BACKGROUND: Lutein is an antioxidant compound with potential biological effects. The present study investigated the protective role of Lutein against I/R injury in skeletal muscle. METHODS: Animals were divided into three groups. Group I - sham operated; Group II- IR injury- Hind limb ischemia was induced by clamping the common femoral artery and vein. After 4 h of ischemia, the clamp was removed and the animals underwent 2 h of reperfusion. Group III-Lutein + IR injury- Rats with Lutein treatment received intraperitoneal injection 1 h before reperfusion. The skeletal tissues were analyzed for oxidative stress parameters (reactive oxygen species, protein carbonylation and sulfhydryls, lipid peroxidation). Antioxidant status was determined by evaluating Nrf-2 levels and antioxidant enzyme activities. The inflammatory mechanism was determined through NF-κB and COX-2 expressions. Pro-inflammatory cytokines were determined by ELISA. RESULTS: The results showed that Lutein treatment significantly decreased the oxidative stress by reducing reactive oxygen species, protein carbonylation and sulphydryls, lipid peroxidation. Further, the levels of Nrf-2 and antioxidant status was significantly declined during IR injury compared to sham operated rats. Lutein treatment reduced the oxidative stress by enhancing Nrf-2 levels and antioxidant status. Skeletal IR injury enhanced the inflammatory signaling by up regulating NF-κB, COX-2 and various pro-inflammatory cytokines. NF-κB, COX-2 expressions were down regulated by Lutein treatment. CONCLUSION: The study shows that Lutein protects against skeletal IR injury by down regulating oxidative stress and inflammatory mechanisms.
BACKGROUND: Lutein is an antioxidant compound with potential biological effects. The present study investigated the protective role of Lutein against I/R injury in skeletal muscle. METHODS: Animals were divided into three groups. Group I - sham operated; Group II- IR injury- Hind limb ischemia was induced by clamping the common femoral artery and vein. After 4 h of ischemia, the clamp was removed and the animals underwent 2 h of reperfusion. Group III-Lutein + IR injury- Rats with Lutein treatment received intraperitoneal injection 1 h before reperfusion. The skeletal tissues were analyzed for oxidative stress parameters (reactive oxygen species, protein carbonylation and sulfhydryls, lipid peroxidation). Antioxidant status was determined by evaluating Nrf-2 levels and antioxidant enzyme activities. The inflammatory mechanism was determined through NF-κB and COX-2 expressions. Pro-inflammatory cytokines were determined by ELISA. RESULTS: The results showed that Lutein treatment significantly decreased the oxidative stress by reducing reactive oxygen species, protein carbonylation and sulphydryls, lipid peroxidation. Further, the levels of Nrf-2 and antioxidant status was significantly declined during IR injury compared to sham operated rats. Lutein treatment reduced the oxidative stress by enhancing Nrf-2 levels and antioxidant status. Skeletal IR injury enhanced the inflammatory signaling by up regulating NF-κB, COX-2 and various pro-inflammatory cytokines. NF-κB, COX-2 expressions were down regulated by Lutein treatment. CONCLUSION: The study shows that Lutein protects against skeletal IR injury by down regulating oxidative stress and inflammatory mechanisms.
Authors: Javier Ávila-Román; Sara García-Gil; Azahara Rodríguez-Luna; Virginia Motilva; Elena Talero Journal: Mar Drugs Date: 2021-09-23 Impact factor: 5.118