[1]张彩霞 曾彬 廖小婷.心肌梗死模型中三碘甲状腺原氨酸对心肌的保护作用研究[J].心血管病学进展,2020,(11):1209-1214.[doi:10.16806/j.cnki.issn.1004-3934.20.11.000]
　ZHANG Caixia,ZENG Bin,LIAO Xiaoting.Protective Effect of Triiodothyronine on Myocardium in Myocardial Infarction Model[J].Advances in Cardiovascular Diseases,2020,(11):1209-1214.[doi:10.16806/j.cnki.issn.1004-3934.20.11.000]
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心肌梗死模型中三碘甲状腺原氨酸对心肌的保护作用研究()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2020年11期
页码:
1209-1214
栏目:
论著
出版日期:
2020-11-25

文章信息/Info

Title:
Protective Effect of Triiodothyronine on Myocardium in Myocardial Infarction Model
文章编号:
202004075
作者:
张彩霞 曾彬 廖小婷
(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 武汉 430060)
Author(s):
ZHANG Caixia;  ZENG Bin;  LIAO Xiaoting
(Department of CardiologyRenmin Hospital of Wuhan University, Cardiovascular Research Institute of Wuhan University, Hubei Key Laboratory of Cardiology, Wuhan 430060, Hubei, China)
关键词:
三碘甲状腺原氨酸; 心肌梗死; 炎症反应; 细胞凋亡; PI3K/AKT通路
Keywords:
Triiodothyronine;  Myocardial infarction;  Inflammation;  Apoptosis;  PI3K-AKT signaling pathway
DOI:
10.16806/j.cnki.issn.1004-3934.20.11.000
摘要:
目的 探讨三碘甲状腺原氨酸（T3）预处理对心肌梗死后心脏的保护作用及其机制。方法 随机将24只小鼠分为4组，分别为：假手术组、手术组、＋T3组、＋T3磷脂酰肌醇3激酶/蛋白激酶B（PI3K/AKT）抑制剂LY294002组（＋T3＋LY294002组T3[2μg/(100 g·d)]，第四组给予T3＋LY294002[2 mg/(100 g·d)]。术后4周，采用心脏超声检测小鼠心功能；采用苏木精-伊红6和肿瘤坏死因子（TNF）-α水平；并用蛋白免疫印迹法检测心肌组织中凋亡相关蛋白Cleaved caspase-3、Bax、Bcl-2T/p-PI3K和T/p-AKT的表达变化。结果 与假手术组相比，手术组左室射血分数（LVEF）、左室短轴缩短率（FS）和Bcl-2蛋白水平明显下降，左室收缩末期内径（LVESD）、左室舒张末期内径（LVEDD）、心重/体重和心肌组织中白介素-6、TNF-αBax、Cleaved caspase-3、p-PI3Kp-AKT水平明显升高（P＜0.05），心肌结构受损严重伴炎性细胞浸润；与手术组相比，手术＋T组LVEF、FSBcl-2、p-PI3Kp-AKT蛋白水平升高，LVESD、LVEDD6、TNF-αBax和Cleaved caspase-3蛋白水平下降（P＜0.05），心肌结构受损程度减轻伴炎性细胞浸润减少；与手术＋T组＋T3＋LY294002组LVEF、FSBcl-2、p-PI3Kp-AKT蛋白水平明显下降，LVESD、LVEDD6、TNF-αBax、Cleaved caspase-3P＜0.05），心肌结构受损程度加重伴炎性细胞浸润增加。结论 T3可通过PI3K/AKT信号通路发挥抗心肌纤维化、抗炎症损伤和抗凋亡作用以保护梗死后心肌。
Abstract:
Objective To explore the protective effect and mechanism of triiodothyronine （T3） pretreatment on the heart after myocardial infarction（MI）. Methods ivide 24 mice into 4 groups randomly: Sham, MI, MI＋T3 and MI＋T3＋PI3K/AKT inhibitor LY294002MI＋T3＋LY294002group, and 6 animals in each group. Acute MI was induced by ligating the left anterior descending coronary artery in mice. Pretreatment was injected intraperitoneally three days before operation. The first two groups were given normal saline, the third group was given T3 [2 μg/(100 g?d)], and the fourth group was given T3＋LY2940022 mg/(100 g?d)]. Cardiac ultrasound was used to detect cardiac function in mice four weeks after operation, H&E staining method was used to observe the pathological changes of myocardial tissue, ELISA was used to detect the level of inflammatory factors IL-6 and TNF-αin the tissue around the infarct border, and Western blotting was used to detect the expression changes of apoptosis-related proteins Cleaved caspase-3, Bax, Bcl-2 and pathway-related proteins T/p-PI3K and T/p-AKT in myocardial tissue. Results Compared with the Sham group, the left ventricular ejection fraction (LVEF), fractional shortening(FS), Bcl-2 protein level in the MI group decreased significantly, the left ventricular end-systolic dimension(LVESD), left ventricular end-diastolic dimension (LVEDD), heart/body weight ratio, and IL-6, TNF-α and Bax, Cleaved caspase-3, p-PI3K, p-AKT levels in myocardial tissue increased significantly(P＜0.05, and myocardial structure was severely damaged with inflammatory cell infiltration. Compared with MI group, LVEF, FS and the protein levels of Bcl-2, p-PI3K and p-AKT increased in the MI＋T3 group LVESD, LVEDD, IL-6 and TNF-α in myocardial tissue and the protein levels of Bax and Cleaved caspase-3 were decreased (P＜0.05he degree of myocardial structural damage was reduced with reduced inflammatory cell infiltration. Compared with the MI＋T3 group, LVEF, FS, protein levels Bcl-2, p-PI3K and p-AKT in the MI＋T3＋LY294002 group decreased significantly, and LVESD, LVEDD, IL-6 and TNF-α in myocardial tissue and protein levelsBax, Cleaved caspase-3 increased (P＜0.05he degree of damage to myocardial structure increased with increased inflammatory cell infiltration. Conclusion Triiodothyronine can play the role of anti-myocardial fibrosis, anti-inflammatory damage and anti-apoptosis through PI3K-AKT signaling pathway to protect the myocardium after infarction

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备注/Memo

备注/Memo:
收稿日期：2020-04-12(基金项目：国家自然科学基金(8127027181570333)；中央高校基本科研业务费专项资金（2042020kf1014）
更新日期/Last Update: 2021-02-04