细胞凋亡
自噬
脂多糖
流式细胞术
污渍
药理学
生物
小RNA
细胞生物学
化学
内分泌学
分子生物学
生物化学
基因
作者
Qiuning Wang,Yang Xue-feng,Ying Song,Xiaowei Sun,Wentao Li,Ling Zhang,Xueling Hu,Hong Wang,Nan Zhao,Ruming Zhuang,Xinling Xie,Futian Tang,Hongxin Wang
出处
期刊:Life Sciences
[Elsevier]
日期:2021-06-01
卷期号:275: 119414-119414
被引量:22
标识
DOI:10.1016/j.lfs.2021.119414
摘要
Astragaloside IV (AS-IV), the major active constituent purified from Astragalus membranaceus, was previously reported to have protective effects against cardiac dysfunction. However, the underlying mechanism remains unknown. In the present study, we investigated the protective effect of AS-IV on lipopolysaccharide (LPS)-induced cardiac dysfunction and explored the potential mechanism by focusing on miRNA-1 (miR-1) at the animal and cellular levels. A series of methods were used, including echocardiography, flow cytometry, ELISA, immunofluorescence, transmission electron microscopy, RT-PCR, and western blotting. The results showed that both AS-IV and the miR-1 inhibitor improved cardiac dysfunction, reduced heart injury, inhibited apoptosis and autophagy, and regulated the expression of calcium- and mitochondrial energy metabolism-related proteins in the heart tissue of rats treated with LPS. Importantly, AS-IV downregulated the expression of miR-1 mRNA in heart tissue. All effects of AS-IV were at least partly abolished by miR-1 mimics. In the in vitro study, both AS-IV and the miR-1 inhibitor inhibited apoptosis and autophagy and regulated the expression of calcium- and mitochondrial energy metabolism-related proteins in heart cells treated with LPS. Similarly, AS-IV downregulated the expression of miR-1 mRNA in heart cells. All effects of AS-IV on cells were at least partly abolished by miR-1 mimics. Furthermore, miR-1 mimics exhibited effects similar to LPS both in animal and cellular studies. Taken together, these results suggest that AS-IV protects against LPS-induced cardiac dysfunction by inhibiting calcium-mediated apoptosis and autophagy by targeting miR-1, highlighting a new mechanism for the therapeutic effect of AS-IV on cardiac dysfunction.
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