Preventive effect of rutin, a bioflavonoid, on lipid peroxides and antioxidants in isoproterenol-induced myocardial infarction in rats

Karthick, M.; Prince, P. Stanely Mainzen

doi:10.1211/jpp.58.5.0016

Cited by 84 publications

(58 citation statements)

References 30 publications

(25 reference statements)

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“…There was a significant elevation in serum CK-MB confirming the acute myocardial infarction in rats. These observations were in line with previous studies conducted on rats treated with iso (26). CK-MB is localized predominantly in the heart, and this makes it a valuable diagnostic marker for MI, as damages specific to the myocardium would result in the elevation of serum CK-MB levels (10,11,27).…”

Section: Discussionsupporting

confidence: 91%

Morinda Citrifolia (Noni) and Low Dose Aspirin Prevent Apoptotic Cell Death and Oxidative Stress on Isoproterenol Induced Myocardial Infarction in Rats

Ol¹,

Kanbak²,

İlhan³

et al. 2017

Erciyes Med J

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Objective: Isoproterenol (iso)-induced myocardial infarction is a widely used experimental model to study the beneficial effects of many drugs. Morinda citrifolia (noni) has traditionally been used for treating many diseases. Low-dose aspirin may have been protected heart tissueThis study aimed to investigate the possible protective effects of noni (20%) and low-dose aspirin (30 mg/kg) against iso-induced acute myocardial infarction in male Wistar rats. Materials and Methods:Rats were divided into control, iso, iso+noni, iso+aspirin, and iso+aspirin+noni groups (n=8). Myocardial infarction was induced by subcutaneous injection of iso (100 mg/kg) for two consecutive days. Iso-induced rats showed increased serum Creatine kinase-muscle brain CK-MB activity. The effects of noni (20%) and low-dose aspirin (30 mg/kg) were evaluated in response to iso-induced changes, Malondialdehyde (MDA), Superoxide Dismutase (SOD), Catalase (CAT), DNA fragmentation, caspase-3, and cathepsins B and L.Results: Oral treatment with 20% noni juice and low-dose aspirin (30 mg/kg) for 7 days significantly decreased apoptotic markers such as DNA fragmentation, caspase-3, and cathepsins B and L; increased antioxidant enzymes such as SOD and catalase activities; and decreased MDA levels. Conclusion:We propose that the protective effect, antiapoptotic and antioxidant mechanisms of noni and low dose aspirin may be on iso-induced myocardial infarction.

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Section: Discussionsupporting

confidence: 91%

Morinda Citrifolia (Noni) and Low Dose Aspirin Prevent Apoptotic Cell Death and Oxidative Stress on Isoproterenol Induced Myocardial Infarction in Rats

Ol¹,

Kanbak²,

İlhan³

et al. 2017

Erciyes Med J

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“…Normal control and ISO control rats were received CMC alone (1 ml/rat). Rutin pretreatment and dosage fixation was based on our earlier study [9]. Twelve hours after the second dose of ISO injection (on 45th day), all the rats were anesthetized and then killed by cervical decapitation.…”

Section: Experimental Designmentioning

confidence: 99%

“…A wide variety of pharmacological actions of rutin were reported-antibacterial, anti-tumor, anti-inflammatory, anti-diarrheal, antiulcer, anti-mutagenic, vasodilator, immunomodulatory and hepatoprotective [7]. Previously, we reported the preventive effects of rutin on lipids, lipoproteins, ATPases, lipid peroxides and antioxidants in ISO-induced rats [8,9].…”

Section: Introductionmentioning

confidence: 98%

Protective Effects of Rutin on Mitochondrial Damage in Isoproterenol-Induced Cardiotoxic Rats: An In Vivo and In Vitro Study

2010

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Consumption of diets rich in flavonoids is associated with reduced risk of cardiovascular diseases such as myocardial infarction. Cardiotoxicity was induced in rats by subcutaneous injection of isoproterenol at an interval of 24 h for 2 days. Isoproterenol-induced rats showed a significant increase in the levels of heart mitochondrial lipids, lipid peroxidation products, calcium and a significant decrease in the activities/levels of mitochondrial antioxidants, enzymes and adenosine triphosphate. Isoproterenol-induced rats also showed an increase in the intensities of serum lactate dehydrogenase-1 and 2 isoenzyme bands. Pretreatment with rutin at the dose of 80 mg/kg daily for 42 days to isoproterenol-induced rats prevented all the biochemical alterations. Transmission electron microscopic study also confirmed the protective effects of rutin on the structure of heart mitochondria. Thus, rutin reduced the extent of mitochondrial damage induced by isoproterenol and prevented cardiac mitochondrial dysfunction. The possible mechanisms for the observed effects of rutin could be due to scavenging free radicals, lowering lipid peroxides, lipids and calcium, improving multienzyme activities, glutathione levels, adenosine triphosphate levels, thereby improving cardiac mitochondrial structure and function. This study may have a significant impact on myocardial infarcted patients.

