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Capsanthin Inhibits Atherosclerotic Plaque Formation and Vascular Inflammation in ApoE−/− Mice

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Capsanthin is a red pigment and the major carotenoid component of red paprika (Capsicum annuum L.). However, its role in atherosclerosis is yet to be fully elucidated. This study investigated the role of dietary capsanthin in vascular inflammation in atherosclerotic mice. We evaluated the anti-atherosclerotic effects of daily oral administration of capsanthin (0.5 mg/kg of body weight/day) in apolipoprotein E-deficient (ApoE−/−) mice fed a Western-type diet (WD). Capsanthin treatment inhibited vascular cell adhesion molecule 1 expression and nuclear factor-κB ser536 phosphorylation in tumor necrosis factor-α-stimulated cultured endothelial cells. Dietary capsanthin significantly inhibited the WD-induced elevation in the plasma levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglyceride in mice. Interestingly, capsanthin reduced aortic plaque formation and VCAM-1 expression, which is vascular inflammation, in atherosclerotic mice. In addition, the neutrophil–lymphocyte ratio, a systemic inflammatory marker, was inhibited in capsanthin-treated mice. Furthermore, capsanthin significantly reduced the levels of proinflammatory cytokines, such as TNF-α, interleukin-6, and monocyte chemoattractant protein-1, in the plasma of atherosclerotic mice. Collectively, our data demonstrate that dietary capsanthin plays a protective role against atherosclerosis in hyperlipidemic mice. This protective effect could be attributed to the anti-inflammatory properties of capsanthin.
Title: Capsanthin Inhibits Atherosclerotic Plaque Formation and Vascular Inflammation in ApoE−/− Mice
Description:
Capsanthin is a red pigment and the major carotenoid component of red paprika (Capsicum annuum L.
).
However, its role in atherosclerosis is yet to be fully elucidated.
This study investigated the role of dietary capsanthin in vascular inflammation in atherosclerotic mice.
We evaluated the anti-atherosclerotic effects of daily oral administration of capsanthin (0.
5 mg/kg of body weight/day) in apolipoprotein E-deficient (ApoE−/−) mice fed a Western-type diet (WD).
Capsanthin treatment inhibited vascular cell adhesion molecule 1 expression and nuclear factor-κB ser536 phosphorylation in tumor necrosis factor-α-stimulated cultured endothelial cells.
Dietary capsanthin significantly inhibited the WD-induced elevation in the plasma levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglyceride in mice.
Interestingly, capsanthin reduced aortic plaque formation and VCAM-1 expression, which is vascular inflammation, in atherosclerotic mice.
In addition, the neutrophil–lymphocyte ratio, a systemic inflammatory marker, was inhibited in capsanthin-treated mice.
Furthermore, capsanthin significantly reduced the levels of proinflammatory cytokines, such as TNF-α, interleukin-6, and monocyte chemoattractant protein-1, in the plasma of atherosclerotic mice.
Collectively, our data demonstrate that dietary capsanthin plays a protective role against atherosclerosis in hyperlipidemic mice.
This protective effect could be attributed to the anti-inflammatory properties of capsanthin.

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