Astaxanthin limits atherosclerosis and dysmetabolism in mice by attenuating inflammatory cell recruitment and signaling

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Introduction Astaxanthin (ASX) has demonstrated various cardioprotective effects, including reductions in body weight, adipose tissue mass, hypertension, myocardial infarct size, and oxidative stress markers. Despite these findings, the underlying mechanisms remain unclear. This study examines the role of ASX in murine atherosclerosis and metabolic derangements induced by atherogenic diet, aiming to gain a deeper understanding of its biological effects and potential therapeutic applications. Methods Ldlr-/- mice were fed a high-fat, high-cholesterol diet (HCD) for 16 weeks, receiving 70 mg/kg ASX or vehicle every other day. A week before the study ended, glucose and insulin tolerance tests were performed. Plaque size in the aorta was analyzed via histology (Oil-red-O and Masson's trichrome). Flow cytometry assessed immune cells from blood, aorta, adipose tissue, and cytokines in plasma. Additional mice underwent intravital microscopy for further investigation. Results The overall body weight of animals treated with ASX or vehicle did not differ. ASX-treated mice showed a reduced abundance of peripheral monocytes by 34%, lower numbers of leukocytes in adipose tissue depots, and improved glucose metabolism and insulin sensitivity compared with animals receiving vehicle. White adipose mass decreased while brown adipose and muscle mass increased in mice treated with ASX. Atheroscle

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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