广州医科大学学报
廣州醫科大學學報
엄주의과대학학보
Academic Journal of Guangzhou Medical College
2014年
6期
30-33
,共4页
龙训辉%王齐国%李颖%宋云林
龍訓輝%王齊國%李穎%宋雲林
룡훈휘%왕제국%리영%송운림
葛根素%Toll样受体4%心肌缺血再灌注损伤
葛根素%Toll樣受體4%心肌缺血再灌註損傷
갈근소%Toll양수체4%심기결혈재관주손상
puerarin%Toll ̄like receptor 4%myocardium ischemia ̄reperfusion injury
目的::探讨葛根素对大鼠心肌缺血再灌注损伤的保护机制。方法:24只雌性Sprague ̄Dawley (SD)大鼠随机分为假手术组、缺血再灌注组和葛根素干预组,RT ̄PCR和Western blotting法检测心肌中TLR4 mRNA及TLR4蛋白的表达,同时四唑氮蓝染色测定心肌梗死范围。结果:大鼠心肌缺血再灌注损伤模型造模成功;葛根素干预组的心肌梗死范围明显小于缺血再灌注组(P<0.01),且该组大鼠TLR4 mRNA及蛋白的表达也显著低于缺血再灌注组( P<0.01)。结论:葛根素干预可减轻大鼠心肌缺血再灌注的损伤,其机制可能与抑制TLR4的表达相关。
目的::探討葛根素對大鼠心肌缺血再灌註損傷的保護機製。方法:24隻雌性Sprague ̄Dawley (SD)大鼠隨機分為假手術組、缺血再灌註組和葛根素榦預組,RT ̄PCR和Western blotting法檢測心肌中TLR4 mRNA及TLR4蛋白的錶達,同時四唑氮藍染色測定心肌梗死範圍。結果:大鼠心肌缺血再灌註損傷模型造模成功;葛根素榦預組的心肌梗死範圍明顯小于缺血再灌註組(P<0.01),且該組大鼠TLR4 mRNA及蛋白的錶達也顯著低于缺血再灌註組( P<0.01)。結論:葛根素榦預可減輕大鼠心肌缺血再灌註的損傷,其機製可能與抑製TLR4的錶達相關。
목적::탐토갈근소대대서심기결혈재관주손상적보호궤제。방법:24지자성Sprague ̄Dawley (SD)대서수궤분위가수술조、결혈재관주조화갈근소간예조,RT ̄PCR화Western blotting법검측심기중TLR4 mRNA급TLR4단백적표체,동시사서담람염색측정심기경사범위。결과:대서심기결혈재관주손상모형조모성공;갈근소간예조적심기경사범위명현소우결혈재관주조(P<0.01),차해조대서TLR4 mRNA급단백적표체야현저저우결혈재관주조( P<0.01)。결론:갈근소간예가감경대서심기결혈재관주적손상,기궤제가능여억제TLR4적표체상관。
Objective:To investigate the mechanism underlying the protective effects of puerarin on myocardial ischemia ̄reperfusion injury ( MIRI) in rats. Methods:Twenty ̄four female Sprague ̄Dawley ( SD) rats were randomly divided into the sham operation group, ischemia ̄reperfusion group and puerarin intervention group. The expressions of TLR4 mRNA and protein were assessed by RT ̄PCR and Western blotting. Meanwhile, the area of myocardial infarction ( MI) was measured by nitroblue tetrazolium ( NBT) staining. Results: The model of MIRI was successfully built in rats. The MI area in the puerarin intervention group was significantly smaller than that in the ischemia ̄reperfusion group ( P<0.01) , and the expressions of TLR4 mRNA and protein were significantly lower than those in the ischemia ̄reperfusion group as well (P<0.01). Conclusion: Puerarin intervention can relieve MIRI in rats and its underlying mechanism may be related to the inhibition of TLR4 expression.