Li Bei, Yu Junjian, Liu Peipei, Zeng Taohui, Zeng Xueliang
Department of Pharmacy, First Affiliated Hospital of Gannan Medical University, Ganzhou, China.
Cardiovascular and Thoracis Surgery Department 2, First Affiliated Hospital of Gannan Medical University, Ganzhou, China.
Ann Transl Med. 2021 Sep;9(18):1435. doi: 10.21037/atm-21-4080.
Hypoxia is an important cause of myocardial injury due to the heart's high susceptibility to hypoxia. Astragaloside IV (AS-IV) is the main component of and could exert cardiac protective role. Here, the effect of AS-IV on hypoxia-injured H9c2 cardiomyocytes was elucidated.
First, H9c2 cells were exposed to hypoxia and/or AS-IV treatment. Cell apoptosis, death, and viability as well as () expression and apoptotic proteins were analyzed. Next, transfection of si- into H9c2 cells was carried out to test whether upregulation and stabilization of influences the effect of AS-IV on hypoxia-treated H9c2 cells. Furthermore, the regulatory role of () signaling on levels was examined.
Hypoxia suppressed viability and promoted the apoptosis and death of H9c2 cells. AS-IV eliminated hypoxia-induced H9c2 injury. Moreover, signaling was further activated and stabilized by AS-IV in hypoxia-challenged H9c2 cells. Downregulation of suppressed the function of AS-IV in hypoxia-challenged H9c2 cells. AS-IV promoted signaling in hypoxia-induced injury. The beneficial functions of AS-IV in hypoxia-exposed H9c2 cells were linked to upregulation and signaling activation.
AS-IV relieved H9c2 cardiomyocyte injury after hypoxia, possibly by activating -mediated signaling.
由于心脏对缺氧高度敏感，缺氧是心肌损伤的重要原因。黄芪甲苷IV（AS-IV）是黄芪的主要成分，可发挥心脏保护作用。在此，阐明了AS-IV对缺氧损伤的H9c2心肌细胞的影响。
首先，将H9c2细胞暴露于缺氧和/或AS-IV处理。分析细胞凋亡、死亡和活力以及（）表达和凋亡蛋白。接下来，将si-转染到H9c2细胞中，以测试的上调和稳定是否影响AS-IV对缺氧处理的H9c2细胞的作用。此外，研究了（）信号对水平的调节作用。
缺氧抑制了H9c2细胞的活力，促进了其凋亡和死亡。AS-IV消除了缺氧诱导的H9c2损伤。此外，在缺氧挑战的H9c2细胞中，AS-IV进一步激活并稳定了信号。的下调抑制了AS-IV在缺氧挑战的H9c2细胞中的功能。AS-IV在缺氧诱导的损伤中促进了信号。AS-IV在缺氧暴露的H9c2细胞中的有益作用与上调和信号激活有关。
AS-IV可能通过激活介导的信号减轻缺氧后H9c2心肌细胞损伤。
