Department of Cardiology, The First Afliated Hospital of Nanjing Medical University, Huaian City, Jiangsu Province, China.
Bioengineered. 2022 Mar;13(3):5653-5662. doi: 10.1080/21655979.2022.2037366.
Myocardial infarction (MI), caused by continuous ischemia and hypoxia of the coronary artery, is one of the major causes of human mortality. This study aimed to investigate the role of notoginsenoside R1 (NGR1) in MI therapy. and models of MI were established by hypoxia/reoxygenation (H/R)-treatment of H9C2 cells and through the ligation of the left anterior descending coronary artery of rats, respectively. CCK-8 and EdU assays were performed to measure cell viability and proliferation, respectively. Flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were performed to determine the apoptotic rate of cells. Western blot was used to determine protein expression. The MI area was analyzed by 2,3,5-triphenyltetrazolium chloride (TTC) staining. NGR1 promoted viability and proliferation, and inhibited the apoptotic rate of H/R-treated H9C2 cells. In addition, NGR1 downregulated the protein expression of caspase-3 and Bax, and upregulated Bcl-2 expression in H/R-treated H9C2 cells. The JAK2/STAT3 signaling pathway was activated following NGR1 treatment and , and inhibition of the JAK2/STAT3 signaling pathway reversed the effects of NGR1 on H/R-treated H9C2 cells. Finally, NGR1 reduced the area of MI. NGR1 relieved MI and by activating the JAK2/STAT3 signaling pathway.
心肌梗死（MI）是由冠状动脉持续缺血和缺氧引起的，是人类死亡的主要原因之一。本研究旨在探讨三七总皂苷 R1（NGR1）在 MI 治疗中的作用。通过缺氧/复氧（H/R）处理 H9C2 细胞和结扎大鼠左前降支冠状动脉分别建立 MI 模型。通过 CCK-8 和 EdU 测定分别检测细胞活力和增殖。通过流式细胞术和末端脱氧核苷酸转移酶 dUTP 缺口末端标记（TUNEL）染色检测细胞凋亡率。通过 Western blot 检测蛋白表达。通过 2,3,5-氯化三苯基四氮唑（TTC）染色分析 MI 面积。NGR1 促进 H/R 处理的 H9C2 细胞的活力和增殖，并抑制其凋亡率。此外，NGR1 下调 H/R 处理的 H9C2 细胞中 caspase-3 和 Bax 的蛋白表达，并上调 Bcl-2 的表达。NGR1 处理后激活 JAK2/STAT3 信号通路，抑制 JAK2/STAT3 信号通路可逆转 NGR1 对 H/R 处理的 H9C2 细胞的作用。最后，NGR1 减少了 MI 面积。NGR1 通过激活 JAK2/STAT3 信号通路缓解 MI。
