Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion
(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...
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| Format: | Article |
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MDPI AG
2019-06-01
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| Series: | Marine Drugs |
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| Online Access: | https://www.mdpi.com/1660-3397/17/6/354 |
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| author | Marisol Zuluaga Tamayo Laurence Choudat Rachida Aid-Launais Olivier Thibaudeau Liliane Louedec Didier Letourneur Virginie Gueguen Anne Meddahi-Pellé Anne Couvelard Graciela Pavon-Djavid |
| author_facet | Marisol Zuluaga Tamayo Laurence Choudat Rachida Aid-Launais Olivier Thibaudeau Liliane Louedec Didier Letourneur Virginie Gueguen Anne Meddahi-Pellé Anne Couvelard Graciela Pavon-Djavid |
| author_sort | Marisol Zuluaga Tamayo |
| collection | DOAJ |
| description | (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. |
| first_indexed | 2024-04-11T13:25:54Z |
| format | Article |
| id | doaj.art-a355a46a2c254a56b85b4799594c04d9 |
| institution | Directory Open Access Journal |
| issn | 1660-3397 |
| language | English |
| last_indexed | 2024-04-11T13:25:54Z |
| publishDate | 2019-06-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Marine Drugs |
| spelling | doaj.art-a355a46a2c254a56b85b4799594c04d92022-12-22T04:22:05ZengMDPI AGMarine Drugs1660-33972019-06-0117635410.3390/md17060354md17060354Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-ReperfusionMarisol Zuluaga Tamayo0Laurence Choudat1Rachida Aid-Launais2Olivier Thibaudeau3Liliane Louedec4Didier Letourneur5Virginie Gueguen6Anne Meddahi-Pellé7Anne Couvelard8Graciela Pavon-Djavid9INSERM U1148, Laboratory for Vascular Translational Science, Cardiovascular Bioengineering, Université Paris 13, Av. Jean-Baptiste Clément 93430 Villetaneuse France/ CHU X. Bichat, 46 rue H. Huchard, 75018 Paris, FrancePathology Department, Bichat Hospital, AP-HP, 46 rue H. Huchard, 75018 Paris, FranceINSERM U1148, Laboratory for Vascular Translational Science, Cardiovascular Bioengineering, Université Paris 13, Av. Jean-Baptiste Clément 93430 Villetaneuse France/ CHU X. Bichat, 46 rue H. Huchard, 75018 Paris, FrancePlateau de Morphologie UMR 1152 Université Paris Diderot, Université de Paris, Bichat Hospital, AP-HP, 46 rue H. Huchard, 75018 Paris, FranceINSERM U1148, Laboratory for Vascular Translational Science, Cardiovascular Bioengineering, Université Paris 13, Av. Jean-Baptiste Clément 93430 Villetaneuse France/ CHU X. Bichat, 46 rue H. Huchard, 75018 Paris, FranceINSERM U1148, Laboratory for Vascular Translational Science, Cardiovascular Bioengineering, Université Paris 13, Av. Jean-Baptiste Clément 93430 Villetaneuse France/ CHU X. Bichat, 46 rue H. Huchard, 75018 Paris, FranceINSERM U1148, Laboratory for Vascular Translational Science, Cardiovascular Bioengineering, Université Paris 13, Av. Jean-Baptiste Clément 93430 Villetaneuse France/ CHU X. Bichat, 46 rue H. Huchard, 75018 Paris, FranceINSERM U1148, Laboratory for Vascular Translational Science, Cardiovascular Bioengineering, Université Paris 13, Av. Jean-Baptiste Clément 93430 Villetaneuse France/ CHU X. Bichat, 46 rue H. Huchard, 75018 Paris, FrancePathology Department, Bichat Hospital, AP-HP, 46 rue H. Huchard, 75018 Paris, FranceINSERM U1148, Laboratory for Vascular Translational Science, Cardiovascular Bioengineering, Université Paris 13, Av. Jean-Baptiste Clément 93430 Villetaneuse France/ CHU X. Bichat, 46 rue H. Huchard, 75018 Paris, France(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.https://www.mdpi.com/1660-3397/17/6/354astaxanthinischemia/reperfusion injuryreactive oxygen speciesoxidative stresscyclodextrin |
| spellingShingle | Marisol Zuluaga Tamayo Laurence Choudat Rachida Aid-Launais Olivier Thibaudeau Liliane Louedec Didier Letourneur Virginie Gueguen Anne Meddahi-Pellé Anne Couvelard Graciela Pavon-Djavid Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion Marine Drugs astaxanthin ischemia/reperfusion injury reactive oxygen species oxidative stress cyclodextrin |
| title | Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion |
| title_full | Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion |
| title_fullStr | Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion |
| title_full_unstemmed | Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion |
| title_short | Astaxanthin Complexes to Attenuate Muscle Damage after In Vivo Femoral Ischemia-Reperfusion |
| title_sort | astaxanthin complexes to attenuate muscle damage after in vivo femoral ischemia reperfusion |
| topic | astaxanthin ischemia/reperfusion injury reactive oxygen species oxidative stress cyclodextrin |
| url | https://www.mdpi.com/1660-3397/17/6/354 |
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