Ameliorative effect of allicin on vascular calcification via inhibiting endoplasmic reticulum stress. (October 2022)

• Record Type: Journal Article
• Authors: Wang, Qin; Lin, Ping; Feng, Li; Ren, Qian; Xie, Xiaofeng; Zhang, Bin
• Is Part Of: Vascular. Volume 30:Number 5(2022)
• Page Start: 999
• Page End: 1007
• Publication Date: 2022-10
• Subjects: Allicin -- aorta -- endoplasmic reticulum stress -- vascular calcification -- vascular smooth muscle cells; 616.13
• DOI: 10.1177/17085381211035291
• Languages: English
• ISSNs: 1708-5381

Abstract

Objectives: Vascular calcification (VC) is an independent predictor for cardiovascular events and mortality. However, there are currently no effective methods to reverse or prevent it. The present study aimed to determine the ameliorative effect of allicin on VC. Methods: VC model of rats was induced by high-dose vitamin D3, which was valued by Alizarin Red staining, calcium contents, and alkaline phosphatase in the aorta. Systolic blood pressure, pulse pressure, and pulse wave velocity were measured to determine aortic stiffness. Protein levels were detected by Western blot. Results: Allicin treatment rescued aortic VC and stiffness. The increased protein levels of RUNX2 and BMP2, two markers of osteoblastic phenotype of vascular smooth muscle cells, in the calcified aorta were attenuated by allicin, whereas the decreased levels of calponin and SM22α induced by calcification were improved. Allicin treatment significantly attenuated the increased protein levels of GRP78, GRP94, and CHOP, which are key markers of endoplasmic reticulum stress, in the calcified aorta. The activation of PERK/eIF2α/ATF4 cascades was also prevented by allicin. Conclusions: Allicin could ameliorate aortic VC and stiffness. The ameliorative effect of allicin on VC might be mediated by inhibiting PERK/eIF2α/ATF4 cascades. Our results might provide a new proof for VC treatment.