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“…37 Although this rat model does not exactly reflect the clinical situation in terms of coronary occlusion and regional MI, animals develop "infarct-like" lesions when injected with isoproterenol. In a rabbit model of coronary artery ligation, Krieg et al 38 recently showed that cinaciguat elicited an infarct-reducing effect.…”

Section: Study Limitationsmentioning

confidence: 99%

Pharmacological Activation of Soluble Guanylate Cyclase Protects the Heart Against Ischemic Injury

et al. 2009

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Background-The role of the nitric oxide/cGMP/cGMP-dependent protein kinase G pathway in myocardial protection and preconditioning has been the object of intensive investigations. The novel soluble guanylate cyclase activator cinaciguat has been reported to elevate intracellular [cGMP] and activate the nitric oxide/cGMP/cGMP-dependent protein kinase G pathway in vivo. We investigated the effects of cinaciguat on myocardial infarction induced by isoproterenol in rats. Methods and Results-Rats were treated orally twice a day for 4 days with vehicle or cinaciguat (10 mg/kg). Isoproterenol (85 mg/kg) was injected subcutaneously 2 days after the first treatment at an interval of 24 hours for 2 days to produce myocardial infarction. After 17 hours, histopathological observations and left ventricular pressure-volume analysis to assess cardiac function with a Millar microtip pressure-volume conductance catheter were performed, and levels of biochemicals of the heart tissues were measured. Gene expression analysis was performed by quantitative real-time polymerase chain reaction. Isolated canine coronary arterial rings exposed to peroxynitrite were investigated for vasomotor function, and immunohistochemistry was performed for cGMP and nitrotyrosine. The present results show that cinaciguat treatment improves histopathological lesions, improves cardiac performance, improves impaired cardiac relaxation, reduces oxidative stress, ameliorates intracellular enzyme release, and decreases cyclooxygenase 2, transforming growth factor-␤, and ␤-actin mRNA expression in experimentally induced myocardial infarction in rats.In vitro exposure of coronary arteries to peroxynitrite resulted in an impairment of endothelium-dependent vasorelaxation, increased nitro-oxidative stress, and reduced intracellular cGMP levels, which were all improved by cinaciguat. A cardioprotective effect of postischemic cinaciguat treatment was shown in a canine model of global ischemia/reperfusion. Conclusion-Pharmacological soluble guanylate cyclase activation could be a novel approach for the prevention and treatment of ischemic heart disease. (Circulation. 2009;120:677-686.) Key Words: contractility Ⅲ genes Ⅲ myocardial infarction Ⅲ nitric oxide M yocardial infarction (MI) is the rapid development of myocardial necrosis that occurs when a coronary artery is severely blocked so that there is a significant imbalance between the oxygen supply and the demand of the myocardium, causing damage or death of a portion of the myocardium. A better understanding of the processes involved in myocardial injury has stimulated the search for new drugs that could limit the myocardial damage. It has been proposed that the nitric oxide (NO)/soluble guanylate cyclase (sGC)/ cGMP/cGMP-dependent protein kinase G pathway may play a pivotal role in myocardial protection and preconditioning. In the healthy endothelium, vascular NO binds to the ferrous heme iron (Fe 2ϩ ) and activates a key signal transduction enzyme, sGC, resulting in cGMP generation. This activation promotes...

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Preventive effect of rutin, a bioflavonoid, on lipid peroxides and antioxidants in isoproterenol-induced myocardial infarction in rats

Cited by 84 publications

References 30 publications

Morinda Citrifolia (Noni) and Low Dose Aspirin Prevent Apoptotic Cell Death and Oxidative Stress on Isoproterenol Induced Myocardial Infarction in Rats

Morinda Citrifolia (Noni) and Low Dose Aspirin Prevent Apoptotic Cell Death and Oxidative Stress on Isoproterenol Induced Myocardial Infarction in Rats

Protective Effects of Rutin on Mitochondrial Damage in Isoproterenol-Induced Cardiotoxic Rats: An In Vivo and In Vitro Study

Pharmacological Activation of Soluble Guanylate Cyclase Protects the Heart Against Ischemic Injury

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