世界科学技术-中医药现代化
世界科學技術-中醫藥現代化
세계과학기술-중의약현대화
WORLD SCIENCE AND TECHNOLOGY-MODERNIZATION OF TRADITIONAL CHINESE MEDICINE
2014年
6期
1377-1383
,共7页
臧文华%李冰冰%唐德才%殷沈华
臧文華%李冰冰%唐德纔%慇瀋華
장문화%리빙빙%당덕재%은침화
补气活血药%血管生成%心肌缺血%SDF-1%CXCR4
補氣活血藥%血管生成%心肌缺血%SDF-1%CXCR4
보기활혈약%혈관생성%심기결혈%SDF-1%CXCR4
Qi-reinforcing and blood-activating herbs%angiogenesis%myocardial ischemia%SDF-1%CXCR4
目的:观察补气活血药对急性心肌梗死模型大鼠梗死心肌边缘区新生微血管数目以及基质细胞衍生因子-1(SDF-1)、趋化因子受体(CXCR4)蛋白及mRNA表达的影响。方法:建立大鼠急性心肌梗死动物模型,采用免疫组化SP法检测心肌组织中VIII因子相关抗原(vWF)蛋白的表达,计数微血管数目(MVC);用Western Blot和Real-Time PCR技术检测各组大鼠梗死心肌边缘区域的SDF-1因子和其特异性受体CXCR4蛋白和基因表达情况。结果:假手术组、模型组、各给药组大鼠梗死心肌边缘区域均可见vWF因子标记染色的新生微血管,假手术组大鼠心肌中新生微血管不明显,模型组大鼠梗死心肌边缘区域可见到少量新生成的微血管,各给药组大鼠梗死心肌边缘区域可见较多新生微血管。模型组与假手术组比较差异有统计学意义(P约0.05);各给药组与模型组相比较差异有统计学意义(P约0.05或P约0.01)。与假手术组比较,模型组大鼠心肌中SDF-1、CXCR4蛋白和mRNA表达明显增多(P约0.05或P约0.01);与模型组比较,各给药组SDF-1、CXCR4蛋白和mRNA表达均明显增多(P约0.05或P约0.01)。结论:丹参、丹参黄芪药对等药物可以促进血管的生成,推测这些药物促进血管生成的机制可能是通过促进SDF-1、CXCR4蛋白及mR原NA表达水平,从而增加SDF-1、CXCR4的含量以促进新生血管的生成。
目的:觀察補氣活血藥對急性心肌梗死模型大鼠梗死心肌邊緣區新生微血管數目以及基質細胞衍生因子-1(SDF-1)、趨化因子受體(CXCR4)蛋白及mRNA錶達的影響。方法:建立大鼠急性心肌梗死動物模型,採用免疫組化SP法檢測心肌組織中VIII因子相關抗原(vWF)蛋白的錶達,計數微血管數目(MVC);用Western Blot和Real-Time PCR技術檢測各組大鼠梗死心肌邊緣區域的SDF-1因子和其特異性受體CXCR4蛋白和基因錶達情況。結果:假手術組、模型組、各給藥組大鼠梗死心肌邊緣區域均可見vWF因子標記染色的新生微血管,假手術組大鼠心肌中新生微血管不明顯,模型組大鼠梗死心肌邊緣區域可見到少量新生成的微血管,各給藥組大鼠梗死心肌邊緣區域可見較多新生微血管。模型組與假手術組比較差異有統計學意義(P約0.05);各給藥組與模型組相比較差異有統計學意義(P約0.05或P約0.01)。與假手術組比較,模型組大鼠心肌中SDF-1、CXCR4蛋白和mRNA錶達明顯增多(P約0.05或P約0.01);與模型組比較,各給藥組SDF-1、CXCR4蛋白和mRNA錶達均明顯增多(P約0.05或P約0.01)。結論:丹參、丹參黃芪藥對等藥物可以促進血管的生成,推測這些藥物促進血管生成的機製可能是通過促進SDF-1、CXCR4蛋白及mR原NA錶達水平,從而增加SDF-1、CXCR4的含量以促進新生血管的生成。
목적:관찰보기활혈약대급성심기경사모형대서경사심기변연구신생미혈관수목이급기질세포연생인자-1(SDF-1)、추화인자수체(CXCR4)단백급mRNA표체적영향。방법:건립대서급성심기경사동물모형,채용면역조화SP법검측심기조직중VIII인자상관항원(vWF)단백적표체,계수미혈관수목(MVC);용Western Blot화Real-Time PCR기술검측각조대서경사심기변연구역적SDF-1인자화기특이성수체CXCR4단백화기인표체정황。결과:가수술조、모형조、각급약조대서경사심기변연구역균가견vWF인자표기염색적신생미혈관,가수술조대서심기중신생미혈관불명현,모형조대서경사심기변연구역가견도소량신생성적미혈관,각급약조대서경사심기변연구역가견교다신생미혈관。모형조여가수술조비교차이유통계학의의(P약0.05);각급약조여모형조상비교차이유통계학의의(P약0.05혹P약0.01)。여가수술조비교,모형조대서심기중SDF-1、CXCR4단백화mRNA표체명현증다(P약0.05혹P약0.01);여모형조비교,각급약조SDF-1、CXCR4단백화mRNA표체균명현증다(P약0.05혹P약0.01)。결론:단삼、단삼황기약대등약물가이촉진혈관적생성,추측저사약물촉진혈관생성적궤제가능시통과촉진SDF-1、CXCR4단백급mR원NA표체수평,종이증가SDF-1、CXCR4적함량이촉진신생혈관적생성。
This study was aimed to observe the influence of qi-reinforcing and blood-activating(QRBA) herbs onan-giogenesis of the myocardial microvascular, SDF-1 and CXCR4 protein expression as well as mRNA expression in the infarcted myocardium edge area of acute myocardial infarction (AMI) ratmodel. The AMI rat model was estab-lished. The immunohistochemical staining method was used in the detection of vWF protein expression in the myocar-dial tissues. The MVC account was recorded. The SDF-1 factor and its specific receptor factor CXCR4 were detected by the western blot and realtime-PCR technique in the infarcted myocardium edge area of rats from each group. The results showed that in the new generated microvessels which were staining marked by the vWF factor can be seen in infarcted myocardium edge area of rats from the sham-operated group, model group, each medication group. The new generated microvessels in the myocardium of rats in the sham-operated group were not obvious. Small amount of new generated microvessels can be seen in rats from the model group. More new generated microvessels can be seen in rats from each medication group. The comparison between the model group and the sham-operated group showed sta-tistical difference (P<0.05). The comparison between each medication group and the model group showed statistical difference(P<0.05 or P<0.01). Compared with the sham-operated group, SDF-1, CXCR4 and mRNA expression were obviously increased in the myocardium of rats in the model group (P<0.05 or P<0.01). Compared with the model group, SDF-1, CXCR4 protein and mRNA expression were obviously increased in the myocardium of rats from each medication group (P<0.05 or P<0.01). It was concluded that herbs such as Salvia, couplet herbs of Salvia and Astra-galushad stimulation effectonangiogenesis. Mechanism of these drugs in angiogenesismay be through the promotion of SDF-1 and CXCR4 protein as well as mRNA express.