重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2013年
25期
3004-3007
,共4页
陈章荣%吴新华%罗开良%何泉%杨瑛%向玉鸾%王小平
陳章榮%吳新華%囉開良%何泉%楊瑛%嚮玉鸞%王小平
진장영%오신화%라개량%하천%양영%향옥란%왕소평
心肌梗死%心肌重塑%二硫代氨基甲酸吡咯烷%核转录因子κB%基质金属蛋白酶-2
心肌梗死%心肌重塑%二硫代氨基甲痠吡咯烷%覈轉錄因子κB%基質金屬蛋白酶-2
심기경사%심기중소%이류대안기갑산필각완%핵전록인자κB%기질금속단백매-2
myocardial infraction%myocardial remolding%PDTC%NF-κB%MMP-2
目的:探讨二硫代氨基甲酸吡咯烷(PDTC)对大鼠心肌梗死后核转录因子κB(NF-κB)、基质金属蛋白酶-2(MMP-2)的表达及胶原重塑的影响。方法:制作大鼠心肌梗死模型,分为 PDTC干预(PD)组和心肌梗死对照(MI)组,另设假手术(SH)组,每组大鼠6只。PD组于术后24 h腹腔注射PDTC 80 mg · kg -1· d-1,连续给药28 d后行超声心动图检查评定心功能,处死动物,计算总胶原、Ⅰ型胶原、Ⅲ型胶原含量和梗死面积,实时荧光定量逆转录聚合酶链反应和免疫印迹法分别检测N F-κBp65及MMP-2的mRNA和蛋白质表达量。结果与SH组比较,MI组和 PD组的总胶原、Ⅰ型胶原、Ⅰ/Ⅲ胶原比值明显增大,NF-κBp65和MMP-2的mRNA及蛋白质表达量明显增加,差异均具有统计学意义(P<0.01)。与MI组比较,PD组总胶原、Ⅰ型胶原、Ⅰ/Ⅲ胶原比值改变明显减轻,NF-κBp65和 MMP-2的 mRNA 及蛋白质表达量明显降低,差异有统计学意义(P<0.01)。结论: PDTC在一定程度上能改善大鼠心肌梗死后心肌胶原重塑,其机制可能与抑制 NF-κB激活,下调基质金属蛋白酶(如MMP-2)表达有关。
目的:探討二硫代氨基甲痠吡咯烷(PDTC)對大鼠心肌梗死後覈轉錄因子κB(NF-κB)、基質金屬蛋白酶-2(MMP-2)的錶達及膠原重塑的影響。方法:製作大鼠心肌梗死模型,分為 PDTC榦預(PD)組和心肌梗死對照(MI)組,另設假手術(SH)組,每組大鼠6隻。PD組于術後24 h腹腔註射PDTC 80 mg · kg -1· d-1,連續給藥28 d後行超聲心動圖檢查評定心功能,處死動物,計算總膠原、Ⅰ型膠原、Ⅲ型膠原含量和梗死麵積,實時熒光定量逆轉錄聚閤酶鏈反應和免疫印跡法分彆檢測N F-κBp65及MMP-2的mRNA和蛋白質錶達量。結果與SH組比較,MI組和 PD組的總膠原、Ⅰ型膠原、Ⅰ/Ⅲ膠原比值明顯增大,NF-κBp65和MMP-2的mRNA及蛋白質錶達量明顯增加,差異均具有統計學意義(P<0.01)。與MI組比較,PD組總膠原、Ⅰ型膠原、Ⅰ/Ⅲ膠原比值改變明顯減輕,NF-κBp65和 MMP-2的 mRNA 及蛋白質錶達量明顯降低,差異有統計學意義(P<0.01)。結論: PDTC在一定程度上能改善大鼠心肌梗死後心肌膠原重塑,其機製可能與抑製 NF-κB激活,下調基質金屬蛋白酶(如MMP-2)錶達有關。
목적:탐토이류대안기갑산필각완(PDTC)대대서심기경사후핵전록인자κB(NF-κB)、기질금속단백매-2(MMP-2)적표체급효원중소적영향。방법:제작대서심기경사모형,분위 PDTC간예(PD)조화심기경사대조(MI)조,령설가수술(SH)조,매조대서6지。PD조우술후24 h복강주사PDTC 80 mg · kg -1· d-1,련속급약28 d후행초성심동도검사평정심공능,처사동물,계산총효원、Ⅰ형효원、Ⅲ형효원함량화경사면적,실시형광정량역전록취합매련반응화면역인적법분별검측N F-κBp65급MMP-2적mRNA화단백질표체량。결과여SH조비교,MI조화 PD조적총효원、Ⅰ형효원、Ⅰ/Ⅲ효원비치명현증대,NF-κBp65화MMP-2적mRNA급단백질표체량명현증가,차이균구유통계학의의(P<0.01)。여MI조비교,PD조총효원、Ⅰ형효원、Ⅰ/Ⅲ효원비치개변명현감경,NF-κBp65화 MMP-2적 mRNA 급단백질표체량명현강저,차이유통계학의의(P<0.01)。결론: PDTC재일정정도상능개선대서심기경사후심기효원중소,기궤제가능여억제 NF-κB격활,하조기질금속단백매(여MMP-2)표체유관。
Objective Toinvestigatetheeffectsofpyrrolidinedithiocarbamate(PDTC)onexpressionofNF-κB,MMP-2andleft ventricular collagen remodeling following acute myocardial infarction in rats .Methods The myocardial infarction model in rat was induced by ligation of left anterior descending coronary artery .12 adult Sprague-Dawley rats survived 24 for h after acute myocardial infarction were randomly divided into the myocardial infarction (MI) group and the PDTC-treated(PD) group .Six rats were desig-nated as sham-operated group(SH group) .The PD group was intraperitoneally injected with PDTC (80 mg · kg -1 · d-1 ) for 28 d , the MI group and SH group were given normal saline as control .On 28 d ,the cardiac function of left ventricle was measured by ech-ocardiography .The infarct size was evaluated .The total collgen ,typeⅠcollgen ,typeⅢcollgen ,and Ⅰ /Ⅲ collgen ratio were quanti-fied histomorphometry .The mRNA and protein levels of NF-kappaBp65 and MMP-2 were determined by reverse transcription-poly-merase chain reaction(RT-PCR) and by Western blot ,respectively .Results Compared with the SH group ,the values of the total collgen ,typeⅠcollgen ,typeⅢcollgen ,and Ⅰ /Ⅲ collgen ratio in the MI group and the PD group were significantly increased ,the differen had statistical significance (P<0 .01) .The values of the total collgen ,typeⅠcollgen ,typeⅢcollgen ,and Ⅰ /Ⅲ collgen ratio in the PD group were notably decreased than those in the MI group(P<0 .01) .Moreover ,the mRNA and protein levels of NF-kap-paBp65 and MMP-2 in the PD group were lower than those in the MI group ,the difference had statistical significance(P<0 .01) . Conclusion Left ventricular collagen remodeling following acute myocardial infarction could be improved by PDTC to some extent , which mechanism could be related with inhibiting NF-kappaB activation and down -regulating the expression of MMP-2 in rats .