PMID- 32218307 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20200928 IS - 2076-3921 (Print) IS - 2076-3921 (Electronic) IS - 2076-3921 (Linking) VI - 9 IP - 4 DP - 2020 Mar 25 TI - Corylin Inhibits Vascular Cell Inflammation, Proliferation and Migration and Reduces Atherosclerosis in ApoE-Deficient Mice. LID - 10.3390/antiox9040275 [doi] LID - 275 AB - Atherosclerosis is a complex disease that includes several events, including reactive oxygen species (ROS) stress, inflammation, endothelial dysfunction, lipid deposition, and vascular smooth muscle cell (VSMC) proliferation and migration, which result in atherosclerotic plaque formation. Corylin, a flavonoid compound, is known to exhibit antioxidative, anti-inflammatory and antiproliferative effects. However, it remains unknown whether corylin could modulate atherogenesis. Here, we identified the anti-inflammatory effect of corylin in tumor necrosis factor-alpha (TNF-alpha)-induced vascular cells. In human umbilical vein endothelial cells (HUVECs), corylin suppressed TNF-alpha-induced monocyte adhesion to the HUVECs and transmigration by downregulating the ROS/JNK/nuclear factor-kappa beta (NF-kappaB) p65 pathway. In VSMCs, corylin inhibited TNF-alpha-induced monocyte adhesion by suppressing ROS production, mitogen-activated protein kinase (MAPK) phosphorylation and NF-kappaB p65 translocation. In platelet-derived growth factor-BB (PDGF-BB)-induced VSMCs, corylin inhibited PDGF-BB-induced VSMC proliferation and migration through regulating the mammalian target of rapamycin (mTOR)/dynamin-1-like protein 1 (Drp1) signaling cascade. In addition, corylin treatment not only attenuated atherosclerotic lesions, ROS production, vascular cell adhesion protein-1 (VCAM-1) expression, monocyte adhesion and VSMC proliferation in apolipoprotein E (ApoE)-deficient mice but also inhibited neointimal hyperplasia in endothelial-denuded mice. Thus, corylin may be a potential prevention and treatment for atherosclerosis. FAU - Chen, Chin-Chuan AU - Chen CC AD - Graduate Institute of Natural Products, Chang Gung University, Taoyuan 33302, Taiwan. AD - Chinese Herbal Medicine Research Team, Healthy Aging Research Center, Chang Gung University, Taoyuan 33302, Taiwan. AD - Tissue Bank, Chang Gung Memorial Hospital, Taoyuan 33305, Taiwan. FAU - Li, Hung-Yuan AU - Li HY AD - Department of Internal Medicine, National Taiwan University Hospital, Taipei 10002, Taiwan. FAU - Leu, Yann-Lii AU - Leu YL AD - Graduate Institute of Natural Products, Chang Gung University, Taoyuan 33302, Taiwan. AD - Chinese Herbal Medicine Research Team, Healthy Aging Research Center, Chang Gung University, Taoyuan 33302, Taiwan. AD - Center for Traditional Chinese Medicine, Chang Gung Memorial Hospital, Taoyuan 33305, Taiwan. FAU - Chen, Yu-Ju AU - Chen YJ AD - Graduate Institute of Natural Products, Chang Gung University, Taoyuan 33302, Taiwan. FAU - Wang, Chia-Jen AU - Wang CJ AD - Cell Therapy Center, Chang Gung Memorial Hospital, Taoyuan 33378, Taiwan. FAU - Wang, Shu-Huei AU - Wang SH AD - Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan. LA - eng GR - NSC 108-2320-B-002 -045/National Science Council/ PT - Journal Article DEP - 20200325 PL - Switzerland TA - Antioxidants (Basel) JT - Antioxidants (Basel, Switzerland) JID - 101668981 PMC - PMC7222202 OTO - NOTNLM OT - ROS OT - atherosclerosis OT - corylin OT - inflammation OT - mitofission COIS- The authors declare no conflict of interest. EDAT- 2020/03/29 06:00 MHDA- 2020/03/29 06:01 PMCR- 2020/03/25 CRDT- 2020/03/29 06:00 PHST- 2020/02/11 00:00 [received] PHST- 2020/03/11 00:00 [revised] PHST- 2020/03/23 00:00 [accepted] PHST- 2020/03/29 06:00 [entrez] PHST- 2020/03/29 06:00 [pubmed] PHST- 2020/03/29 06:01 [medline] PHST- 2020/03/25 00:00 [pmc-release] AID - antiox9040275 [pii] AID - antioxidants-09-00275 [pii] AID - 10.3390/antiox9040275 [doi] PST - epublish SO - Antioxidants (Basel). 2020 Mar 25;9(4):275. doi: 10.3390/antiox9040275.