Open AccessRoles of NOD1/Rip2 signal pathway in carotid artery remodelling in spontaneous hypertensive rats
Author(s) -
Jingsi Zhang,
Bingqian Fang,
Lixian Sun,
Xiuzhen Zhang,
Jinli Liu,
Yang Ying,
Wenhua Zhang,
Xiuli Wang,
Yanchun Ding
Publication year - 2022
Publication title -
general physiology and biophysics
Language(s) - English
Resource type - Journals
eISSN - 1338-4325
pISSN - 0231-5882
DOI - 10.4149/gpb_2021042
Subject(s) - oxidative stress , yeast , saccharomyces cerevisiae , chemistry , oxidative phosphorylation , reactive oxygen species , microbiology and biotechnology , biophysics , biochemistry , biology
Nucleotide-binding and oligomerization domain (NOD) receptor is a member of inherent immunity recognition receptor family. We investigated the NOD1/Rip2 signalling pathway on carotid arterial remodelling in spontaneously hypertensive rats (SHRs). SHRs were treated with NOD1 agonist (iE-DAP), inhibitor (ML130), or normal saline. We determined the NOD1 and Rip2 expression in carotid artery tissues, serum tumour necrosis factor-α (TNF-α) and monocyte chemotactic protein-1 (MCP-1). The carotid artery remodelling in 16-week SHRs was higher than that of 8-week SHRs and 16-week Wistar-Kyoto (WKY) rats. Expression of NOD1, Rip2, MCP-1 and TNF-α in 16-week SHRs was higher than that of 8-week SHRs and 16-week WKY rats. Blood pressure in iE-DAP-treated SHRs was higher than SHR-C group (no treatment), together with MCP-1, TNF-α, NOD1 and Rip2 expression, as well as carotid artery remodelling. In ML130-treated group, these aspects were completely the opposite. Taken together, inhibition of NOD1/Rip2 signalling pathway could delay the vascular remodelling process.