Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion

• Published in: Marine drugs Vol. 17; no. 6; p. 354
• Main Authors: Zuluaga Tamayo, Marisol, Choudat, Laurence, Aid-Launais, Rachida, Thibaudeau, Olivier, Louedec, Liliane, Letourneur, Didier, Gueguen, Virginie, Meddahi-Pellé, Anne, Couvelard, Anne, Pavon-Djavid, Graciela
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 14-06-2019; MDPI
• Subjects: 3T3 Cells; Animal models; Animals; Antioxidants; Antioxidants - pharmacology; Apoptosis; Astaxanthin; Biocompatibility; Blood flow; CD163 antigen; Cell Line; cyclodextrin; Damage; Disease Models, Animal; Expected values; Femoral artery; Femur; Free radicals; Heme; Iron; Ischemia; ischemia/reperfusion injury; Kidneys; Life Sciences; Macrophages; Macrophages - drug effects; Male; Mice; Muscle, Skeletal; Muscle, Skeletal - drug effects; Muscles; Oxidative Stress; Oxidative Stress - drug effects; Polysaccharides; Rats; reactive oxygen species; Reperfusion; Reperfusion Injury; Reperfusion Injury - drug therapy; Tissue; Toxicity; Veins & arteries; Xanthophylls; Xanthophylls - pharmacology; France; ischemia/reperfusion injury; oxidative stress; cyclodextrin; reactive oxygen species; astaxanthin
• ISSN: 1660-3397; 1660-3397
• DOI: 10.3390/md17060354

(1) Background: Reperfusion injury refers to the cell and tissue damage induced, when blood flow is restored after an ischemic period. While reperfusion reestablishes oxygen supply, it generates a high concentration of radicals, resulting in tissue dysfunction and damage. Here, we aimed to challenge and achieve the potential of a delivery system based on astaxanthin, a natural antioxidant, in attenuating the muscle damage in an animal model of femoral hind-limb ischemia and reperfusion. (2) Methods: The antioxidant capacity and non-toxicity of astaxanthin was validated before and after loading into a polysaccharide scaffold. The capacity of astaxanthin to compensate stress damages was also studied after ischemia induced by femoral artery clamping and followed by varied periods of reperfusion. (3) Results: Histological evaluation showed a positive labeling for CD68 and CD163 macrophage markers, indicating a remodeling process. In addition, higher levels of Nrf2 and NQO1 expression in the sham group compared to the antioxidant group could reflect a reduction of the oxidative damage after 15 days of reperfusion. Furthermore, non-significant differences were observed in non-heme iron deposition in both groups, reflecting a cell population susceptible to free radical damage. (4) Conclusions: Our results suggest that the in situ release of an antioxidant molecule could be effective in improving the antioxidant defenses of ischemia/reperfusion (I/R)-damaged muscles.