Article Publish Status: FREE
Abstract Title:

Astragaloside IV inhibits oxidized low‑density lipoprotein‑induced endothelial damage via upregulation of miR‑140‑3p.

Abstract Source:

Int J Mol Med. 2019 Sep ;44(3):847-856. Epub 2019 Jun 26. PMID: 31257467

Abstract Author(s):

Weibin Qian, Qiuhai Qian, Xinrui Cai, Ru Han, Wenjun Yang, Xinyue Zhang, Hongmin Zhao, Ranran Zhu

Article Affiliation:

Weibin Qian


Oxidized low‑density lipoprotein (ox‑LDL)‑mediated endothelial cell injury has an important role in the vascular complications of type 2 diabetes. Astragaloside IV (ASV) is an active component of Radix Astragali, which has been demonstrated to exert protective effects against endothelial damage. The present study explored whether microRNAs (miRNAs) are involved in mediating the protective effects of ASV on ox‑LDL‑induced damage in human umbilical vein endothelial cells (HUVECs). RNA sequencing and reverse transcription‑quantitative PCR analyses revealed that ox‑LDL treatment significantly downregulated miR‑140‑3p expression in HUVECs. miR‑140‑3p overexpression promoted cell proliferation and inhibited apoptosis in ox‑LDL‑induced HUVECs. However, inhibition of miR‑140‑3p expression could reverse the effects of ASV on ox‑LDL‑induced HUVECs and reactivate ASV‑inhibited PI3K/Akt signaling in ox‑LDL‑induced HUVECs. In addition, Krüppel‑like factor 4 (KLF4) was identified as a target of miR‑140‑3p in ox‑LDL‑treated HUVECs. Subsequent experiments revealed that KLF4 overexpression partially counteracted the protective effects of miR‑140‑3p or ASVtreatment in ox‑LDL‑induced HUVECs. Taken together, the current findings demonstrated that the protective effects of ASV on HUVECs were dependent on miR‑140‑3p upregulation and subsequent inhibition of KLF4 expression, which in turn suppressed the PI3K/Akt signaling pathway. The present results shed light to the molecular mechanism by which ASV alleviated ox‑LDL‑induced endothelial cell damage.

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