조조각시점고골두 VEGF mRNA 표체량균저우실험조(P =0.000,P =0.000,P =0.000,P =0.000,P =0.000);약물간예후1、3、6、9주시대조조고골두 VEGF mRNA 표체량균저우모형조(P =0.020,P =0.003,P =0.027,P =0.046);약물간예후3、6、9、12주시모형조고골두 VEGF mRNA 표체량균저우실험조(P =0.011,P =0.000,P =0.000,P =0.000);기여각시점조간량량비교,차이균무통계학의의。결론:활골주사액관관절강관주가지속촉진토고골두배사모형배사고골두국부 VEGF 표체,저가능시기치료고골두배사적주요작용궤제지일。
Objective:To observe the dynamic effect of intra-articular hip injection of Huogu injection on the expression of vascular en-dothelial growth factor(VEGF)in rabbit models with osteonecrosis of the femoral head(ONFH).Methods:Ninety New Zealand white rab-bits were randomly divided into control group,model group and experimental group,30 cases in each group.The rabbits in model group and experimental group were administrated with liquid-nitrogen refrigeration to build ONFH models,and then they were intra-articular injected with normal saline and Huogu injection respectively in the hip,while the rabbits in the control group were not be treated.At 1 ,3,6,9 and 1 2weeks after the beginning of drug intervention,6 rabbits were randomly selected from each group respectively and were executed,then their femoral heads were fetched out and were sectioned for detecting the expression of VEGF by immunohistochemical method and real-time quantitative PCR method.Results:There was statistical difference in the expression of VEGF protein in femoral head between the 3 groups at each timepoint after the beginning of drug intervention(490.56 +/-60.62,661 .99 +/-64.51 ,796.09 +/-86.1 7,F =27.670,P =0.000;501 .41 +/-58.85,781 .71 +/-87.32,854.71 +/-76.97,F =36.81 0,P =0.000;489.33 +/-53.1 9,592.42 +/-1 1 7.35, 905.51 +/-1 07.95,F =29.930,P =0.000;498.96 +/-40.37,571 .31 +/-1 1 1 .38,1 1 58.20 +/-1 47.35,F =65.820,P =0.000;500.47 +/-33.67,508.01 +/-1 38.76,1 528.20 +/-1 46.09,F =1 50.770,P =0.000).The expression of VEGF protein in femoral head was lower in control group compared to experimental group at each timepoint after the beginning of drug intervention(P =0.000,P =0.000,P =0.000,P =0.000,P =0.000).The expression of VEGF protein in femoral head were lower in control group compared to model group at 1 and 3 weeks after the beginning of drug intervention(P =0.001 ,P =0.000)and were lower in model group compared to experi-mental group at 1 ,6,9 and 1 2 weeks after the beginning of drug intervention(P =0.005,P =0.000,P =0.000,P =0.000),while there was no statistical difference between the paired groups at other timepoints.There was statistical difference in VEGF mRNA expression in the femoral head between the 3 groups at each timepoint after the beginning of drug intervention (1 .000 +/-0.000,1 .31 3 +/-0.380, 1 .546 +/-0.204,F =9.650,P =0.001 ;1 .000 +/-0.000.1 .41 2 +/-0.345,1 .750 +/-0.236,F =1 9.361 ,P =0.000;1 .000 +/-0.000, 1 .235 +/-0.095,1 .807 +/-0.21 1 ,F =35.21 6,P =0.000;1 .000 +/-0.000,1 .234 +/-0.250,2.691 +/-0.289,F =1 37.743,P =0.000;1 .000 +/-0.000,1 .1 1 3 +/-0.1 80,3.1 06 +/-0.287,F =293.245,P =0.000).The VEGF mRNA expression in the femoral head was lower in control group compared to experimental group at each timepoint after the beginning of drug intervention(P =0.000,P =0.000,P =0.000,P =0.000,P =0.000),and were lower in control group compared to model group at 1 ,3,6 and 9 weeks after the begin-ning of drug intervention(P =0.020,P =0.003,P =0.027,P =0.046),and were lower in model group compared to experimental group at 3,6,9 and 1 2 weeks after the beginning of drug intervention(P =0.01 1 ,P =0.000,P =0.000,P =0.000),while there was no statistical difference between the paired groups at other timepoints.Conclusion:Intra-articular hip injection of Huogu injection can promote the ex-pression of VEGF in necrotic femoral head of rabbit ONFH model,which may be one of the mechanisms of action for treatment of ONFH.