Moxifloxacin induces aortic aneurysm and dissection by increasing osteopontin in mice.

Biochem Biophys Res Commun

Department of Pharmaceutical Care and Health Sciences, Faculty of Pharmaceutical Sciences, Fukuoka University, 8-19-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.

Published: November 2022

AI Article Synopsis

  • Fluoroquinolones, commonly prescribed antibiotics, are linked to an increased risk of aortic aneurysm and dissection (AAD), but the exact mechanism of this side effect is not well understood.
  • A study was conducted on male mice to assess the impact of moxifloxacin, a type of fluoroquinolone, on AAD, showing that it induced the condition and caused damage to aortic tissues.
  • The findings revealed that moxifloxacin increased levels of osteopontin and matrix metalloproteinases-2 while decreasing smooth muscle protein 22α, suggesting it promotes AAD development by weakening aortic wall structure.

Article Abstract

Fluoroquinolones are one of the most frequently prescribed antibiotics. However, their use increases the risk of Aortic aneurysm and dissection (AAD). The mechanism underlying this effect remains unclear. AAD are caused by weakening of the aortic wall and loss of vascular smooth muscle cells. Osteopontin is involved in the occurrence and development of AAD. The aim of the present study was to examine the role of moxifloxacin, a fluoroquinolone, in the occurrence of AAD using a moderate-severity AAD mouse model. Four-week-old male C57BL/6J mice were fed a high-fat diet. At 8 weeks of age, the mice were infused with saline or angiotensin II (1000 ng kg min) via osmotic minipumps for 4 weeks, and then orally administered water (vehicle) or moxifloxacin (30 and 100 mg kg day) for another 3 weeks. Moxifloxacin (30 and 100 mg kg day) induced AAD and elastin degradation in aortic tissues, as revealed by hematoxylin and eosin staining and elastica-van Gieson staining. Additionally, immunohistochemical staining and Western blot analyses showed that moxifloxacin 100 mg kg day decreased the protein expression of smooth muscle protein 22α, one of the markers of the contractile phenotype of vascular smooth muscle cells, in aortic tissues compared to vehicle and moxifloxacin 30 mg kg day. Furthermore, moxifloxacin (100 mg kg day) increased the protein expression of osteopontin and matrix metalloproteinases-2 in the aortic tissues when compared to control. Moxifloxacin may induce the onset of AAD and weakening of the aortic media by increasing the expression of osteopontin and matrix metalloproteinase-2 and decreasing that of smooth muscle protein 22α in aortic tissue.

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Source
http://dx.doi.org/10.1016/j.bbrc.2022.08.080DOI Listing

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