(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.