Lin Zhao, Yanghong Liu, Ye Chen, Zaixin Yu, Huijuan Luo
{"title":"减轻大鼠心肌缺血再灌注损伤的新型后处理方法","authors":"Lin Zhao, Yanghong Liu, Ye Chen, Zaixin Yu, Huijuan Luo","doi":"10.31083/j.rcm2502067","DOIUrl":null,"url":null,"abstract":"Background : Ischaemia-reperfusion injury (IRI) is the damage that occurs when blood flow is restored to a tissue or organ after a period of ischaemia. Postconditioning is a therapeutic strategy aimed at reducing the tissue damage caused by IRI. Postconditioning in rodents is a useful tool to investigate the potential mechanisms of postconditioning. Currently, there is no convenient approach for postconditioning rodents. Methods : Rats were subjected to a balloon postconditioning procedure. A balloon was used to control the flow in the vessel. This allowed for easy and precise manipulation of perfusion. Evans blue and triphenyltetrazolium chloride (TTC) double staining were used to determine the infarct size. Apoptosis in the myocardium was visualised and quantified by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Western blotting was performed to assess the expression of key apoptotic proteins, i.e. , B-cell lymphoma 2 (Bcl-2), Bcl-2 Associated X (Bax), and cleaved caspase-3. Results : The balloon control approach to postconditioning provided accurate control of coronary blood flow and simplified the postconditioning manipulation. Infarct size reduction was observed in IRI rats after post-conditioning. There was a decrease in cardiac apoptosis in IRI rats after conditioning, as detected by TUNEL staining. IRI rats showed increased Bcl-2 levels and decreased Bax and cleaved caspase-3 levels in the myocardium. Conclusions : Postconditioning was successfully applied in rats using this novel approach. Postconditioning with this approach reduced infarct size and apoptosis in the area at risk.","PeriodicalId":507771,"journal":{"name":"Reviews in Cardiovascular Medicine","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2024-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A Novel Postconditioning Approach Attenuates Myocardial Ischaemia-Reperfusion Injury in Rats\",\"authors\":\"Lin Zhao, Yanghong Liu, Ye Chen, Zaixin Yu, Huijuan Luo\",\"doi\":\"10.31083/j.rcm2502067\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Background : Ischaemia-reperfusion injury (IRI) is the damage that occurs when blood flow is restored to a tissue or organ after a period of ischaemia. Postconditioning is a therapeutic strategy aimed at reducing the tissue damage caused by IRI. Postconditioning in rodents is a useful tool to investigate the potential mechanisms of postconditioning. Currently, there is no convenient approach for postconditioning rodents. Methods : Rats were subjected to a balloon postconditioning procedure. A balloon was used to control the flow in the vessel. This allowed for easy and precise manipulation of perfusion. Evans blue and triphenyltetrazolium chloride (TTC) double staining were used to determine the infarct size. Apoptosis in the myocardium was visualised and quantified by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Western blotting was performed to assess the expression of key apoptotic proteins, i.e. , B-cell lymphoma 2 (Bcl-2), Bcl-2 Associated X (Bax), and cleaved caspase-3. Results : The balloon control approach to postconditioning provided accurate control of coronary blood flow and simplified the postconditioning manipulation. Infarct size reduction was observed in IRI rats after post-conditioning. There was a decrease in cardiac apoptosis in IRI rats after conditioning, as detected by TUNEL staining. IRI rats showed increased Bcl-2 levels and decreased Bax and cleaved caspase-3 levels in the myocardium. Conclusions : Postconditioning was successfully applied in rats using this novel approach. 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引用次数: 0
摘要
背景:缺血再灌注损伤(IRI)是指组织或器官在缺血一段时间后血流恢复时发生的损伤。后调节是一种治疗策略,旨在减少 IRI 造成的组织损伤。在啮齿动物中进行后调节是研究后调节潜在机制的有用工具。目前,还没有方便的方法对啮齿动物进行后调节。方法 :对大鼠进行气球后调节程序。气球用于控制血管中的流量。这样就能轻松精确地控制灌注量。伊文思蓝和三苯基氯化四氮唑(TTC)双重染色用于确定梗死的大小。通过末端脱氧核苷酸转移酶 dUTP 缺口标记(TUNEL)观察和量化心肌凋亡。用 Western 印迹法评估关键凋亡蛋白的表达,即 B 细胞淋巴瘤 2(Bcl-2)、Bcl-2 相关 X(Bax)和裂解的 caspase-3。结果:球囊控制后处理方法可精确控制冠状动脉血流量,简化后处理操作。后调节后,IRI 大鼠的梗死面积缩小。通过 TUNEL 染色法检测,调节后 IRI 大鼠心脏凋亡减少。IRI 大鼠心肌中的 Bcl-2 水平升高,Bax 和裂解的 Caspase-3 水平降低。结论 :使用这种新方法成功地对大鼠进行了后处理。使用这种方法进行后处理可缩小梗死面积,减少危险区域的细胞凋亡。
A Novel Postconditioning Approach Attenuates Myocardial Ischaemia-Reperfusion Injury in Rats
Background : Ischaemia-reperfusion injury (IRI) is the damage that occurs when blood flow is restored to a tissue or organ after a period of ischaemia. Postconditioning is a therapeutic strategy aimed at reducing the tissue damage caused by IRI. Postconditioning in rodents is a useful tool to investigate the potential mechanisms of postconditioning. Currently, there is no convenient approach for postconditioning rodents. Methods : Rats were subjected to a balloon postconditioning procedure. A balloon was used to control the flow in the vessel. This allowed for easy and precise manipulation of perfusion. Evans blue and triphenyltetrazolium chloride (TTC) double staining were used to determine the infarct size. Apoptosis in the myocardium was visualised and quantified by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Western blotting was performed to assess the expression of key apoptotic proteins, i.e. , B-cell lymphoma 2 (Bcl-2), Bcl-2 Associated X (Bax), and cleaved caspase-3. Results : The balloon control approach to postconditioning provided accurate control of coronary blood flow and simplified the postconditioning manipulation. Infarct size reduction was observed in IRI rats after post-conditioning. There was a decrease in cardiac apoptosis in IRI rats after conditioning, as detected by TUNEL staining. IRI rats showed increased Bcl-2 levels and decreased Bax and cleaved caspase-3 levels in the myocardium. Conclusions : Postconditioning was successfully applied in rats using this novel approach. Postconditioning with this approach reduced infarct size and apoptosis in the area at risk.