中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2008年
6期
453-457
,共5页
心肌梗死%细胞凋亡%凋亡调节蛋白类
心肌梗死%細胞凋亡%凋亡調節蛋白類
심기경사%세포조망%조망조절단백류
Myocardial infarction%Apoptosis%Apoptosis regulatory protein
目的 建立成年和老年Wistar大鼠急性心肌梗死模型,比较鼠龄对大鼠冠状动脉(冠脉)结扎后不同时间点的凋亡指数及凋亡相关蛋白Bcl-2和Bax表达的影响.方法 115只6～24月龄大鼠中,95只结扎冠脉左前降支,80只(成年、老年大鼠各40只)术后存活,根据鼠龄分为老年心肌梗死组(40只)和成年心肌梗死组(40只),按结扎前降支后的1 h、3 h、5 h、1 d和7 d各分为5组(每组8只).假手术老年组和假手术成年组各10只.心肌梗死组分别于冠脉结扎后1、3、5 h和1、7d时记录血流动力学参数,包括心率、左室收缩压(LVSP)、左室终末舒张压(LVEDP)和左室内压最大收缩和舒张速率(±dp/dtmax).采用伊文蓝-红四氮唑(TTC)染色和原位末端标记(TUNEL)法检测心肌坏死和凋亡程度.免疫组化染色检测心肌内Bcl-2和Bax的形成.结果 大鼠心肌在冠脉结扎后的1 h内即有凋亡出现,并且凋亡达高峰的时间老年心肌梗死组较成年心肌梗死组早.在冠脉结扎3 h,老年心肌梗死组与成年心肌梗死组的凋亡指数分别为(51.90±23.15)%与(18.67±17.15)%,差异有统计学意义(P<0.01).Bcl-2蛋白的表达值老年假手术组和成年假手术组分别为(2.7±0.9)分和(1.8±0.8)分,差异有统计学意义(P<0.05).Bax蛋白的表达两组分别为(6.2±2.9)分和(4.2±1.5)分,差异有统计学意义(P<0.05).结论 老年大鼠抵抗心肌缺血的能力差,鼠龄可能会改变Bcl-2和Bax蛋白的表达而增加心肌细胞凋亡.
目的 建立成年和老年Wistar大鼠急性心肌梗死模型,比較鼠齡對大鼠冠狀動脈(冠脈)結扎後不同時間點的凋亡指數及凋亡相關蛋白Bcl-2和Bax錶達的影響.方法 115隻6～24月齡大鼠中,95隻結扎冠脈左前降支,80隻(成年、老年大鼠各40隻)術後存活,根據鼠齡分為老年心肌梗死組(40隻)和成年心肌梗死組(40隻),按結扎前降支後的1 h、3 h、5 h、1 d和7 d各分為5組(每組8隻).假手術老年組和假手術成年組各10隻.心肌梗死組分彆于冠脈結扎後1、3、5 h和1、7d時記錄血流動力學參數,包括心率、左室收縮壓(LVSP)、左室終末舒張壓(LVEDP)和左室內壓最大收縮和舒張速率(±dp/dtmax).採用伊文藍-紅四氮唑(TTC)染色和原位末耑標記(TUNEL)法檢測心肌壞死和凋亡程度.免疫組化染色檢測心肌內Bcl-2和Bax的形成.結果 大鼠心肌在冠脈結扎後的1 h內即有凋亡齣現,併且凋亡達高峰的時間老年心肌梗死組較成年心肌梗死組早.在冠脈結扎3 h,老年心肌梗死組與成年心肌梗死組的凋亡指數分彆為(51.90±23.15)%與(18.67±17.15)%,差異有統計學意義(P<0.01).Bcl-2蛋白的錶達值老年假手術組和成年假手術組分彆為(2.7±0.9)分和(1.8±0.8)分,差異有統計學意義(P<0.05).Bax蛋白的錶達兩組分彆為(6.2±2.9)分和(4.2±1.5)分,差異有統計學意義(P<0.05).結論 老年大鼠牴抗心肌缺血的能力差,鼠齡可能會改變Bcl-2和Bax蛋白的錶達而增加心肌細胞凋亡.
목적 건립성년화노년Wistar대서급성심기경사모형,비교서령대대서관상동맥(관맥)결찰후불동시간점적조망지수급조망상관단백Bcl-2화Bax표체적영향.방법 115지6～24월령대서중,95지결찰관맥좌전강지,80지(성년、노년대서각40지)술후존활,근거서령분위노년심기경사조(40지)화성년심기경사조(40지),안결찰전강지후적1 h、3 h、5 h、1 d화7 d각분위5조(매조8지).가수술노년조화가수술성년조각10지.심기경사조분별우관맥결찰후1、3、5 h화1、7d시기록혈류동역학삼수,포괄심솔、좌실수축압(LVSP)、좌실종말서장압(LVEDP)화좌실내압최대수축화서장속솔(±dp/dtmax).채용이문람-홍사담서(TTC)염색화원위말단표기(TUNEL)법검측심기배사화조망정도.면역조화염색검측심기내Bcl-2화Bax적형성.결과 대서심기재관맥결찰후적1 h내즉유조망출현,병차조망체고봉적시간노년심기경사조교성년심기경사조조.재관맥결찰3 h,노년심기경사조여성년심기경사조적조망지수분별위(51.90±23.15)%여(18.67±17.15)%,차이유통계학의의(P<0.01).Bcl-2단백적표체치노년가수술조화성년가수술조분별위(2.7±0.9)분화(1.8±0.8)분,차이유통계학의의(P<0.05).Bax단백적표체량조분별위(6.2±2.9)분화(4.2±1.5)분,차이유통계학의의(P<0.05).결론 노년대서저항심기결혈적능력차,서령가능회개변Bcl-2화Bax단백적표체이증가심기세포조망.
Objective To compare the influence of aging on apoptosis and the expression of apoptosis-related protein in adult and aged male Wistar rat hearts after acute coronary artery occlusion. Methods The acute myocardial infarction rat model was established by left anterior descending(LAD)occlusion.A total of 115 adult and aged rats,aged 6-24 months,were included in the study.The rats were divided into 4 groups:aged model group,aged control group,adult model group and adult control group.Animals were killed 1,3,5 hours,1 and 7 days after coronary occlusion.Hemodynamic parameters[heart rate(HR),left ventricular systolic pressure(LUSP),left ventricular end-diastolic pressure(LVEDP),±dp/dtmax)]were obtained from each group at every time points.The apoptosis and necrosis of myocardium were detected with TUNEL way and TTC stain.The expressions of Bcl-2 and Bax were analyzed with immumohistochemical stain. Results DNA fragmentation occured 1 hour after coronary occlusion and apparently peaked earlier in the aged than in the adult rat hearts.At 3 hour,the apoptotic index of aged model group was obviousily higher than that in adult model group[(51.90±23.15)%us.(18.67±17.15)%,P<0.01].The basal levels of Bcl-2 and Bax were higher in the aged than in the adult rat hearts.The expression of Bcl-2 in aged model group and adult model group were 2.7±0.9 and 1.8±0.8,P<0.05.The expression of Bax in aged model group and adult model group were 6.2±2.9 and 4.2±1.5,P<0.05. Conclusions The ability of aged rats to resist ischemia is poor,aging may alter the expressions of Bcl-2 and/or Bax,increase cardiomyocyte apoptosis,thereby,enhance the myocardial dysfunction during acute myocardial infarction.
