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Luteolin promotes mitochondrial protection during acute and chronic periods of isoproterenol induced myocardial infarction in rats
Author(s) -
Murugesan Madhesh,
Manju Vaiyapuri
Publication year - 2013
Publication title -
the egyptian heart journal /the egyptian heart journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.212
H-Index - 9
eISSN - 2090-911X
pISSN - 1110-2608
DOI - 10.1016/j.ehj.2013.02.005
Subject(s) - tbars , medicine , luteolin , lipid peroxidation , myocardial infarction , mitochondrion , mitochondrial ros , pharmacology , antioxidant , endocrinology , oxidative stress , biochemistry , chemistry , flavonoid
ObjectiveAn attempt has been made to evaluate the mitochondrial protection in acute and chronic periods after isoproterenol (ISO)-induced myocardial-infarction (MI) in male Wistar rats.Materials and methodsLuteolin was supplemented by intra-gastric intubation at a daily dose of 0.3mg/kg body weight for 30days. In the acute MI model, luteolin had been administered once per day to rat groups during 30days. On 29th and 30th days, the rats of the acute MI control groups were administered 85mg/kg body weight, isoproterenol, intra-peritoneally at an interval of 24h. In the chronic MI model luteolin was supplemented to the rat group during 30days. On the 1st and 2nd days, the rats of the chronic MI control and luteolin treatment groups were administered ISO by the same way.ResultsThe isoproterenol-treated rats both in acute and chronic models showed an increase in the level of TBARS and a decrease in the activities of mitochondrial antioxidants in MI rats, an increase in levels of mitochondrial lipid profile except phospholipids and the activities of mitochondrial enzymes were decreased in isoproterenol-treated rats. Oral treatments with luteolin in both acute and chronic models showed a significant decrease in the levels of mitochondrial lipid peroxidation, increase in the mitochondrial antioxidant levels and also decrease in the mitochondrial enzymes.ConclusionThus the present study revealed that luteolin ameliorates mitochondrial damage in isoproterenol induced myocardial infarction by maintaining lipid peroxidation metabolism due to its free radical scavenging, mitochondrial lipids, antioxidants and mitochondrial enzymes. Histopathological observations were also in correlation with the biochemical parameters

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