中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2015年
4期
811-814
,共4页
微小RNA-29b%心肌缺血%再灌注损伤%心室重塑
微小RNA-29b%心肌缺血%再灌註損傷%心室重塑
미소RNA-29b%심기결혈%재관주손상%심실중소
MicroRNA-29b%Myocardial ischemia%Reperfusion injury%Ventricular remodeling
目的 探讨微小RNA(miRNA,miR)-29b对心肌缺血再灌注损伤的保护作用及机制.方法 将成年雄性Wister大鼠40只随机分为假手术组、缺血再灌注损伤组、miR-29b治疗组和缺血再灌注阴性对照组4组.假手术组大鼠,放置6-0缝合线不结扎,其余3组均按缺血再灌注模型处理,其中miR-29b治疗组在缺血再灌注模型前24 h,心肌内注射agomiR-29b(1×103 mol/L),阴性对照组在缺血再灌注模型前24 h,心肌内注射阴性对照序列.监测各组大鼠术后1、3、7、15、30 d各时相点的心率、左室射血分数(LVEF)、心肌细胞凋亡率、Ⅰ型胶原蛋白及miR-29b的mRNA表达.结果 各组大鼠术后1、3、7、15、30 d各组时相点心率差异无统计学意义(P＞0.05);与假手术组比较,缺血再灌注组大鼠术后1、3、7、15、30 d左室射血分数(LVEF)分别为(70.42±2.06)％、(64.37±1.84)％、(54.61±1.37)％、(51.92±1.07)％、(47.38±1.02)％,LVEF变化均显著下降;与缺血再灌注组比较,miR-29b治疗组大鼠术后1、3、7、15、30 d心肌LVEF分别为(80.62±2.48)％、(78.37±2.03)％、(72.15±2.34)％、(65.18±1.73)％、(60.08±1.16)％,LVEF变化均显著上调;阴性对照组与缺血再灌注组比较差异无统计学意义(P＞0.05).与假手术组比较,缺血再灌注组大鼠术后1、3、7、15、30 d心肌细胞凋亡率分别为(33.6±4.2)％、(53.7±6.3)％、(41.9±5.8)％、(39.3±6.7)％、(32.7±4.8)％,心肌细胞凋亡率均显著升高;与缺血再灌注组比较,miR-29b治疗组大鼠术后1、3、7、15、30 d心肌细胞凋亡率分别为(18.2±3.9)％、(29.6±5.2)％、(32.7±3.8)％、(28.4±6.0)％、(21.5±4.6)％,心肌细胞凋亡率均显著下降;阴性对照组与缺血再灌注组间各指标比较差异无统计学意义(P＞0.05).与假手术组比较,缺血再灌注组大鼠术后各时相点Ⅰ型胶原蛋白表达均显著升高;而与缺血再灌注组比较,给予miR-29b治疗组大鼠术后各时相点Ⅰ型胶原蛋白表达均显著下降;阴性对照组与缺血再灌注组比较差异无统计学意义(P＞0.05).与假手术组比较,缺血再灌注组大鼠术后各时相点miRNA-29b的mRNA表达均显著下降;而与缺血再灌注组比较,给予miR-29b治疗组大鼠术后各时相点miRNA-29b的mRNA表达均显著上调;阴性对照组与缺血再灌注组比较差异无统计学意义(P＞0.05).结论 心肌缺血再灌注后miR-29b表达明显下降,表明miR-29b参与大鼠心肌缺血再灌注损伤过程,而上调miR-29b可有效组织心肌缺血再灌注后心室重塑,保护心脏功能.
