carnosine/infarction

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Effects of carnosine on prooxidant-antioxidant status in heart tissue, plasma and erythrocytes of rats with isoproterenol-induced myocardial infarction.

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Rats were injected with isoproterenol (ISO; 110 mg/kg, ip, 2 doses, 24 h interval) to induce acute myocardial infarction (AMI) and were sacrificed 6 and 24 h after the last ISO injection. The heart tissue, plasma and erythrocytes of these rats were evaluated for cardiac markers and oxidative stress

Differential neuroprotective effects of carnosine, anserine, and N-acetyl carnosine against permanent focal ischemia.

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Carnosine (beta-alanyl-L-histidine) has been shown to exhibit neuroprotection in rodent models of cerebral ischemia. In the present study, we further characterized the effects of carnosine treatment in a mouse model of permanent focal cerebral ischemia and compared them with its related peptides

Investigation on Beneficial Role of L-Carnosine in Neuroprotective Mechanism of Ischemic Postconditioning in Mice: Possible role of Histidine Histamine Pathway.

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The present study was undertaken to investigate the possible role of histidine-histamine pathway in the neuroprotective effects produced by L-carnosine hand in hand with ischemic postconditioning in the animal model of cerebral ischemia. Cerebral ischemia was induced in swiss albino mice by

Protective effects of beef decoction rich in carnosine on cerebral ischemia injury by permanent middle cerebral artery occlusion in rats.

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Inflammation has a role in the cerebral injury induced by ischemia and the present study aimed to determine the mechanism of the protective effect of beef decoction (BD) with carnosine against it. A rat model of permanent middle cerebral artery occlusion was established using a suture method in the

[The effect of carnosine on the activity of Na,K,ATPase: prospective uses in clinical cardiology].

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The effects of carnosine on erythrocyte membrane Na,K-ATPase and isolated enzyme in vitro as well as on membrane Na,K-ATPase activity and lipid peroxidation (LPO) in chronic heart failure (CHF) and acute myocardial infarction (AMI) have been studied. CHF and AMI have been shown to be associated with

L-carnosine inhibits neuronal cell apoptosis through signal transducer and activator of transcription 3 signaling pathway after acute focal cerebral ischemia.

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Considerable studies have showed that L-carnosine provides anti-oxidative and anti-apoptotic roles in the animal models of global or focal cerebral ischemia. However, the anti-apoptotic mechanisms of L-carnosine in the focal cerebral ischemia model have yet to be elucidated. To investigate the

Structural Elucidation of a Carnosine-Acrolein Adduct and its Quantification in Human Urine Samples.

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Aldehydes accumulate in inflammation, during myocardial infarction and have been associated with pain symptoms. One pathway of aldehyde detoxification is the conjugation with carnosine. A 3-methylpyridinium carnosine adduct from the reaction of carnosine and acrolein was characterized using

Carnosine is neuroprotective against permanent focal cerebral ischemia in mice.

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OBJECTIVE Carnosine is a naturally occurring dipeptide with multiple neuroprotective properties. In addition, it is well tolerated in high doses with minimal side effects. The purposes of this study were to determine whether carnosine is neuroprotective in permanent focal cerebral ischemia and to

Systematic review and stratified meta-analysis of the efficacy of carnosine in animal models of ischemic stroke.

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Carnosine is a naturally occurring pleotropic dipeptide which influences multiple deleterious mechanisms that are activated during stroke. Numerous published studies have reported that carnosine has robust efficacy in ischemic stroke models. To further evaluate these data, we have conducted a

Carnosine pretreatment protects against hypoxia-ischemia brain damage in the neonatal rat model.

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Perinatal hypoxia-ischemia brain injury is a major cause of mortality and morbidity in neonates and lacks an effective treatment thus far. Carnosine has been demonstrated to play a neuroprotective role in the adult brain injuries. However, there is no information available concerning its

[Study of the neuroprotective effects of carnosine in an experimental model of focal cerebral ischemia/reperfusion].

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Oxidative stress is one of the key factors in brain tissue damage in ischemia, which indicates the appropriateness of using antioxidants under these conditions. One of the promising antioxidants for the therapy of ischemic stroke is the natural dipeptide carnosine. The neuroprotective effect of

The neuroprotective effects of carnosine in early stage of focal ischemia rodent model.

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OBJECTIVE This study was conducted to elucidate neuroprotective effect of carnosine in early stage of stroke. METHODS Early stage of rodent stroke model and neuroblastoma chemical hypoxia model was established by middle cerebral artery occlusion and antimycin A. Neuroprotective effect of carnosine

Carnosine protects against permanent cerebral ischemia in histidine decarboxylase knockout mice by reducing glutamate excitotoxicity.

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Recently, we showed that carnosine protects against NMDA-induced excitotoxicity in differentiated PC12 cells through a histaminergic pathway. However, whether the protective effect of the carnosine metabolic pathway also occurs in ischemic brain is unknown. Utilizing the model of permanent middle

Involvement of reactive oxygen species in cardiac preconditioning in rats.

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To date, the involvement of reactive oxygen species in ischemic preconditioning in vivo in rats is not clearly demonstrated. The aim of the present study was to determine whether N-(2-mercaptopropionyl)glycine (MPG), a cell-diffusible hydroxyl radical scavenger, and carnosine, a potent singlet

Evidence for the role of histaminergic pathways in neuroprotective mechanism of ischemic postconditioning in mice.

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The present study has been designed to investigate the possible role of histaminergic pathway in neuroprotective mechanism of ischemic postconditioning (iPoCo). Bilateral carotid artery occlusion (BCAO) for 12 min followed by reperfusion for 24 h was employed to produce I/R-induced cerebral injury

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