title: Lycopene attenuates inflammation and apoptosis in post-myocardial infarction remodeling by inhibiting the nuclear factor-κB signaling pathway.
abstract: Inflammatory response and cardiomyocyte apoptosis are important processes in ventricular remodeling post-myocardial infarction (MI) and may form the basic mechanisms in the development of chronic heart failure. The nuclear factor κB (NF-κB) signaling pathway could promote inflammation and apoptosis and it has been demonstrated that lycopene inhibits cigarette smoke extract-mediated NF-κB activation. Therefore, it was hypothesized that the NF-κB signaling pathway may be a key target of lycopene in the reversal of ventricular remodeling post MI. An MI model was established by left anterior descending coronary artery ligation in mice. Following ligation, the mice were administered with lycopene (10 mg/kg/day) or saline. The mice underwent echocardiography and were sacrificed after 4 weeks. The mRNA expression of fibrosis markers transforming growth factor-β1 (TGF-β1), collagen I and III and inflammatory markers tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were examined by quantitative polymerase chain reaction. The protein expression of apoptotic markers, including caspase-3, -8, -9 and activation of the NF-κB signaling pathway were analyzed by western blotting. Lycopene reduced the expression of TGF-β1, collagen I, collagen III, TNF-α, IL-1β, caspase-3, -8 and -9 and inhibited the activation of the NF-κB signaling pathway. The level of ventricular remodeling post-MI was also attenuated following treatment with lycopene. Lycopene may inhibit the NF-κB signaling pathway thereby reducing the inflammatory response and cardiomyocyte apoptosis post-MI, which could be a key mechanism of lycopene in attenuating ventricular remodeling.
authors.affiliation: Department of Cardiology, The Central Hospital of Wuhan, Wuhan, Hubei 430014, P.R. China.
authors.forename: Qin
authors.initials: Q
authors.lastname: He
authors.affiliation: Department of Cardiology, The Central Hospital of Wuhan, Wuhan, Hubei 430014, P.R. China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhou
authors.affiliation: Department of Cardiology, The Central Hospital of Wuhan, Wuhan, Hubei 430014, P.R. China.
authors.forename: Caijin
authors.initials: C
authors.lastname: Xiong
authors.affiliation: Department of Cardiology, The Central Hospital of Wuhan, Wuhan, Hubei 430014, P.R. China.
authors.forename: Gang
authors.initials: G
authors.lastname: Tan
authors.affiliation: Department of Cardiology, The Central Hospital of Wuhan, Wuhan, Hubei 430014, P.R. China.
authors.forename: Manhua
authors.initials: M
authors.lastname: Chen
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D002338:Carotenoids / Q000008:administration & dosage / Q000494:pharmacology*; D004195:Disease Models, Animal; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology*; D000077276:Lycopene; D008297:Male; D051379:Mice; D009203:Myocardial Infarction / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D000975:Antioxidants; D016328:NF-kappa B; D002338:Carotenoids; D000077276:Lycopene