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基因对急性心肌梗死的保护作用。

Protective effects of gene on acute myocardial infarction.

作者信息

Gong Ge, Yang Xin-Xing, Li Yan-Yan, Geng Hong-Yu, Wang Hui, Wang Lian-Sheng, Yang Zhi-Jian

机构信息

Departments of Geriatrics, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.

Departments of Geriatrics, General Hospital of Nanjing Military Region, Nanjing 210002, China.

出版信息

J Thorac Dis. 2018 Feb;10(2):941-953. doi: 10.21037/jtd.2018.01.59.

DOI:10.21037/jtd.2018.01.59
PMID:29607167
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5864685/
Abstract

BACKGROUND

To study the protective effects of recombinant phosphatidylinositol 3-kinase p110 gamma () lentiviral vector in Sprague-Dawley (SD) rats with acute myocardial infarction (AMI).

METHOD

The AMI rat models were established by ligaturing left anterior descending coronary artery. The or empty lentiviral vectors were injected at the edge of the infarct zone. The experiment was divided randomly into four groups (n=8): (I) Sham group; (II) AMI group; (III) AMI + empty vector injection group (AMI + E group); and (IV) AMI + PLV-PI3KCG injection group (AMI + PLV-PI3KCG group). The ultrasonic cardiogram (UCG) was used to compare the structural or functional changes among the four groups after operation for 10 days. Meanwhile, the rats were sacrificed and HE staining was used to compare the myocardial tissue changes among the four groups. The immunofluorescence and western blots were performed to compare the angiogenesis in the infarct region and explore the mechanism of the protective effects of gene on AMI rats.

RESULTS

Compared with AMI group and AMI + E group, in the AMI + PLV-PI3KCG group, left ventricular end diastolic diameter (LVEDd) was decreased, left ventricular ejection fraction (LVEF%) was significantly increased, and vascular endothelial growth factor (VEGF) expression was significantly increased in the infarct region (P<0.05); PI3KCG, pAkt/Akt, HIF-1a, and Bcl-2/Bax protein expressions were significantly increased (P<0.05).

CONCLUSIONS

The injection could improve the cardiac function, relieve the cardiac injury after the AMI operation. gene could play the protection role in the AMI process possibly by activating PI3K/Akt signal pathway, inhibiting apoptosis and promoting angiogenesis.

摘要

背景

研究重组磷脂酰肌醇3激酶p110γ()慢病毒载体对急性心肌梗死(AMI)的Sprague-Dawley(SD)大鼠的保护作用。

方法

通过结扎左冠状动脉前降支建立AMI大鼠模型。在梗死区域边缘注射或空慢病毒载体。实验随机分为四组(n = 8):(I)假手术组;(II)AMI组;(III)AMI + 空载体注射组(AMI + E组);(IV)AMI + PLV-PI3KCG注射组(AMI + PLV-PI3KCG组)。术后10天用超声心动图(UCG)比较四组之间的结构或功能变化。同时,处死大鼠,用HE染色比较四组之间的心肌组织变化。进行免疫荧光和蛋白质免疫印迹以比较梗死区域的血管生成,并探讨基因对AMI大鼠保护作用的机制。

结果

与AMI组和AMI + E组相比,AMI + PLV-PI3KCG组左心室舒张末期内径(LVEDd)减小,左心室射血分数(LVEF%)显著增加,梗死区域血管内皮生长因子(VEGF)表达显著增加(P < 0.05);PI3KCG、pAkt/Akt、HIF-1α和Bcl-2/Bax蛋白表达显著增加(P < 0.05)。

结论

注射可改善心脏功能,减轻AMI手术后的心脏损伤。基因可能通过激活PI3K/Akt信号通路、抑制细胞凋亡和促进血管生成在AMI过程中发挥保护作用。

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