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17.08.2017

Diosmin Prevents Isoproterenol-Induced Heart Mitochondrial Oxidative Stress in Rats

verfasst von: S. Sharmila Queenthy, P. Stanely Mainzen Prince, Babu John

Erschienen in: Cardiovascular Toxicology | Ausgabe 2/2018

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Abstract

Cardiac mitochondrial oxidative stress causes mitochondrial damage that plays an important role in the pathology of myocardial infarction. The preventive effects of diosmin on cardiac mitochondrial oxidative stress in isoproterenol-induced myocardial infarcted rats were evaluated. Rats were pretreated with diosmin (10 mg/kg body weight) daily for 10 days. Myocardial infarction was induced in rats by isoproterenol (100 mg/kg body weight) injection twice at an interval of 24 h (on 11th and 12th day). Isoproterenol-induced myocardial infarcted rats showed a significant increase in the levels of cardiac diagnostic markers, heart mitochondrial lipid peroxidation, calcium ion, and a significant decrease in the levels of heart mitochondrial glutathione peroxidase, reduced glutathione, glutathione-S-transferase, isocitrate, malate, α-ketoglutarate, and succinate dehydrogenases. Transmission electron microscopic findings revealed damaged mitochondria with loss of cristae, swelling, and vacuolation in isoproterenol-induced rats’ heart. Diosmin pretreatment showed significant preventive effects on all the biochemical parameters, and the structure of mitochondria was evaluated. Furthermore, the transmission electron microscopic study confirms the biochemical findings. The antioxidant and negative inotropic effects of diosmin inhibited cardiac mitochondrial oxidative stress and prevented mitochondrial damage in myocardial infarcted rats.
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Metadaten
Titel
Diosmin Prevents Isoproterenol-Induced Heart Mitochondrial Oxidative Stress in Rats
verfasst von
S. Sharmila Queenthy
P. Stanely Mainzen Prince
Babu John
Publikationsdatum
17.08.2017
Verlag
Springer US
Erschienen in
Cardiovascular Toxicology / Ausgabe 2/2018
Print ISSN: 1530-7905
Elektronische ISSN: 1559-0259
DOI
https://doi.org/10.1007/s12012-017-9422-2