2013
DOI: 10.1016/j.metabol.2012.06.003
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Ellagic acid inhibits cardiac arrhythmias, hypertrophy and hyperlipidaemia during myocardial infarction in rats

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Cited by 112 publications
(71 citation statements)
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“…In addition to intercellular and interstitial inflammatory cellular infiltration with endothelial damage associated with hemorrhage and extravasation of blood cells in between the myocytes. These histopathological changes are in agreement with previous researchers confirming the success of the current MI model [8,12,26,30] . These changes are most probably consequential to the increase in the radical oxygen species (ROS) such as superoxide anion and hydroxyl radicals in ischemic tissues, thus resulting in oxidative damage to membrane lipids, proteins, carbohydrates and DNA [31] .…”
Section: Discussionsupporting
confidence: 92%
See 1 more Smart Citation
“…In addition to intercellular and interstitial inflammatory cellular infiltration with endothelial damage associated with hemorrhage and extravasation of blood cells in between the myocytes. These histopathological changes are in agreement with previous researchers confirming the success of the current MI model [8,12,26,30] . These changes are most probably consequential to the increase in the radical oxygen species (ROS) such as superoxide anion and hydroxyl radicals in ischemic tissues, thus resulting in oxidative damage to membrane lipids, proteins, carbohydrates and DNA [31] .…”
Section: Discussionsupporting
confidence: 92%
“…Isoproterenol generates highly cytotoxic free radicals that stimulate membrane phospholipids peroxidation thus causing severe damage to the myocardial membrane in addition to many metabolic and morphologic alterations. Therefore, it is commonly used to produce MI model in rats [7,8] .…”
Section: Introductionmentioning
confidence: 99%
“…Thus, in the present study, the increase in cardiac MDA content (an indicator for lipid peroxidation) and decrease in cardiac SOD content in the ISO group could be expected. The current results are in line with the work of other investigators (Panda and Naik 2009;Gayathri et al 2011;Kannan and Quine 2013). Reactive oxygen species (ROS) participate in cardiomyocyte apoptosis and inflammation, especially in AMI (Sun 2007).…”
Section: Discussionsupporting
confidence: 92%
“…In all cases, a period of 1 week was allowed to elapse between randomization and this would allow time for each rat to adapt to new cage mates and re-establish relationships and hierarchy and thereby reduce stresses to the animals that could potentially have an impact on the study outcomes. The groups were designated: (1) Control (vehicle only), in which rats were to receive two subcutaneous (SC) injections of saline (ISO vehicle) in a volume of 10 ml and only normal saline per os daily (100 ml/dosing) in the 28-day ''post-MI induction'' period; (2) ISO only, in which rats were to be given ISO (250 mg/kg, SC; Sigma, St. Louis, MO) dissolved in saline once daily for 2 successive days to induce MI (dose was chosen based on Kannan and Quine 2013) and then only normal saline in the post-MI induction period; (3) BM-MNC group, in which rats were to be given an IV injection of 14 Â 10 6 newly-isolated BM-MNC in 10 ml PBS via the lateral tail vein on Day 1, 24 h after induction of MI by ISO and then normal saline per os daily in the 28-day ''post-MI induction'' period; (4) PRAV group, in which rats were to be given PRAV (20 mg/kg) per os daily in the 28-day post-MI induction period (dose was selected based on Kassan et al, 2009) on Day 1, 24 h after induction of MI; and (5) PRAV + BM-MNC group, in which rats were to be given both the IV injection of BM-MNC and daily oral PRAV as described above. As this study was meant to evaluate the effects of the drug ± BM-MNC on MIrelated outcomes, there were no formal control groups assessed that solely measured effects of PRAV, BM-MNC or the two regimens in combination on the endpoints outlined below.…”
Section: Animalsmentioning
confidence: 99%
“…Subsequently, the inflammation event takes place with infiltration of neutrophils into the infarcted area where it can promote myocardial cell damage through the release of proteolytic enzymes. It intern produces cytotoxic reactive oxygen species (Kannan and Quine, 2013). Thus, the model is used as a novel method to produce myocardial infarction in experimental animals.…”
Section: Introductionmentioning
confidence: 99%