Protective Effect of Natural Antioxidants on Heart Against Ischemia-Reperfusion Damage

Zhao, Yan; Zhao, Baolu

doi:10.2174/138920110793262105

Cited by 18 publications

(10 citation statements)

References 44 publications

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“…20, 21, 22 Myocardial ischemia is due to blockage of the blood flow in the myocardium, leading to a significant change in the energy balance including depletion of ATP. A compensatory response emerges in the cardiomyocytes from the inhibition of fatty acid oxidation to an increase in the flux toward anaerobic glycolysis.…”

Section: Discussionmentioning

confidence: 99%

“…To our knowledge no other studies have examined the potential of labdane diterpenes for cardioprotection. There are a few that describe a protective role for natural products, such as antioxidant polyphenols, 22, 26, 27 and by the triterpene saponins. 28, 29 In the present study, we have focused on the molecular mechanisms underlying the effects of labdanes to protect cardiomyocytes against A/R-induced injury.…”

Section: Discussionmentioning

confidence: 99%

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Labdane diterpenes protect against anoxia/reperfusion injury in cardiomyocytes: involvement of AKT activation

2011

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Several labdane diterpenes exert anti-inflammatory and cytoprotective actions; therefore, we have investigated whether these molecules protect cardiomyocytes in an anoxia/reperfusion (A/R) model, establishing the molecular mechanisms involved in the process. The cardioprotective activity of three diterpenes (T1, T2 and T3) was studied in the H9c2 cell line and in isolated rat cardiomyocyte subjected to A/R injury. In both cases, treatment with diterpenes T1 and T2 protected from A/R-induced apoptosis, as deduced by a decrease in the percentage of apoptotic and caspase-3 active positive cells, a decrease in the Bcl-2/Bax ratio and an increase in the expression of antiapoptotic proteins. Analysis of cell survival signaling pathways showed that diterpenes T1 and T2 added after A/R increased phospho-AKT and phospho-ERK 1/2 levels. These cardioprotective effects were lost when AKT activity was pharmacologically inhibited. Moreover, the labdane-induced cardioprotection involves activation of AMPK, suggesting a role for energy homeostasis in their mechanism of action. Labdane diterpenes (T1 and T2) also exerted cardioprotective effects against A/R-induced injury in isolated cardiomyocytes and the mechanisms involved activation of specific survival signals (PI3K/AKT pathways, ERK1/2 and AMPK) and inhibition of apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Labdane diterpenes protect against anoxia/reperfusion injury in cardiomyocytes: involvement of AKT activation

2011

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“…However, ROS formation may be increased during periods of ischemia and reperfusion. Previous studies have suggested that the increased rate of ROS production during reperfusion is a major cause of the pathophysiology of ischemia/reperfusion injury in both the heart and brain [1, 12 , 30, 13, 31]. …”

Section: Reactive Oxygen Speciesmentioning

confidence: 99%

Redox Signaling Pathways Involved in Neuronal Ischemic Preconditioning

Thompson¹,

Narayanan²,

Pérez-Pinzón³

2012

Current Neuropharmacology

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There is extensive evidence that the restoration of blood flow following cerebral ischemia contributes greatly to the pathophysiology of ischemia mediated brain injury. The initiating stimulus of reperfusion injury is believed to be the excessive production of reactive oxygen (ROS) and nitrogen (RNS) species by the mitochondria. ROS and RNS generation leads to mitochondrial protein, lipid and DNA oxidation which impedes normal mitochondrial physiology and initiates cellular death pathways. However not all ROS and RNS production is detrimental. It has been demonstrated that low levels of ROS production are protective and may serve as a trigger for activation of ischemic preconditioning. Ischemic preconditioning is a neuroprotective mechanism which is activated upon a brief sublethal ischemic exposure and is sufficient to provide protection against a subsequent lethal ischemic insult. Numerous proteins and signaling pathways have been implicated in the ischemic preconditioning neuroprotective response. In this review we examine the origin and mechanisms of ROS and RNS production following ischemic/reperfusion and the role of free radicals in modulating proteins associated with ischemic preconditioning neuroprotection.

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“…[13][14][15][16] CAR exerts a protective potential against tissue damage in oxidative stress-induced pathologies and is accepted as a cardioprotective agent. 14-17 It protected cardiomyocytes from damage and improved contractility of heart in cardiac ischemia 18,19 and DOX-induced cardiotoxicity. 20, 21 We recently reported that CAR treatment diminished isoproterenol-induced myocardial damage by reducing oxidative stress in rats.…”

Section: Introductionmentioning

confidence: 99%

Beneficial effects of carnosine and carnosine plus vitamin E treatments on doxorubicin-induced oxidative stress and cardiac, hepatic, and renal toxicity in rats

et al. 2015

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Objective: Oxidative stress plays an important role in doxorubicin (DOX)-induced toxicity. Carnosine (CAR) is a dipeptide with antioxidant properties. The aim of this study was to evaluate the decreasing or preventive effect of CAR alone or combination with vitamin E (CAR + Vit E) on DOX-induced toxicity in heart, liver, and brain of rats. Methods: Rats were treated with CAR (250 mg kg−1 day−1; intraperitoneally (i.p.)) or CAR + Vit E (equals 200 mg kg−1 α-tocopherol; once every 3 days; intramuscularly) for 12 consecutive days. On the 8th day of treatment, rats were injected with a single dose of DOX (30 mg kg−1, i.p.). Serum cardiac troponin I (cTnI), urea, and creatinine levels; alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities; and oxidative stress parameters in tissues were measured. We also determined thiobarbituric acid reactive substances, diene conjugate, protein carbonyl (PC), and glutathione levels and antioxidant enzyme activities. Results: DOX resulted in increased serum cTnI, ALT, AST, urea, and creatinine levels and increased lipid peroxide and PC levels in tissues. CAR or CAR + Vit E treatments led to decreases in serum cTnI levels and ALT and AST activities. These treatments reduced prooxidant status and ameloriated histopathologic findings in the examined tissues. Conclusion: Our results may indicate that CAR alone, especially in combination with Vit E, protect against DOX-induced toxicity in heart, liver, and kidney tissues of rats. This was evidenced by improved cardiac, hepatic, and renal markers and restoration of the prooxidant state and amelioration of histopathologic changes.

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Protective Effect of Natural Antioxidants on Heart Against Ischemia-Reperfusion Damage

Cited by 18 publications

References 44 publications

Labdane diterpenes protect against anoxia/reperfusion injury in cardiomyocytes: involvement of AKT activation

Labdane diterpenes protect against anoxia/reperfusion injury in cardiomyocytes: involvement of AKT activation

Redox Signaling Pathways Involved in Neuronal Ischemic Preconditioning

Beneficial effects of carnosine and carnosine plus vitamin E treatments on doxorubicin-induced oxidative stress and cardiac, hepatic, and renal toxicity in rats

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