目的 探討微小RNA(miRNA,miR)-29b對心肌缺血再灌註損傷的保護作用及機製.方法 將成年雄性Wister大鼠40隻隨機分為假手術組、缺血再灌註損傷組、miR-29b治療組和缺血再灌註陰性對照組4組.假手術組大鼠,放置6-0縫閤線不結扎,其餘3組均按缺血再灌註模型處理,其中miR-29b治療組在缺血再灌註模型前24 h,心肌內註射agomiR-29b(1×103 mol/L),陰性對照組在缺血再灌註模型前24 h,心肌內註射陰性對照序列.鑑測各組大鼠術後1、3、7、15、30 d各時相點的心率、左室射血分數(LVEF)、心肌細胞凋亡率、Ⅰ型膠原蛋白及miR-29b的mRNA錶達.結果 各組大鼠術後1、3、7、15、30 d各組時相點心率差異無統計學意義(P＞0.05);與假手術組比較,缺血再灌註組大鼠術後1、3、7、15、30 d左室射血分數(LVEF)分彆為(70.42±2.06)％、(64.37±1.84)％、(54.61±1.37)％、(51.92±1.07)％、(47.38±1.02)％,LVEF變化均顯著下降;與缺血再灌註組比較,miR-29b治療組大鼠術後1、3、7、15、30 d心肌LVEF分彆為(80.62±2.48)％、(78.37±2.03)％、(72.15±2.34)％、(65.18±1.73)％、(60.08±1.16)％,LVEF變化均顯著上調;陰性對照組與缺血再灌註組比較差異無統計學意義(P＞0.05).與假手術組比較,缺血再灌註組大鼠術後1、3、7、15、30 d心肌細胞凋亡率分彆為(33.6±4.2)％、(53.7±6.3)％、(41.9±5.8)％、(39.3±6.7)％、(32.7±4.8)％,心肌細胞凋亡率均顯著升高;與缺血再灌註組比較,miR-29b治療組大鼠術後1、3、7、15、30 d心肌細胞凋亡率分彆為(18.2±3.9)％、(29.6±5.2)％、(32.7±3.8)％、(28.4±6.0)％、(21.5±4.6)％,心肌細胞凋亡率均顯著下降;陰性對照組與缺血再灌註組間各指標比較差異無統計學意義(P＞0.05).與假手術組比較,缺血再灌註組大鼠術後各時相點Ⅰ型膠原蛋白錶達均顯著升高;而與缺血再灌註組比較,給予miR-29b治療組大鼠術後各時相點Ⅰ型膠原蛋白錶達均顯著下降;陰性對照組與缺血再灌註組比較差異無統計學意義(P＞0.05).與假手術組比較,缺血再灌註組大鼠術後各時相點miRNA-29b的mRNA錶達均顯著下降;而與缺血再灌註組比較,給予miR-29b治療組大鼠術後各時相點miRNA-29b的mRNA錶達均顯著上調;陰性對照組與缺血再灌註組比較差異無統計學意義(P＞0.05).結論 心肌缺血再灌註後miR-29b錶達明顯下降,錶明miR-29b參與大鼠心肌缺血再灌註損傷過程,而上調miR-29b可有效組織心肌缺血再灌註後心室重塑,保護心髒功能.
목적 탐토미소RNA(miRNA,miR)-29b대심기결혈재관주손상적보호작용급궤제.방법 장성년웅성Wister대서40지수궤분위가수술조、결혈재관주손상조、miR-29b치료조화결혈재관주음성대조조4조.가수술조대서,방치6-0봉합선불결찰,기여3조균안결혈재관주모형처리,기중miR-29b치료조재결혈재관주모형전24 h,심기내주사agomiR-29b(1×103 mol/L),음성대조조재결혈재관주모형전24 h,심기내주사음성대조서렬.감측각조대서술후1、3、7、15、30 d각시상점적심솔、좌실사혈분수(LVEF)、심기세포조망솔、Ⅰ형효원단백급miR-29b적mRNA표체.결과 각조대서술후1、3、7、15、30 d각조시상점심솔차이무통계학의의(P＞0.05);여가수술조비교,결혈재관주조대서술후1、3、7、15、30 d좌실사혈분수(LVEF)분별위(70.42±2.06)％、(64.37±1.84)％、(54.61±1.37)％、(51.92±1.07)％、(47.38±1.02)％,LVEF변화균현저하강;여결혈재관주조비교,miR-29b치료조대서술후1、3、7、15、30 d심기LVEF분별위(80.62±2.48)％、(78.37±2.03)％、(72.15±2.34)％、(65.18±1.73)％、(60.08±1.16)％,LVEF변화균현저상조;음성대조조여결혈재관주조비교차이무통계학의의(P＞0.05).여가수술조비교,결혈재관주조대서술후1、3、7、15、30 d심기세포조망솔분별위(33.6±4.2)％、(53.7±6.3)％、(41.9±5.8)％、(39.3±6.7)％、(32.7±4.8)％,심기세포조망솔균현저승고;여결혈재관주조비교,miR-29b치료조대서술후1、3、7、15、30 d심기세포조망솔분별위(18.2±3.9)％、(29.6±5.2)％、(32.7±3.8)％、(28.4±6.0)％、(21.5±4.6)％,심기세포조망솔균현저하강;음성대조조여결혈재관주조간각지표비교차이무통계학의의(P＞0.05).여가수술조비교,결혈재관주조대서술후각시상점Ⅰ형효원단백표체균현저승고;이여결혈재관주조비교,급여miR-29b치료조대서술후각시상점Ⅰ형효원단백표체균현저하강;음성대조조여결혈재관주조비교차이무통계학의의(P＞0.05).여가수술조비교,결혈재관주조대서술후각시상점miRNA-29b적mRNA표체균현저하강;이여결혈재관주조비교,급여miR-29b치료조대서술후각시상점miRNA-29b적mRNA표체균현저상조;음성대조조여결혈재관주조비교차이무통계학의의(P＞0.05).결론 심기결혈재관주후miR-29b표체명현하강,표명miR-29b삼여대서심기결혈재관주손상과정,이상조miR-29b가유효조직심기결혈재관주후심실중소,보호심장공능.
