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Antiatherosclerotic effect of dehydrocorydaline on ApoE−/− mice: inhibition of macrophage inflammation

   
@article{APS10576,
	author = {Bin Wen and Yuan-ye Dang and Su-hua Wu and Yi-min Huang and Kong-yang Ma and Yi-ming Xu and Xi-Long Zheng and Xiao-yan Dai},
	title = {Antiatherosclerotic effect of dehydrocorydaline on ApoE −/−  mice: inhibition of macrophage inflammation},
	journal = {Acta Pharmacologica Sinica},
	volume = {43},
	number = {6},
	year = {2022},
	keywords = {},
	abstract = {Despite improvements in cardiovascular disease (CVD) outcomes by cholesterol-lowering statin therapy, the high rate of CVD is still a great concern worldwide. Dehydrocorydaline (DHC) is an alkaloidal compound isolated from the traditional Chinese herb Corydalis yanhusuo. Emerging evidence shows that DHC has anti-inflammatory and antithrombotic benefits, but whether DHC exerts any antiatherosclerotic effects remains unclear. Our study revealed that intraperitoneal (i.p.) injection of DHC in apolipoprotein E-deficient (ApoE−/−) mice not only inhibited atherosclerosis development but also improved aortic compliance and increased plaque stability. In addition, DHC attenuated systemic and vascular inflammation in ApoE−/− mice. As macrophage inflammation plays an essential role in the pathogenesis of atherosclerosis, we next examined the direct effects of DHC on bone marrow-derived macrophages (BMDMs) in vitro. Our RNA-seq data revealed that DHC dramatically decreased the levels of proinflammatory gene clusters. We verified that DHC significantly downregulated proinflammatory interleukin (IL)-1β and IL-18 mRNA levels in a time- and concentration-dependent manner. Furthermore, DHC decreased lipopolysaccharide (LPS)-induced inflammation in BMDMs, as evidenced by the reduced protein levels of CD80, iNOS, NLRP3, IL-1β, and IL-18. Importantly, DHC attenuated LPS-induced activation of p65 and the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway. Thus, we conclude that DHC ameliorates atherosclerosis in ApoE−/− mice by inhibiting inflammation, likely by targeting macrophage p65- and ERK1/2- mediated pathways.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/10576}
}