magnolol/infarction

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Magnolol reduces infarct size and suppresses ventricular arrhythmia in rats subjected to coronary ligation.

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1. Magnolol is an active component of Magnolia officinalis. It is 1000-times more potent than alpha-tocopherol in inhibiting lipid peroxidation in rat heart mitochondria. In the present study, the in vivo antiarrhythmic and anti-ischaemic effects of magnolol in coronary ligated rats were

Effect of magnolol on coronary vascular resistance in rabbits: measurement with pulsed Doppler velocimetry.

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OBJECTIVE Magnolol is an active component purified from Magnolia officinalis that has been reported to protect the myocardium against infarction and reperfusion injury. The purpose of this study was to investigate the effect of magnolol on the coronary circulation and to determine whether a change

Anti-apoptotic effect of magnolol in myocardial ischemia and reperfusion injury requires extracellular signal-regulated kinase1/2 pathways in rat in vivo.

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Magnolol, an active component extracted from Magnolia officinalis, has been reported to have protective effect on ischemia and reperfusion (I/R)-induced injury in experimental animals. The aim of the present investigation was to further evaluate the mechanism(s) by which magnolol reduces I/R-induced

Magnolol Reduces Renal Ischemia and Reperfusion Injury via Inhibition of Apoptosis.

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Magnolol, a constituent of the bark of Magnolia officinalis, has been reported to decrease myocardial stunning and infarct size. In this study, we investigated whether magnolol can reduce renal ischemia and reperfusion (I/R) injury. Renal I/R, induced by a 60-min occlusion of bilateral renal

Resuscitation from experimental traumatic brain injury by magnolol therapy.

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BACKGROUND The purpose of the present study was to determine whether magnolol, a free radical scavenger, mitigates the deleterious effects of traumatic brain injury (TBI). METHODS Traumatic brain injuries were induced in anesthetized male Sprague-Dawley rats using fluid percussion, and the rats were

Effect of magnolol on cerebral injury and blood brain barrier dysfunction induced by ischemia-reperfusion in vivo and in vitro.

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Magnolol, a neolignan compound isolated from traditional Chinese medicine Magnolia officinalis, has a potentially therapeutic influence on ischemic stroke. Previous studies have demonstrated that cerebral ischemia-reperfusion (I-R) and blood-brain barrier (BBB) are involved in the pathogeneses of

Magnolol reduces glutamate-induced neuronal excitotoxicity and protects against permanent focal cerebral ischemia up to 4 hours.

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Neuroprotective efficacy of magnolol, 5,5'-dially-2,2'-dihydroxydiphenyl, was investigated in a model of stroke and cultured neurons exposed to glutamate-induced excitotoxicity. Rats were subjected to permanent middle cerebral artery occlusion (pMCAO). Magnolol or vehicle was administered

Magnolol protects neurons against ischemia injury via the downregulation of p38/MAPK, CHOP and nitrotyrosine.

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Magnolol is isolated from the herb Magnolia officinalis, which has been demonstrated to exert pharmacological effects. Our aim was to investigate whether magnolol is able to act as an anti-inflammatory agent that brings about neuroprotection using a global ischemic stroke model and to determine the

CYP3A Excipient-Based Microemulsion Prolongs the Effect of Magnolol on Ischemia Stroke Rats

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Magnolol, which is a CYP3A substrate, is a well-known agent that can facilitate neuroprotection and reduce ischemic brain damage. However, a well-controlled release formulation is needed for the effective delivery of magnolol due to its poor water solubility. In this study, we have developed a

Magnolol reduces myocardial ischemia/reperfusion injury via neutrophil inhibition in rats.

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The accumulation of oxygen-free radicals and activation of neutrophils are strongly implicated as important pathophysiological mechanisms mediating myocardial ischemia/reperfusion injury. It has been proven that various antioxidants have cardioprotective effects. Magnolol, an active component

Magnolol derivative 002C-3 protects brain against ischemia-reperfusion injury via inhibiting apoptosis and autophagy.

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Neuroprotective agents can rescue ischemic penumbra in cerebral ischemia. However, the clinically effective neuroprotective agents for cerebral ischemic injury remain deficient in clinic so far. This study was undertaken to investigate the brain protective effect of 002C-3 and its potential

Magnolol protects against ischemic-reperfusion brain damage following oxygen-glucose deprivation and transient focal cerebral ischemia.

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In the present study, the neuroprotective potential of magnolol against ischemia-reperfusion brain injury was examined via in vivo and in vitro experiments. Magnolol exhibited strong radical scavenging and antioxidant activity, and significantly inhibited the production of interleukin‑6, tumor

Magnolol attenuates the inflammation and apoptosis through the activation of SIRT1 in experimental stroke rats.

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BACKGROUND Silent information regulator 1 (SIRT1), a histone deacetylase, plays a protective role in ischemic brain injury. Previous studies have shown that magnolol has a beneficial effect on ischemic stroke; however, the role of SIRT1 in the protective effect of magnolol against cerebral ischemia

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