Synergistic interactions of Ferulic acid with Ascorbic acid: Its cardioprotective role during isoproterenol induced myocardial infarction in rats

Yogeeta, Surinder Kumar; Arunachalam, Gnanapragasam; Senthilkumar, Subramanian; Subhashini, Rajakannu; Sathivel, Arumugam; Devaki, Thiruvengadam

doi:10.1007/s11010-006-2494-0

Cited by 64 publications

(47 citation statements)

References 45 publications

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“…Many studies have reported that increased levels of AST, ALT, LDH, GGT, and CPK are consistently correlated with cardiac infarcts (Yogeeta et al, 2006;Rajadurai and Stanely, 2007). Myocardial cell damage induced by heat stress was observed through the gradual elevation of LDH, AST, and CK levels in the present study.…”

Section: Discussionsupporting

confidence: 66%

Temporal variations of Hsp60 and HSF-1 in primary rat myocardial cells in vitro under heat stress

Rehana

Lv²,

Islam³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. The mechanisms involved in sudden animal death due to acute heart failure during heat stress are not well understood. We examined the relationship between heat stress-induced variations of protective Hsp60 and expression of its regulatory factor, HSF-1, in heat-stressed primary myocardial cells of neonatal rats in vitro through cardiac enzyme detection, immunoblotting, immunocytochemistry, and qPCR. Increases in cardiac damage-related enzyme levels demonstrated injury to myocardial cells after heat exposure at 42°C. Hsp60 expression levels fluctuated during heat stress; they decreased significantly after 20 min, then increased at 120 min and decreased again at 360 min after initiation of heat stress. The highest levels of Hsp60 were observed at 240 min, while the lowest were at 60 min. Damage to myocardial cells was characterized by increases in cardiac enzyme levels and low levels of Hsp60 due to functional disorder of myocardial cells at early stages of heat stress. However, the significant induction of hsp60 mRNA levels from the beginning up to 240 min of heat stress was not consistent with the classic regulatory mechanisms that link transcription and translation, suggesting that Hsp60 expression is delayed due to loss of Hsp60 during the early stages of heat stress. hsf-1 mRNA levels were significantly increased from 10 min of heat stress; however, HSF-1 protein levels did not simultaneously increase, indicating that HSF-1 is not the sole regulator of Hsp60 expression.

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Section: Discussionsupporting

confidence: 66%

Temporal variations of Hsp60 and HSF-1 in primary rat myocardial cells in vitro under heat stress

Rehana

Lv²,

Islam³

et al. 2013

Genet. Mol. Res.

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“…AST starts to rise about 12 hours after infarction and reaches a peak on the 1 st or 2 nd day 30 . The sera of rats with myocardial necrosis were worthy of particular attention because of the possibility that destruction of cardiac muscle, rich in transaminase activity, results in a release of this enzyme into blood stream and thus increase the serum transaminase activity.…”

Section: Discussionmentioning

confidence: 99%

Modulation of oxidative stress by enalapril and valsartan in adrenaline treated rats: a comparative study

Huda¹,

Akhter

2014

Bangladesh Med Res Counc Bull

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Angiotensin (Ang II) II is known to promote oxidative stress in acute myocardial infarction (AMI). Inhibition of renin angiotensin system (RAS) or blockade of Ang II receptors may therefore be effective in reducing oxidative stress during AMI. The study evaluates and compares the protective effect of Angiotensin Converting Enzyme (ACE) inhibitor and AT 1 receptor blocker in adrenaline induced oxidative stress in rats. Rats were treated with two successive injections of adrenaline subcutaneously at a dose of 2 mg/kg administered 24 hours apart. In other two groups of rats enalapril (30 mg/kg) or valsartan (30 mg/kg) were given orally once daily through intragastric tube for 2 weeks and then two injections of adrenaline were administered 24 hours apart. Serum Aspertate Transaminase (AST), plasma Malonde Aldehyde (MDA), erythrocyte GSH and serum vitamin E levels were measured 24 hours after the 2 nd injection of adrenaline in all the groups. Administration of adrenaline caused significant increase (p<0.001) in serum AST and plasma MDA levels and decrease (p<0.001) in erythrocyte GSH and serum vitamin E levels. Pre-treatment of enalapril or valsartan for 14 days reduced (p<0.001) serum AST and plasma MDA levels and increased the concentration of erythrocyte GSH in enalapril pre-treated group (p<0.01) and in valsartan pre-treated group (p<0.05). Pre-treatment of enalapril or valsartan also increased (p<0.01) serum vitamin E levels in adrenaline treated rats. However, no significant difference was noted between the effect of enalapril and valsartan on serum AST, plasma MDA, erythrocyte GSH and serum vitamin E levels. It may be concluded that both enalapril and valsartan offered cardioprotection in adrenaline induced oxidative stress, but the protection afforded by valsartan was not superior to enalapril.

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“…Lipid peroxidation and anti-oxidant change and their significance during myocardial injury have provided a new insight in the pathogenesis of heart disease (Yogeeta et al, 2006). The increased level of free radical generating system and malondialdehyde (MDA) and lowered levels of free radical scavenging systems seem to have critical role in ischemic heart condition (Pandry et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective effect of amlodipine in oxidative stress induced by experimental myocardial infarction in rats

Begum

Akhter

2008

Bangladesh J Pharmacol

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The present study investigated whether the administration of amlodipine ameliorates oxidative stress induced by experimental myocardial infarction in rats. Adrenaline was administered and myocardial damage was evaluated biochemically [significantly increased serum aspertate aminotransferase (AST), lactate dehydrogenase (LDH) and malondialdehyde (MDA) levels of myocardial tissue] and histologically (morphological changes of myocardium). Amlodipine was administered as pretreatment for 14 days in adrenaline treated rats. Statistically significant amelioration in all the biochemical parameters supported by significantly improved myocardial morphology was observed in amlodipine pretreatment. It was concluded that amlodipine afforded cardioprotection by reducing oxidative stress induced in experimental myocardial infarction of catecholamine assault.

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Synergistic interactions of Ferulic acid with Ascorbic acid: Its cardioprotective role during isoproterenol induced myocardial infarction in rats

Cited by 64 publications

References 45 publications

Temporal variations of Hsp60 and HSF-1 in primary rat myocardial cells in vitro under heat stress

Temporal variations of Hsp60 and HSF-1 in primary rat myocardial cells in vitro under heat stress

Modulation of oxidative stress by enalapril and valsartan in adrenaline treated rats: a comparative study

Cardioprotective effect of amlodipine in oxidative stress induced by experimental myocardial infarction in rats

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