三碘甲三碘甲状腺原氨酸预处理对小鼠心肌梗死后心室重构心室重构的影响  

Effect of T3 pretreatment on ventricular remodeling after myocardial infarction in mice

作　　者：张彩霞[1] 曾彬[1] 廖小婷 ZHANG Cai-xia;ZENG Bin;LIAO Xiao-ting(Department of Cardiology,Renmin Hospital of Wuhan University,Cardiovascular Research Institute of Wuhan University,Hubei Key Laboratory of Cardiology,Wuhan 430060,China)

机构地区：[1]武汉大学人民医院心内科,武汉大学心血管病研究所,心血管病湖北省重点实验室,湖北省武汉市430060

出　　处：《中国心血管病研究》2021年第3期242-246,共5页Chinese Journal of Cardiovascular Research

基　　金：国家自然科学基金青年基金资助项目(30900609);国家自然科学基金资助项目(81270271,81570333);中央高校基本科研业务费专项资金资助项目(2042020kf1014)。

摘　　要：目的探讨三碘甲状腺原氨酸(triiodothyronine,T3)预处理对小鼠心肌梗死(myocardial infarction,MI)后心室重构的影响。方法采用随机数字法将24只昆明小鼠分为4组:假手术组(Sham组)、手术组(MI组)、手术+T3组(MI+T3组)、手术+T3+PI3K/Akt信号通路抑制剂LY294002组(MI+T3+LY294002组),每组各6只。连续3天腹腔注射生理盐水、T3(2μg·100 g^(-1)·d-1)和LY294002(2 mg·100 g^(-1)·d-1)进行预处理,每天一次。结扎左冠状动脉前降支诱导小鼠发生急性心肌梗死。手术4周后,称量小鼠体质量、全心重和左心室重量;采用TUNEL染色法检测小鼠非梗死区心肌细胞凋亡情况;采用CD31免疫荧光染色检测梗死边缘区血管新生情况;采用Masson染色检测梗死后心肌梗死面积及纤维化程度。结果与Sham组小鼠术后的心重/体质量(6.5±0.6)和左室质量/体质量(4.1±0.4)相比,MI组(8.3±0.5、5.4±0.2)明显增加(P<0.05),造模成功;与MI组小鼠的心肌细胞凋亡(28.0±4.0)、新生血管密度(42.22±3.33)、心肌梗死面积(30.0±1.3)、纤维化程度(30.67±1.33)相比,MI+T3组分别为(11.0±5.0、57.78±6.67、22.0±4.6、24.0±2.33)(P<0.05);与MI+T3组相比,MI+T3+LY294002组小鼠的心肌细胞凋亡增加(36.0±5.0)、新生血管密度减少(41.11±4.44)、心肌梗死面积增加(37.0±3.3)、纤维化程度加重(37.33±4.0)(P<0.05)。结论T3在心肌梗死后可通过PI3K/Akt信号通路发挥抑制凋亡、促进血管新生、减少心肌纤维化和抗心室重构的作用。Objective To investigate the effect of triiodothyronine(T3)pretreatment on ventricular remodeling after myocardial infarction(MI)in mice.Methods Random number method was used to divide 24 Kunming mice into 4 groups:Sham,MI,MI+T3 and MI+T3+LY294002 group,6 animals in each group.Three consecutive days of intraperitoneal injection of saline,T3(2μg·100 g^(-1)·d-1)and LY294002(2 mg·100 g^(-1)·d-1)for pretreatment,once a day.Acute myocardial infarction was induced by ligation of the left anterior descending coronary artery.Four weeks after MI,the body weight,whole heart weight and left ventricular weight of mice were recorded.Using TUNEL staining to detect myocardial cell apoptosis in the non-infarct area,using CD31 immunofluorescence staining to detect angiogenesis in the marginal area of infarction,and using Masson staining to detect the area of myocardial infarction and the degree of fibrosis after myocardial infarction,then the compares were made.Results After the MI,compared with the heart weight/weight(6.5±0.6)and left ventricular weight/weight(4.1±0.4)of the mice in the Sham group,the MI group(8.3±0.5,5.4±0.2)increased significantly(P<0.05),and the modeling was successful;Compared with the myocardial cell apoptosis(28.0±4.0),neovascular density(42.22±3.33),myocardial infarction area(30.0±1.3)and degree of fibrosis(30.67±1.33)in the MI group of mice,the MI+T3 group was respectively(11.0±5.0,57.78±6.67,22.0±4.6,24.0±2.33)(P<0.05);Compared with the MI+T3 group,the MI+T3+LY294002 group had increased myocardial cell apoptosis(36.0±5.0),decreased neovascular density(41.11±4.44),increased myocardial infarction area(37.0±3.3),and the degree of fibrosis the degree aggravated(37.33±4.0)(P<0.05).Conclusion T3 can play the role of inhibiting apoptosis,promoting angiogenesis,reducing myocardial fibrosis and anti-ventricular remodeling through phosphatidyl inositide 3 kinases-protein kinase B(PI3 K/Akt)signaling pathway after myocardial infarction.

关 键 词：三碘甲状腺原氨酸 心肌梗死 心室重构 PI3K/AKT信号通路 

分 类 号：Q95-33[生物学—动物学] R542.22[医药卫生—心血管疾病]