title: Niacin inhibits vascular inflammation via downregulating nuclear transcription factor-κB signaling pathway.
abstract: The study aimed to investigate the effect of niacin on vascular inflammatory lesions in vivo and in vitro as well as its lipid-regulating mechanism. In vivo study revealed that niacin downregulated the levels of inflammatory factors (IL-6 and TNF-α) in plasma, suppressed protein expression of CD68 and NF-κB p65 in arterial wall, and attenuated oxidative stress in guinea pigs that have been fed high fat diet. In vitro study further confirmed that niacin decreased the secretion of IL-6 and TNF-α and inhibited NF-κB p65 and notch1 protein expression in oxLDL-stimulated HUVECs and THP-1 macrophages. Moreover, niacin attenuated oxLDL-induced apoptosis of HUVECs as well. In addition, niacin significantly lessened lipid deposition in arterial wall, increased HDL-C and apoA levels and decreased TG and non-HDL-C levels in plasma, and upregulated the mRNA amount of cholesterol 7 α-hydroxylase A1 in liver of guinea pigs. These data suggest for the first time that niacin inhibits vascular inflammation in vivo and in vitro via downregulating NF-κB signaling pathway. Furthermore, niacin also modulates plasma lipid by upregulating the expression of factors involved in the process of reverse cholesterol transport.
authors.affiliation: Key Laboratory of Atherosclerosis in Universities of Shandong and Institute of Atherosclerosis, Taishan Medical University, Shandong 271000, China ; College of Basic Medical Sciences, Taishan Medical University, Shandong 271000, China.
authors.forename: Yanhong
authors.initials: Y
authors.lastname: Si
authors.affiliation: Key Laboratory of Atherosclerosis in Universities of Shandong and Institute of Atherosclerosis, Taishan Medical University, Shandong 271000, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Shandong Agricultural University, Shandong 271000, China.
authors.forename: Jilong
authors.initials: J
authors.lastname: Zhao
authors.affiliation: Key Laboratory of Atherosclerosis in Universities of Shandong and Institute of Atherosclerosis, Taishan Medical University, Shandong 271000, China.
authors.forename: Shoudong
authors.initials: S
authors.lastname: Guo
authors.affiliation: Key Laboratory of Atherosclerosis in Universities of Shandong and Institute of Atherosclerosis, Taishan Medical University, Shandong 271000, China.
authors.forename: Lei
authors.initials: L
authors.lastname: Zhai
authors.affiliation: Key Laboratory of Atherosclerosis in Universities of Shandong and Institute of Atherosclerosis, Taishan Medical University, Shandong 271000, China ; College of Basic Medical Sciences, Taishan Medical University, Shandong 271000, China.
authors.forename: Shutong
authors.initials: S
authors.lastname: Yao
authors.affiliation: Key Laboratory of Atherosclerosis in Universities of Shandong and Institute of Atherosclerosis, Taishan Medical University, Shandong 271000, China ; College of Basic Medical Sciences, Taishan Medical University, Shandong 271000, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Sang
authors.affiliation: Key Laboratory of Atherosclerosis in Universities of Shandong and Institute of Atherosclerosis, Taishan Medical University, Shandong 271000, China.
authors.forename: Nana
authors.initials: N
authors.lastname: Yang
authors.affiliation: Key Laboratory of Atherosclerosis in Universities of Shandong and Institute of Atherosclerosis, Taishan Medical University, Shandong 271000, China.
authors.forename: Guohua
authors.initials: G
authors.lastname: Song
authors.affiliation: Department of Geriatrics, PLA Navy General Hospital, Beijing 100048, China.
authors.forename: Jue
authors.initials: J
authors.lastname: Gu
authors.affiliation: Key Laboratory of Atherosclerosis in Universities of Shandong and Institute of Atherosclerosis, Taishan Medical University, Shandong 271000, China.
authors.forename: Shucun
authors.initials: S
authors.lastname: Qin
mesh_terms: D000818:Animals; D001053:Apolipoproteins / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D002460:Cell Line; D004591:Electrophoresis, Polyacrylamide Gel; D005434:Flow Cytometry; D006168:Guinea Pigs; D006801:Humans; D007150:Immunohistochemistry; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D016328:NF-kappa B / Q000378:metabolism*; D009525:Niacin / Q000494:pharmacology*; D018384:Oxidative Stress / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D001053:Apolipoproteins; D015850:Interleukin-6; D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D009525:Niacin; D008315:Malondialdehyde; D002097:C-Reactive Protein