Amelioration chloride-induced abdominal aortic aneurysm injury by activation of α7nAChR s calcium in mice
10.12206/j.issn.2097-2024.202409045
- VernacularTitle:激活α7nAChR改善氯化钙诱导的小鼠腹主动脉瘤损伤研究
- Author:
Wenjing ZHANG
1
;
Hui FU
2
;
Xiaobin GUO
1
;
Hao GUO
1
Author Information
1. Department of Pharmacy, Inner Mongolia Autonomous Region People’s Hospital, Hohhot 010017, China.
2. Department of Pharmacy, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China.
- Publication Type:Originalarticles
- Keywords:
α7 nicotinic acetylcholine receptor;
inflammation;
CaCl2;
abdominal aortic aneurysm
- From:
Journal of Pharmaceutical Practice and Service
2026;44(8):400-407
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of activating α7 nicotinic acetylcholine receptor （α7nAChR） on calcium chloride （CaCl2）-induced abdominal aortic aneurysm （AAA） injury in mice. Methods AAA model was induced by CaCl2 in wild type （WT） mice and α7nAChR knockout （α7nAChR−/−） mice. The effects of knockout of α7nAChR on histological damage in CaCl2-induced AAA mice and expression of inflammatory factors were assessed by HE staining, Elasticavan Gieson （EVG） staining and IHC staining. Rat-derived primary vascular smooth muscle cells （VSMC） were stimulated with tumor necrosis factor-α （TNF-α）, which mimicked the inflammatory environment of AAA. The expressions of inflammation-related proteins were detected by using Western-blot （WB） with or without PNU-282987 to activate α7nAChR. Results Aortic dilatation was obvious, and the aortic structure was disrupted in CaCl2-induced AAA mice. Knockout of α7nAChR further exacerbated the histological injury and significantly up-regulated the expression of inflammation-related proteins in aorta of AAA mice. It was showed that TNF-α stimulation of VSMC increased inflammation-related protein expression, whereas activation of α7nAChR prevented the phenomenon. Conclusion Activation of α7nAChR could attenuate CaCl2-induced AAA injury in mice by suppressing the inflammatory response.
