Abstract:

Abstract: Objective To study the protective effect of miR-208b on myocardial infarction mice. Method Construction of a mouse model of myocardial infarction. The mice were randomly divided into the model group ( MI group) , the empty body group ( Ad group without miR-208b antagomir ) , the experimental group ( miR-208b antagomir group with miR-208b antagomir) . The mice without ligation of anterior descending branch were selected as the sham operation group ( sham group) . Echocardiography was used to detect cardiac function, the expression of miR-208b was measured by qRT-PCR, the area of myocardial infarction was measured by TTC staining, the apoptosis of myocardial cells in the periphery of infarction was detected by TUNEL, and the expression of Bcl-2 and Bax in myocardial cells was detected by Western-blot. Result After 7 days of myocardial infarction, the expression of miR-208b in the MI group and the Ad group was significantly increased compared with the Sham group ( P<0. 05) ; The infarct area of the miR-208b antagomir group was significantly smaller than that of the MI group ( P<0. 05) ; The levels of LVEDd and LVESD in the MI group, the Ad group and the miR-208b antagomir group were significantly higher than those in the Sham group, while LVEF and FS were significantly lower ( P<0. 05) ; The levels of LVEDd and LVESD in the miR-208b antagomir group were significantly lower than those in the MI group, while LVEF and FS were significantly higher ( P<0. 05) ; The apoptosis rate of myocardial cells in the MI group, the Ad group and the miR-208b antigomir group was significantly higher than that in the Sham group ( P<0. 05) ; The apoptosis rate of myocardial cells in the miR-208b antigomir group of was significantly lower than that in the MI group( P<0. 05) ; The result of Western blot showed that the heart cells in the group of MI and Ad were significantly lower than those in the group of MI ( P<0. 05) . The expression of Bcl-2 and Bax in myocardial infarction mice was significantly down regulated ( P < 0. 05) . The expression of Bcl-2 in the miR-208b antiagor group was significantly up regulated ( P < 0. 05 ) and Bax was significantly down regulated ( P < 0. 05 ) . Conclusion miR-208b is highly expressed in myocardial infarction mice. Inhibiting the expression of miR-208b can reduce the area of myocardial infarction, inhibit the apoptosis of myocardial cells, and improve the cardiac function of mice, so as to play the role of heart protection.

摘要：

摘要:目的 研究 miR-208b 对心肌梗死( myocardial infarction, MI)小鼠的保护作用。 方法 构建心肌梗死小鼠模型,将造模成功的小鼠随机分为模型组( MI 组) 、空载体组( Ad 组,注射未携带 miR-208b antagomir 腺病毒) 、实验组( miR-208b antagomir 组,注射携带 miR-208b antagomir 腺病毒) ,另选取未进行前降支结扎的小鼠作为假手术组( Sham 组) 。 使用超声心动检测心功能指标,利用 qRT-PCR 测定小鼠心肌 miR-208b 的表达,通过 TTC 染色测定小鼠心肌梗死面积,借助 TUNEL 法检测梗死周边区心肌细胞的凋亡情况,通过 Western blot 检测心肌细胞 Bcl-2 和Bax 的表达水平。 结果 小鼠心肌梗死 7 d 后,与 Sham 组比较,MI 组及 Ad 组小鼠心肌梗死周围区域 miR-208b 的表达显著 上 调 ( P < 0. 05) , miR-208b antagomir 组 小 鼠 miR-208b 的 表 达 显 著 较 MI 组 下 调 ( P < 0. 05) ; miR-208b antagomir 组心肌梗死面积明显小于 MI 组( P<0. 05) ;MI 组、Ad 组、miR-208b antagomir 组小鼠左心室舒张末期内径(LVEDd)、左心室收缩末期内径(LVESD)水平明显高于 Sham 组,而左室射血分数( LVEF)和短轴缩短率( FS)显著降低(P<0. 05);miR-208b antagomir 组小鼠 LVEDd 和 LVESD 水平明显低于 MI 组,而 LVEF 和 FS 显著升高( P<0. 05);MI 组、Ad 组及 miR-208b antagomir 组心肌细胞的凋亡率明显高于 Sham 组( P< 0. 05) ,miR-208b antagomir 组小鼠心肌细胞的凋亡率明显低于 MI 组( P < 0. 05) ;Western blot 实验结果显示,MI 组与 Ad 组心肌梗死小鼠心脏组织中Bcl-2 明显下调( P<0. 05) ,Bax 的表达明显较 Sham 组上调( P<0. 05) ,miR-208b antagomir 组 Bcl-2 的表达明显较 MI组上调( P<0. 05) ,Bax 的表达明显较 MI 组下调( P< 0. 05) 。 结论 miR-208b 在心肌梗死小鼠心肌组织中高表达。抑制 miR-208b 表达可降低心肌梗死小鼠心肌梗死面积,抑制心肌细胞的凋亡,改善小鼠的心功能,进而发挥心脏保护作用。