Dexmedetomidine suppresses the development of abdominal aortic aneurysm by downregulating the mircoRNA‑21/PDCD 4 axis

右美托咪啶通过下调 mircoRNA-21/PDCD 4 轴抑制腹主动脉瘤的发展

阅读:14
作者:Qi Yu, Qianqian Li, Xinglong Yang, Qiang Liu, Jun Deng, Yanping Zhao, Ruilin Hu, Min Dai

Abstract

Abdominal aortic aneurysm (AAA) is a pathological state with permanent dilation, which indicates a fatal potential for aortic rupture. It has been reported that dexmedetomidine (Dex) and microRNA (miR)‑21 are involved in the progression of AAA. Thus, the present study aimed to investigate the joint effects of these factors on AAA treatment. For this purpose, rat models of AAA were established with enzyme perfusion and the rats were then injected with Dex. Alterations in the abdominal aorta in rats with AAA were recorded. miR‑21 expression in the rats with AAA was determined. Inflammatory factor expression was detected by western blot analysis. Subsequently, a dual‑luciferase reporter gene assay was performed to verify the targeting association between miR‑21 and programmed cell death protein 4 (PDCD4). Additionally, AAA‑related indices and inflammatory responses were examined by an injection of a combination of antagomiR (ant)‑miR‑21 and Dex or lentivirus‑PDCD4‑short hairpin RNA. It was found that Dex markedly alleviated the development of AAA and downregulated the expression of inflammatory factors and matrix metalloproteinase in rats with AAA. The high expression of miR‑21, which targets PDCD4, was observed in the rats with AAA. However, ant‑miR‑21 induced AAA development and inflammatory responses. Additionally, the inhibition of PDCD4 reduced AAA development and inflammatory responses. On the whole, the present study demonstrates that Dex inhibits AAA development by downregulating the miR‑21/PCDP4 axis. The findings of the present study may provide novel insight for the treatment of AAA. These findings may provide a reference for the future treatment of AAA and may provide theoretical guidance for the early prevention and development of AAA.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。