Favorable Effects of Astaxanthin on Brain Damage due to Ischemia- Reperfusion Injury

Activated inflammation and oxidant stress during cerebral ischemia reperfusion injury (IRI) lead to brain damage. Astaxanthin (ASX) is a type of carotenoid with a strong antioxidant effect. The aim of this study was to investigate the role of ASX on brain IRI. A total of 42 adult male Sprague-Dawley...

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Published inCombinatorial chemistry & high throughput screening Vol. 23; no. 3; p. 214
Main Authors Cakir, Esra, Cakir, Ufuk, Tayman, Cuneyt, Turkmenoglu, Tugba Taskin, Gonel, Ataman, Turan, Isil O
Format Journal Article
LanguageEnglish
Published United Arab Emirates 01.01.2020
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Summary:Activated inflammation and oxidant stress during cerebral ischemia reperfusion injury (IRI) lead to brain damage. Astaxanthin (ASX) is a type of carotenoid with a strong antioxidant effect. The aim of this study was to investigate the role of ASX on brain IRI. A total of 42 adult male Sprague-Dawley rats were divided into 3 groups as control (n=14) group, IRI (n=14) group and IRI + ASX (n=14) group. Cerebral ischemia was instituted by occluding middle cerebral artery for 120 minutes and subsequently, reperfusion was performed for 48 hours. Oxidant parameter levels and protein degradation products were evaluated. Hippocampal and cortex cell apoptosis, neuronal cell count, neurological deficit score were evaluated. In the IRI group, oxidant parameter levels and protein degradation products in the tissue were increased compared to control group. However, these values were significantly decreased in the IRI + ASX group (p<0.05). There was a significant decrease in hippocampal and cortex cell apoptosis and a significant increase in the number of neuronal cells in the IRI + ASX group compared to the IRI group alone (p<0.05). The neurological deficit score which was significantly lower in the IRI group compared to the control group was found to be significantly improved in the IRI + ASX group (p<0.05). Astaxanthin protects the brain from oxidative damage and reduces neuronal deficits due to IRI injury.
ISSN:1875-5402
DOI:10.2174/1386207323666200219121600