Lycopene inhibits neointimal hyperplasia through regulating lipid metabolism and suppressing oxidative stress.
The present study aimed to investigate the possible mechanism(s) through which lycopene inhibits neointimal hyperplasia in restenosis models. A total of 32 white rabbits were randomly divided into the following four groups: A sham group, a model group, a model group treated with apocynin and a model group treated with lycopene. Immunohistochemistry and transmission electron microscopy (TEM) were used to detect the carotid structures in these groups. Quantitative polymerase chain reaction (qPCR) and western blot analysis were performed to detect the mRNA and protein expression levels of the proteins involved in cell proliferation and oxidative stress, including anti‑proliferating cell nuclear antigen, extracellular signal-regulated kinase, nicotinamide adenine dinucleotide phosphate oxidase 1, hydroxymethyl glutaric acyl coenzyme A reductase, adenosine triphosphate‑binding cassette transporter A1 and human neutrophil cytochrome b light chain. Immunohistochemistry and TEM indicated that lycopene treatment significantly reduced the intima/media ratios, the accumulation of lipids and the formation of foam cells in carotid plaques in rabbit restenosis models. Furthermore, lycopene regulated the blood lipid levels and suppressed the oxidative stress in these models. In addition, qPCR and western blot analyses revealed that lycopene significantly decreased the expression levels of cell proliferation‑associated proteins, as well as proteins involved in lipid synthesis and transportation. The results suggest that lycopene may regulate lipid metabolism and suppress oxidative stress, and thus, represents a promising therapeutic against neointimal hyperplasia.
Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Min
M
Mao
Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Han
H
Lei
Centre for Clinical Research, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Qing
Q
Liu
Department of Cardiology, Chongqing Zhongshan Hospital, Chongqing 400013, P.R. China.
Rui
R
He
Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Zhong
Z
Zuo
Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Nan
N
Zhang
Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Chao
C
Zhou
D064286:ATP Binding Cassette Transporter 1 / Q000235:genetics / Q000378:metabolism; D000098:Acetophenones / Q000494:pharmacology* / Q000627:therapeutic use; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D002338:Carotenoids / Q000494:pharmacology* / Q000627:therapeutic use; D049109:Cell Proliferation / Q000187:drug effects; D004195:Disease Models, Animal; D006965:Hyperplasia / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D050356:Lipid Metabolism / Q000187:drug effects*; D000077276:Lycopene; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000235:genetics / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000235:genetics / Q000378:metabolism; D019255:NADPH Oxidases / Q000235:genetics / Q000378:metabolism; D058426:Neointima / Q000473:pathology; D018384:Oxidative Stress / Q000187:drug effects*; D018809:Proliferating Cell Nuclear Antigen / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D011817:Rabbits
D064286:ATP Binding Cassette Transporter 1; D000098:Acetophenones; D000975:Antioxidants; D018809:Proliferating Cell Nuclear Antigen; D012333:RNA, Messenger; D002338:Carotenoids; C056165:acetovanillone; D019255:NADPH Oxidases; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D000077276:Lycopene