{"title":"Protective function of albiflorin against ferroptosis in exhaustive exerciseinduced myocardial injury via the AKT/Nrf2/HO-1 signaling.","authors":"Zhuang Tian, Zhenyu Li","doi":"10.1590/acb393524","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>It has been reported that exhaustive exercise (EE) causes myocyte injury, and eventually damages the function of the myocardia. Albiflorin (AF) has anti-inflammatory, antioxidant, and anti-apoptosis effects. In this study, we determined whether AF could mitigate the EE-induced myocardial injury and research the potential mechanisms.</p><p><strong>Methods: </strong>The rat model of EE was built by forced treadmill running method. Rats were intraperitoneally injected with AF before EE once daily for one week. The relative factors levels were examined by commercial kits. The apoptosis was appraised using a TdT-mediated dUTP nick end labeling assay kit. The ACSL4, GPX4, Nrf2, pAKT/AKT, and HO-1 contents were assessed by western blot.</p><p><strong>Results: </strong>AF lessened EE-induced cardiac myocytes ischemic/hypoxic injury and reduced the contents of myocardial injury biomarkers in the serum. AF lessened EE-induced cardiac myocyte apoptosis, inflammatory response, oxidative stress, and ferroptosis in myocardial tissues. However, the influences of AF were overturned by the co-treatment of AF and LY294002. AF activated the AKT/Nrf2/HO-1 signaling pathway in myocardial tissues in vivo.</p><p><strong>Conclusions: </strong>AF could curb cardiac myocytes ferroptosis, thus diminishing the EE-induced myocardial injury through activating the AKT/Nrf2/HO-1 cascade.</p>","PeriodicalId":93850,"journal":{"name":"Acta cirurgica brasileira","volume":"39 ","pages":"e393524"},"PeriodicalIF":0.0000,"publicationDate":"2024-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11321502/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta cirurgica brasileira","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1590/acb393524","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Purpose: It has been reported that exhaustive exercise (EE) causes myocyte injury, and eventually damages the function of the myocardia. Albiflorin (AF) has anti-inflammatory, antioxidant, and anti-apoptosis effects. In this study, we determined whether AF could mitigate the EE-induced myocardial injury and research the potential mechanisms.
Methods: The rat model of EE was built by forced treadmill running method. Rats were intraperitoneally injected with AF before EE once daily for one week. The relative factors levels were examined by commercial kits. The apoptosis was appraised using a TdT-mediated dUTP nick end labeling assay kit. The ACSL4, GPX4, Nrf2, pAKT/AKT, and HO-1 contents were assessed by western blot.
Results: AF lessened EE-induced cardiac myocytes ischemic/hypoxic injury and reduced the contents of myocardial injury biomarkers in the serum. AF lessened EE-induced cardiac myocyte apoptosis, inflammatory response, oxidative stress, and ferroptosis in myocardial tissues. However, the influences of AF were overturned by the co-treatment of AF and LY294002. AF activated the AKT/Nrf2/HO-1 signaling pathway in myocardial tissues in vivo.
Conclusions: AF could curb cardiac myocytes ferroptosis, thus diminishing the EE-induced myocardial injury through activating the AKT/Nrf2/HO-1 cascade.
目的：据报道，剧烈运动（EE）会导致心肌细胞损伤，并最终损害心肌功能。阿维菌素（AF）具有抗炎、抗氧化和抗细胞凋亡的作用。在这项研究中，我们确定了阿比福林是否能减轻EE诱导的心肌损伤，并研究了其潜在机制：方法：采用强迫跑步法建立 EE 大鼠模型。方法：采用强迫跑步法建立 EE 大鼠模型，在 EE 前腹腔注射 AF，每天一次，连续一周。用市售试剂盒检测相对因子水平。使用 TdT 介导的 dUTP 缺口标记检测试剂盒评估细胞凋亡。ACSL4、GPX4、Nrf2、pAKT/AKT和HO-1的含量通过Western印迹进行评估：结果：房颤减轻了 EE 诱导的心肌细胞缺血缺氧损伤，降低了血清中心肌损伤生物标志物的含量。房颤减轻了 EE 诱导的心肌细胞凋亡、炎症反应、氧化应激和心肌组织中的铁变态反应。然而，心房颤动与 LY294002 联合治疗会推翻心房颤动的影响。心房颤动激活了体内心肌组织中的AKT/Nrf2/HO-1信号通路：结论：房颤可抑制心肌细胞的铁突变，从而通过激活 AKT/Nrf2/HO-1 级联减轻 EE 诱导的心肌损伤。
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