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Gallic acid and sesame oil exert cardioprotection via mitochondrial protection and antioxidant properties on Ketamine-Induced cardiotoxicity model in rats
Ketamine is a cardiotoxic agent and can deplete ATP in cardiomyocytes through mitochondrial dysfunction. We investigated the effects of gallic acid and sesame oil in ketamine-induced cardiotoxicity in rats. Male Wistar rats were randomly divided into six groups including control; ketamine; ketamine ...
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Published in: | Toxin reviews 2023-04, Vol.42 (2), p.515-526 |
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description | Ketamine is a cardiotoxic agent and can deplete ATP in cardiomyocytes through mitochondrial dysfunction. We investigated the effects of gallic acid and sesame oil in ketamine-induced cardiotoxicity in rats. Male Wistar rats were randomly divided into six groups including control; ketamine; ketamine + gallic acid; ketamine + sesame oil; gallic acid and sesame oil. Serum cardiac marker, cardiac tissue oxidative stress markers, histopathological analysis and mitochondrial toxicity parameters (succinate dehydrogenase activity, mitochondrial swelling, reactive oxygen species (ROS) production and collapse of mitochondria membrane potential) were measured on the fifteen days of the study. The results showed that ketamine administration increased serum cardiac markers, oxidative stress parameters, histopathological alterations and mitochondrial dysfunction in cardiac tissue. Gallic acid and sesame oil administration in presence of ketamine was observed to decrease serum cardiac markers, oxidative stress parameters, histopathological alterations and mitochondrial dysfunction in cardiac tissue. The results suggest that gallic acid and sesame oil exert cardioprotection via mitochondrial protection, antioxidant properties and ultimately improving mitochondrial function and cardiac function. |
doi_str_mv | 10.1080/15569543.2023.2165503 |
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We investigated the effects of gallic acid and sesame oil in ketamine-induced cardiotoxicity in rats. Male Wistar rats were randomly divided into six groups including control; ketamine; ketamine + gallic acid; ketamine + sesame oil; gallic acid and sesame oil. Serum cardiac marker, cardiac tissue oxidative stress markers, histopathological analysis and mitochondrial toxicity parameters (succinate dehydrogenase activity, mitochondrial swelling, reactive oxygen species (ROS) production and collapse of mitochondria membrane potential) were measured on the fifteen days of the study. The results showed that ketamine administration increased serum cardiac markers, oxidative stress parameters, histopathological alterations and mitochondrial dysfunction in cardiac tissue. Gallic acid and sesame oil administration in presence of ketamine was observed to decrease serum cardiac markers, oxidative stress parameters, histopathological alterations and mitochondrial dysfunction in cardiac tissue. 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We investigated the effects of gallic acid and sesame oil in ketamine-induced cardiotoxicity in rats. Male Wistar rats were randomly divided into six groups including control; ketamine; ketamine + gallic acid; ketamine + sesame oil; gallic acid and sesame oil. Serum cardiac marker, cardiac tissue oxidative stress markers, histopathological analysis and mitochondrial toxicity parameters (succinate dehydrogenase activity, mitochondrial swelling, reactive oxygen species (ROS) production and collapse of mitochondria membrane potential) were measured on the fifteen days of the study. The results showed that ketamine administration increased serum cardiac markers, oxidative stress parameters, histopathological alterations and mitochondrial dysfunction in cardiac tissue. Gallic acid and sesame oil administration in presence of ketamine was observed to decrease serum cardiac markers, oxidative stress parameters, histopathological alterations and mitochondrial dysfunction in cardiac tissue. 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subjects | Cardiotoxicity illicit drug mitochondrial dysfunction natural compounds |
title | Gallic acid and sesame oil exert cardioprotection via mitochondrial protection and antioxidant properties on Ketamine-Induced cardiotoxicity model in rats |
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