单击此处阅读完整的文章。通过调节14-3-3η的调节来抑制铁毒性，凋亡和自噬，缺血/再灌注损伤。
摘要来源：
biomed Pharmacother。 2024年5月; 174：116542。 EPUB 2024 4月3日。PMID： 38574620“> 38574620 Ze-Yu Zhang, Ya-Mei Qiao, Wen-Xiong Huang, Yi-Cheng Wang, Xin-Yi Tang, Song-Qing Lai
Article Affiliation:Tie Hu
Abstract:Previous studies have demonstrated that the underlying mechanisms of myocardial ischemia/reperfusion injury (MIRI) are complex and involve multiple types of regulatory cell death, including铁凋亡，凋亡和自噬。因此，我们旨在确定y Miri的基础机制并验证了Epigallocatechin-3-Gallate（EGCG）及其相关机制在MIRI中的保护作用。构建了体内和体外模型的MIRI模型。 The results showed that pretreatment with EGCG could attenuate MIRI, as indicated by increased cell viability, reduced lactate dehydrogenase (LDH) activity and apoptosis, inhibited iron overload, abnormal lipid metabolism, preserved mitochondrial function, decreased infarct size, maintained cardiac function, decreased reactive oxygen species (ROS) level, and reduced TUNEL-positive cells.此外，EGCG预处理可以减弱Miri通过上调14-3-3ηprotein水平引起的肌凋亡，凋亡和自噬。此外，可以用PAD/14-3-3η-shRNA或化合物C11（A 14-3-3-抑制剂）消除EGCG的保护作用，但不能消除EGCG。总之，通过介导14-3-3η和受保护的心肌菌，EGCG预处理减弱了肌凋亡，凋亡和自噬YTES反对Miri。