Objective To discuss the effect and mechanism of microRNA (miR)-29b on the myocardial ischemia-reperfusion (IR) injury.Methods Healthy adult male Wistar rats were divided into four groups:sham group,IR group,miR-29b group and scramble group.In sham group,6-0 linea suturalis was placed without deligation,and in the rest three groups IR model was maded.Rats in miR-29b group were given agomiR-29b (1 × 103 mol/L) at 24 h before IR modelling,and those in scramble group were given agomiR-29b (1 mmol/L) negative control sequence.Heart rate,left ventricular ejection frac-tion (LVEF),apoptosis rate of myocardial cells,collagen Ⅰ and miR-29b at 1,3,7,15 and 30 d after operation were observed.Results Heart rate in all groups showed no significant difference at 1,3,7,15 d,and 30 d.Compared with sham group,I/R rats showed decreased LVEF,as (70.42 ± 2.06) ％,(64.37±1.84)％,(54.61 ±1.37)％,(51.92±1.07)％,(47.38±1.02)％ at 1,3,7,15,30 d,respectively.Compared with I/R group,LVEF in miR-29b group were significandy increased,as (80.62 ± 2.48)％,(78.37 ±2.03)％,(72.15 ±2.34)％,(65.18 ±1.73)％,(60.08 ±1.16)％ at 1,3,7,15,30 d,respectively.There was no significant difference between I/R group and scramble group.Compared with sham group,I/R rats showed increased apoptosis rates of myocardial cell,as (33.6 ± 4.2) ％,(53.7 ±6.3)％,(41.9 ±5.8)％,(39.3 ±6.7)％,(32.7 ±4.8)％ at 1,3,7,15,30 d,respectively.Compared with I/R group,apoptosis rates of myocardial cell in miR-29b group were significantly decreased,as (18.2±3.9)％,(29.6±5.2)％,(32.7±3.8)％,(28.4±6.0)％,(21.5±4.6)％ at 1,3,7,15,30 d,respectively.There was no significant difference between I/R group and scramble group.Compared with sham group,I/R rats showed increased collagen Ⅰ.Compared with I/R group,collagen Ⅰ in miR-29b group were significantly decreased.There was no significant difference between I/R group and scramble group.Compared with sham group,I/R rats showed decreased miRNA-29b mRNA.Compared with I/R group,miRNA-29b mRNA in miR-29b group were significantly increased.Conclusion The expression of miR-29b was significantly decreased after myocardial IR,which indicated that miR-29b took apart in the process of myocardial IR injury.Up-regulation of miR-29b could effectively ameliorate ventricular remodeling after myocardial IR injury and protect cardiac function.
