Journal
NUTRIENTS
Volume 15, Issue 18, Pages -Publisher
MDPI
DOI: 10.3390/nu15184074
Keywords
hyperlipidemia; atherosclerosis; cocktail therapy; oxidative stress; inflammation; high-fat diet; ApoE-knockout mice
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This study investigated the effects of oral ovatodiolide and antcin K (OAK) supplements on high-fat diet-induced cardiovascular dysfunction in apolipoprotein E (ApoE)-knockout mice. Oral OAK supplements significantly alleviated cardiovascular dysfunction in the experimental mice, potentially by reducing lipid accumulation in the artery and oxidative stress and inflammation in the cardiovascular tissue.
A high-fat diet (HFD) is a major risk factor for cardiovascular diseases. Many pure compounds have been demonstrated to be effective in treating cardiovascular diseases. In this study, we investigated the alleviating effects of oral ovatodiolide and antcin K (OAK) supplements on HFD-induced cardiovascular dysfunction in apolipoprotein E (ApoE)-knockout mice. Cardiovascular dysfunction was induced in ApoE-knockout mice by feeding them an HFD for 12 weeks. The degree of cardiovascular dysfunction was assessed through echocardiography, hematological and biochemical analyses, and immunofluorescence and immunohistochemical staining. The HFD-fed mice exhibited cardiovascular dysfunction-abnormal blood biochemical index. The arterial wall tissue exhibited the marked deposition of lipids, upregulated expression of vascular cell adhesion molecule-1 and CD36 receptors, and downregulated expression of the ABCA1 receptor. Macrophages isolated from the peritoneal cavity of the mice exhibited increased levels of lipid accumulation, reactive oxygen species, and CD11b expression but reduced mitochondrial membrane potential. The expression of superoxide dismutase 2 was downregulated and that of tumor necrosis factor-& alpha; was upregulated in the myocardial tissue. Oral OAK supplements twice a day for 12 weeks significantly mitigated HFD-induced cardiovascular dysfunction in the experimental mice. Oral OAK supplements appear to be a promising strategy for treating HFD-induced cardiovascular dysfunction. The underlying mechanisms may involve the reduction of lipid accumulation in the artery and oxidative stress and inflammation in the cardiovascular tissue.
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