疑难病杂志
疑難病雜誌
의난병잡지
JOURNAL OF DIFFICULT AND COMPLICATED CASES
2015年
9期
960-962,968
,共4页
黄湘云%王晞%段慧楠%来欣%党松%王鑫
黃湘雲%王晞%段慧楠%來訢%黨鬆%王鑫
황상운%왕희%단혜남%래흔%당송%왕흠
神经调节蛋白1%急性心肌梗死%瞬时外向钾通道%L型钙通道%大鼠
神經調節蛋白1%急性心肌梗死%瞬時外嚮鉀通道%L型鈣通道%大鼠
신경조절단백1%급성심기경사%순시외향갑통도%L형개통도%대서
Neural regulatory protein 1%Acute myocardial infarction%Transient outward potassium channel%L-type calcium channel%Rats
目的:探讨神经调节蛋白1(NRG-1)对心肌梗死急性期大鼠心肌组织钾、钙离子通道蛋白表达的影响。方法45只健康SD大鼠随机分为3组,假手术组(SO组)、急性心肌梗死模型组(AMI组)、急性心肌梗死rh-NRG-1干预组( NRG-1组),每组15只。建立急性心肌梗死模型24 h后取心脏梗死周边区心肌组织,以Western blot法检测瞬时外向钾通道KV1.4和L型钙通道β亚单位LTCCsβ的蛋白表达情况。结果 AMI组和NRG-1组模型建立成功,心肌梗死面积比较差异无统计学意义[(35.4±3.6)% vs.(33.3±4.9)%, P >0.05]。与SO组比较,AMI组KV1.4降低(0.43±0.23 vs.0.20±0.17, P <0.05);而LTCCsβ差异无统计学意义(1.05±0.31 vs.1.00±0.21, P >0.05)。与AMI组相比,NRG-1组(0.66±0.29)梗死周边区心肌组织KV1.4蛋白表达显著增加,LTCCsβ蛋白表达(0.18±0.11)显著下降,差异均有统计学意义( t =20.95, P <0.05)。结论心肌梗死急性期给予NRG-1干预,能够上调KV1.4,下调LTCCsβ的蛋白表达,可发挥稳定心电保护心肌的作用。
目的:探討神經調節蛋白1(NRG-1)對心肌梗死急性期大鼠心肌組織鉀、鈣離子通道蛋白錶達的影響。方法45隻健康SD大鼠隨機分為3組,假手術組(SO組)、急性心肌梗死模型組(AMI組)、急性心肌梗死rh-NRG-1榦預組( NRG-1組),每組15隻。建立急性心肌梗死模型24 h後取心髒梗死週邊區心肌組織,以Western blot法檢測瞬時外嚮鉀通道KV1.4和L型鈣通道β亞單位LTCCsβ的蛋白錶達情況。結果 AMI組和NRG-1組模型建立成功,心肌梗死麵積比較差異無統計學意義[(35.4±3.6)% vs.(33.3±4.9)%, P >0.05]。與SO組比較,AMI組KV1.4降低(0.43±0.23 vs.0.20±0.17, P <0.05);而LTCCsβ差異無統計學意義(1.05±0.31 vs.1.00±0.21, P >0.05)。與AMI組相比,NRG-1組(0.66±0.29)梗死週邊區心肌組織KV1.4蛋白錶達顯著增加,LTCCsβ蛋白錶達(0.18±0.11)顯著下降,差異均有統計學意義( t =20.95, P <0.05)。結論心肌梗死急性期給予NRG-1榦預,能夠上調KV1.4,下調LTCCsβ的蛋白錶達,可髮揮穩定心電保護心肌的作用。
목적:탐토신경조절단백1(NRG-1)대심기경사급성기대서심기조직갑、개리자통도단백표체적영향。방법45지건강SD대서수궤분위3조,가수술조(SO조)、급성심기경사모형조(AMI조)、급성심기경사rh-NRG-1간예조( NRG-1조),매조15지。건립급성심기경사모형24 h후취심장경사주변구심기조직,이Western blot법검측순시외향갑통도KV1.4화L형개통도β아단위LTCCsβ적단백표체정황。결과 AMI조화NRG-1조모형건립성공,심기경사면적비교차이무통계학의의[(35.4±3.6)% vs.(33.3±4.9)%, P >0.05]。여SO조비교,AMI조KV1.4강저(0.43±0.23 vs.0.20±0.17, P <0.05);이LTCCsβ차이무통계학의의(1.05±0.31 vs.1.00±0.21, P >0.05)。여AMI조상비,NRG-1조(0.66±0.29)경사주변구심기조직KV1.4단백표체현저증가,LTCCsβ단백표체(0.18±0.11)현저하강,차이균유통계학의의( t =20.95, P <0.05)。결론심기경사급성기급여NRG-1간예,능구상조KV1.4,하조LTCCsβ적단백표체,가발휘은정심전보호심기적작용。
Objective To investigate the effects of neural regulatory protein 1 ( NRG-1) on acute myocardial infarc-tion rats myocardium potassium , calcium ion channel protein expression .Methods Forty-five healthy SD rats were randomly divided into 3 groups , the sham operation group ( SO group ) , acute myocardial infarction model group ( AMI group ) , acute myocardial infarction rhNRG-1 intervention group (NRG-1 group), and 15 rats in each group.Establish acute myocardial in-farction model, after 24 h, took peri-infarcted myocardium and used Western blot to detect transient outward potassium chan -nel KV1.4 and L type calcium channel beta subunit ltccs beta protein expression .Results AMI group and NRG-1 group’ model was successfully established .Myocardial infarction area did not show statistical significance [(33.3 ±4.9)% vs. (35.4 ±3.6)%, P >0.05].Compared with the SD group, AMI group’s KV1.4 reduced (0.43 ±0.23 vs.0.20 ±0.17, P <0.05);and the differences of LTCCs beta showed no statistical significance (1.05 ±0.31 vs.1.00 ±0.21).Compared with AMI group, NRG-1 group (0.66 ±0.29) peri-infarcted area of myocardium ’ s KV1.4 protein expression increased sig-nificantly, LTCCs beta protein expression (0.18 ±0.11) decreased significantly , the differences were statistically significant ( t =20.95, P <0.05).Conclusion It demonstrated that the NRG-1 for acute myocardial infarction can increase KV 1.4, reduce the protein expression of LTCCs beta , which can play a role in the stability of ECG of myocardial protection .