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缺血后处理对非罪犯冠状动脉细胞凋亡及相关基因表达的影响。

Effect of ischemic postconditioning on cell apoptosis and expression of relevant genes in non-culprit coronary arteries.

机构信息

Department of Cardiology, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, China

Department of Cardiology, Aerospace Center Hospital, Peking University Aerospace School of Clinical Medicine, Beijing, China.

出版信息

J Investig Med. 2020 Oct;68(7):1276-1281. doi: 10.1136/jim-2020-001328. Epub 2020 Aug 11.

DOI:10.1136/jim-2020-001328
PMID:32784207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7525782/
Abstract

This study was performed to determine the effect of ischemic postconditioning on cell apoptosis and angiotensin II receptor type 1 (AT1), connexin 43 (Cx43), and β-tubulin mRNA expression in non-culprit arteries. Non-culprit arterial tissues were isolated from a rabbit myocardial ischemia-reperfusion model and randomly divided into sham, ischemia-reperfusion, and ischemic postconditioning groups. Cell apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Expression of angiotensin II, AT1, Cx43, and β-tubulin mRNA was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). TUNEL analysis indicated significantly higher ratios of apoptotic cells in the ischemia-reperfusion group than in the sham group. However, significantly fewer apoptotic cells were observed in the ischemic postconditioning group than in the ischemia-reperfusion group. The qRT-PCR results indicated significantly higher expression of AT1, Cx43, and β-tubulin mRNA in the ischemia-reperfusion group than in the sham group. However, expression of AT1, Cx43, and β-tubulin was lower in the ischemic postconditioning group than in the ischemia-reperfusion group. The ratios of apoptotic cells and mRNA expression of AT1, Cx43, and β-tubulin in non-culprit arteries were increased after ischemia-reperfusion. Ischemic postconditioning may decrease these features and inhibit the progression of non-culprit arteries.

摘要

本研究旨在探讨缺血后处理对非罪犯动脉细胞凋亡及血管紧张素 II 受体 1(AT1)、连接蛋白 43(Cx43)和β-微管蛋白 mRNA 表达的影响。取兔心肌缺血再灌注模型非罪犯动脉组织,随机分为假手术组、缺血再灌注组和缺血后处理组。采用末端脱氧核苷酸转移酶 dUTP 缺口末端标记法(TUNEL)检测细胞凋亡。采用实时定量聚合酶链反应(qRT-PCR)检测血管紧张素 II、AT1、Cx43 和β-微管蛋白 mRNA 的表达。TUNEL 分析显示,与假手术组相比,缺血再灌注组细胞凋亡比例显著升高;与缺血再灌注组相比,缺血后处理组细胞凋亡比例显著降低。qRT-PCR 结果显示,与假手术组相比,缺血再灌注组 AT1、Cx43 和β-微管蛋白 mRNA 表达显著升高;与缺血再灌注组相比,缺血后处理组 AT1、Cx43 和β-微管蛋白 mRNA 表达降低。缺血再灌注后非罪犯动脉细胞凋亡比例及 AT1、Cx43 和β-微管蛋白 mRNA 表达增加,缺血后处理可降低这些特征,抑制非罪犯动脉进展。

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