天津医药
天津醫藥
천진의약
TIANJIN MEDICAL JOURNAL
2014年
3期
228-230
,共3页
蒋友旭%张丽华%王小曼%李盼盼
蔣友旭%張麗華%王小曼%李盼盼
장우욱%장려화%왕소만%리반반
热休克蛋白质类%普伐他丁%心肌梗死%急性病%疾病模型,动物%热休克蛋白B7
熱休剋蛋白質類%普伐他丁%心肌梗死%急性病%疾病模型,動物%熱休剋蛋白B7
열휴극단백질류%보벌타정%심기경사%급성병%질병모형,동물%열휴극단백B7
heat-shock proteins%pravastatin%myocardial infarction%acute disease%disease models,animal%HSPB7 protein
目的：观察急性心肌梗死（AMI）大鼠梗死区心肌组织中热休克蛋白B7（HSPB7）mRNA和蛋白的表达水平，研究普伐他汀对HSPB7表达的干预作用。方法80只AMI大鼠随机分为AMI组和普伐他汀（P）组，每组40只，同时设假手术（SH）组大鼠40只，再将3组大鼠分为1、3、6和12 h组，每个时间组10只。SH组开胸后不结扎冠脉；AMI组开胸后结扎冠状动脉左前降支；P组开胸后结扎冠状左前降支，同时给予普伐他汀0.5 mg/（kg·d）灌胃；其余组给予等量蒸馏水灌胃。分别于各时间点处死大鼠，取左心室梗死区心肌组织，SH组取对应部位的心肌组织，分别采用逆转录聚合酶链反应（RT-PCR）和免疫组化法检测HSPB7 mRNA和蛋白的表达。结果 AMI组和P组大鼠各时点梗死区心肌组织HSPB7 mRNA和蛋白表达均高于SH组（P＜0.01）；梗死后1 h，梗死区心肌HSPB7 mRNA和蛋白的表达增加，在3 h时达到高峰，6 h组、12 h组HSPB7 mRNA和蛋白的表达仍高于SH组。且P组中各时间点HSPB7的表达高于AMI组。结论 HSPB7能够在AMI早期表达，普伐他汀可促进AMI后梗死区心肌组织HSPB7表达，可能是其在心梗早期起到保护心肌作用的机制之一。
目的：觀察急性心肌梗死（AMI）大鼠梗死區心肌組織中熱休剋蛋白B7（HSPB7）mRNA和蛋白的錶達水平，研究普伐他汀對HSPB7錶達的榦預作用。方法80隻AMI大鼠隨機分為AMI組和普伐他汀（P）組，每組40隻，同時設假手術（SH）組大鼠40隻，再將3組大鼠分為1、3、6和12 h組，每箇時間組10隻。SH組開胸後不結扎冠脈；AMI組開胸後結扎冠狀動脈左前降支；P組開胸後結扎冠狀左前降支，同時給予普伐他汀0.5 mg/（kg·d）灌胃；其餘組給予等量蒸餾水灌胃。分彆于各時間點處死大鼠，取左心室梗死區心肌組織，SH組取對應部位的心肌組織，分彆採用逆轉錄聚閤酶鏈反應（RT-PCR）和免疫組化法檢測HSPB7 mRNA和蛋白的錶達。結果 AMI組和P組大鼠各時點梗死區心肌組織HSPB7 mRNA和蛋白錶達均高于SH組（P＜0.01）；梗死後1 h，梗死區心肌HSPB7 mRNA和蛋白的錶達增加，在3 h時達到高峰，6 h組、12 h組HSPB7 mRNA和蛋白的錶達仍高于SH組。且P組中各時間點HSPB7的錶達高于AMI組。結論 HSPB7能夠在AMI早期錶達，普伐他汀可促進AMI後梗死區心肌組織HSPB7錶達，可能是其在心梗早期起到保護心肌作用的機製之一。
목적：관찰급성심기경사（AMI）대서경사구심기조직중열휴극단백B7（HSPB7）mRNA화단백적표체수평，연구보벌타정대HSPB7표체적간예작용。방법80지AMI대서수궤분위AMI조화보벌타정（P）조，매조40지，동시설가수술（SH）조대서40지，재장3조대서분위1、3、6화12 h조，매개시간조10지。SH조개흉후불결찰관맥；AMI조개흉후결찰관상동맥좌전강지；P조개흉후결찰관상좌전강지，동시급여보벌타정0.5 mg/（kg·d）관위；기여조급여등량증류수관위。분별우각시간점처사대서，취좌심실경사구심기조직，SH조취대응부위적심기조직，분별채용역전록취합매련반응（RT-PCR）화면역조화법검측HSPB7 mRNA화단백적표체。결과 AMI조화P조대서각시점경사구심기조직HSPB7 mRNA화단백표체균고우SH조（P＜0.01）；경사후1 h，경사구심기HSPB7 mRNA화단백적표체증가，재3 h시체도고봉，6 h조、12 h조HSPB7 mRNA화단백적표체잉고우SH조。차P조중각시간점HSPB7적표체고우AMI조。결론 HSPB7능구재AMI조기표체，보벌타정가촉진AMI후경사구심기조직HSPB7표체，가능시기재심경조기기도보호심기작용적궤제지일。
Objective To observe the effect of pravastatin on the expression of heat shock protein B7 (HSPB7) in acute myocardial infarction (AMI) rats. Methods A total of 80 AMI rats were randomly divided into AMI group and pravas-tatin (P) group. Forty SD rats were used as sham operation (SH) group. Rats were then subdivided into 1 h, 3 h, 6 h and 12 h subgroups (10 for each group). Rats were not ligated after thoracotomy in SH group. The 1eft anterior descending coronary ar-tery was ligated in rats of AMI group. The 1eft anterior descending coronary artery was ligated in P group and given intragas-tric administration of 0.5 mg/(kg · d) pravastatin. The other groups were given the same amount of normal saline via gavage. The left ventricle infarcted myocardial tissues were taken at each time intervals. The corresponding myocardial tissues were harvested in sham-operated rats. The HSPB7 mRNA and protein expressions were measured by RT-PCR and immunohisto-chemistry respectively.Results The expression levels of HSPB7 mRNA and protein were significantly higher in the AMI group and P group than those of SH group(P<0.01). The expression levels of HSPB7 mRNA and protein were significantly increased 1 h after AMI and reached the peak value at 3 h after AMI. The expression levels of HSPB7 mRNA and protein were still higher in 6-h group and 12-h group than those of SH group. The expression levels of HSPB7 were higher in differ-ent time points of P group than those of AMI group. Conclusion HSPB7 could express in the early stage of acute myocardi-al infarction in rats. Pravastatin could promote the upregulation of HSPB7 in myocardial infarcted border zone after AMI, which may play a protective role in early myocardial infarction.
