honokiol/infarction

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Honokiol ameliorates cerebral infarction from ischemia-reperfusion injury in rats.

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Honokiol, a constituent extracted from Magnolia officinalis, had been shown be an antioxidant and an anti-platelet agent in biological systems with an anti-arrhythmic effect and a myocardial protective effect on ischemia-reperfusion injury. We examined the neuroprotective effect of honokiol in rats

Myocardial protective effect of honokiol: an active component in Magnolia officinalis.

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Honokiol is an active component of Magnolia officinalis. It was reported to be 1000 times more potent than alpha-tocopherol in inhibiting lipid peroxidation in rat heart mitochondria. In this study, we investigated the in vivo antiarrhythmic and antiischemic effects of honokiol in coronary ligated

Honokiol, a neuroprotectant against mouse cerebral ischaemia, mediated by preserving Na+, K+-ATPase activity and mitochondrial functions.

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Honokiol, a component of the herb Magnolia officinalis, exhibits antioxidant, anti-inflammatory and anxiolytic properties, increases seizure threshold, and promotes neurite outgrowth. Because stroke has become the second leading cause of death in industrialized countries, an effective

Synthesis, characterization and in vivo evaluation of honokiol bisphosphate prodrugs protects against rats' brain ischemia-reperfusion injury.

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Honokiol (HK) usage is greatly restricted by its poor aqueous solubility and limited oral bioavailability. We synthesized and characterized a novel phosphate prodrug of honokiol (HKP) for in vitro and in vivo use. HKP greatly enhanced the aqueous solubility of HK (127.54 ± 15.53 mg/ml)

Honokiol protects rat brain from focal cerebral ischemia-reperfusion injury by inhibiting neutrophil infiltration and reactive oxygen species production.

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We have previously shown that honokiol, an active component of Magnolia officinalis, displayed protective effect against focal cerebral ischemia-reperfusion (FCI/R) injury in rats. Production of reactive oxygen species (ROS) and infiltration of neutrophils to injured tissue play deleterious roles

Honokiol protects rat hearts against myocardial ischemia reperfusion injury by reducing oxidative stress and inflammation.

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Honokiol, a potent radical scavenger, has been demonstrated to ameliorate cerebral infarction following ischemia/reperfusion (I/R) injury. However, its effects on myocardial I/R injury remain unclear. The present study aimed to examine the effects of honokiol on myocardial I/R injury and to

Honokiol Ameliorates Myocardial Ischemia/Reperfusion Injury in Type 1 Diabetic Rats by Reducing Oxidative Stress and Apoptosis through Activating the SIRT1-Nrf2 Signaling Pathway.

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Reducing oxidative stress is a crucial therapeutic strategy for ameliorating diabetic myocardial ischemia/reperfusion (MI/R) injury. Honokiol (HKL) acts as an effective cardioprotective agent for its strong antioxidative activity. However, its roles and underlying mechanisms against MI/R injury in

Honokiol protects brain against ischemia-reperfusion injury in rats through disrupting PSD95-nNOS interaction.

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Honokiol, a major bioactive constituent of the bark of Magnolia officinalis has been confirmed to have the neuroprotective effect on ischemic stroke in rats. This study was designed to observe the therapeutic time window of honokiol microemulsion on cerebral ischemia-reperfusion injury to support

w007B protects brain against ischemia-reperfusion injury in rats through inhibiting inflammation, apoptosis and autophagy.

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This study was designed to investigate the effect of w007B, a newly synthesized derivative of honokiol, on MCAO reperfusion, and its therapeutic time window and related mechanisms in rats. Neurological deficit scores, infarct size and brain water content were measured after 24 h reperfusion

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