Astragaloside IV protects cardiomyocytes against hypoxia injury via HIF-1α and the JAK2/STAT3 pathway.
Astragaloside IV protects cardiomyocytes against hypoxia injury via HIF-1α and the JAK2/STAT3 pathway.
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黄芪甲苷通过HIF-1α和JAK 2/STAT 3通路保护心肌细胞免受缺氧损伤
DOI：
10.21037/atm-21-4080
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发表时间：
2021-09
影响因子：
--
通讯作者：
Zeng X
中科院分区：
文献类型：
--
作者：
Li B;Yu J;Liu P;Zeng T;Zeng X
由于心脏对低氧的高度敏感性，低氧是导致心肌损伤的重要原因。黄芪皂苷IV(AS-IV)是黄芪的主要成分之一，具有心脏保护作用。本研究旨在阐明AS-IV对缺氧损伤的H9c2心肌细胞的作用。首先，H9c2细胞暴露于低氧和/或AS-IV处理。分析细胞凋亡、死亡、存活率以及缺氧诱导因子1α(HIF-1α)和凋亡蛋白的表达。接下来，将si-HIF-1α导入H9c2细胞，检测HIF-1α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，还检测了Janus kinase2/信号转导和转录激活子3(JAK2/STAT3)信号对HIF-1α水平的调节作用。低氧抑制H9c2细胞的活力，促进细胞的凋亡和死亡。AS-IV可消除缺氧所致的H9c2损伤。此外，AS-IV可进一步激活和稳定缺氧攻击的H9c2细胞中的低氧诱导因子-1α信号。缺氧诱导因子-1α的下调抑制了缺氧攻击的H9c2细胞中AS-IV的功能。AS-IV在缺氧损伤中促进JAK2/STAT3信号转导。AS-IV在低氧暴露的H9c2细胞中的有益作用与上调HIF-1α和激活JAK2/STAT3信号通路有关。AS-IV可能通过激活JAK2/STAT3介导的HIF-1α信号通路减轻缺氧后H9c2心肌细胞的损伤。
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 Astragalus membranaceus 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 hypoxia-inducible factor 1α (HIF-1α) expression and apoptotic proteins were analyzed. Next, transfection of si-HIF-1α into H9c2 cells was carried out to test whether upregulation and stabilization of HIF-1α influences the effect of AS-IV on hypoxia-treated H9c2 cells. Furthermore, the regulatory role of Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling on HIF-1α levels was examined. Hypoxia suppressed viability and promoted the apoptosis and death of H9c2 cells. AS-IV eliminated hypoxia-induced H9c2 injury. Moreover, HIF-1α signaling was further activated and stabilized by AS-IV in hypoxia-challenged H9c2 cells. Downregulation of HIF-1α suppressed the function of AS-IV in hypoxia-challenged H9c2 cells. AS-IV promoted JAK2/STAT3 signaling in hypoxia-induced injury. The beneficial functions of AS-IV in hypoxia-exposed H9c2 cells were linked to HIF-1α upregulation and JAK2/STAT3 signaling activation. AS-IV relieved H9c2 cardiomyocyte injury after hypoxia, possibly by activating JAK2/STAT3-mediated HIF-1α signaling.
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DOI：
10.3390/molecules25215189
发表时间：
2020-11-07
期刊：
Molecules (Basel, Switzerland)
影响因子：
--
作者：
R Amin D;Sink E;Narayan SP;Abdel-Hafiz M;Mestroni L;Peña B
通讯作者：
Peña B
影响因子：
20.1
作者：
Natarajan, R;Salloum, FN;Fowler, AA
通讯作者：
Fowler, AA
影响因子：
3.8
作者：
Gui, Dingkun;Huang, Jianhua;Wang, Niansong
通讯作者：
Wang, Niansong
影响因子：
7.5
作者：
Du, Jian;Liu, Jia;Leng, Ji-Yan
通讯作者：
Leng, Ji-Yan
双功能SDF-1-AnxA5融合蛋白可保护心肌梗塞后的心脏功能。
影响因子：
5.3
作者：
Huang, Fang-Yang;Xia, Tian-Li;Chen, Mao
通讯作者：
Chen, Mao