glycyrrhizic acid/infarction

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Ability of Post-treatment Glycyrrhizic Acid to Mitigate Cerebral Ischemia/Reperfusion Injury in Diabetic Mice

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BACKGROUND Diabetes aggravates cerebral ischemia/reperfusion (I/R) injury by increasing inflammatory reactions, but its specific mechanism is currently unclear. MATERIAL AND METHODS Diabetes was induced in mice with a high-fat diet combined with streptozotocin. These mice were subjected to transient

Brain-targeted glycyrrhizic-acid-loaded surface decorated nanoparticles for treatment of cerebral ischaemia and its toxicity assessment.

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Enhancement of CS-GA-PCL-NPs (Glycyrrhizic Acid-encapsulated-chitosan-coated-PCL-Nanoparticles) bioavailability in brain.Double emulsification solvent evaporation method in order to develop CS-PCL-NPs (Chitosan-coated-PCL-Nanoparticles) followed by

Protective effect of glycyrrhizic acid on cerebral ischemia/reperfusion (I/R) injury via inhibiting HMGB1 mediated TLR4/NF-κB pathway.

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Cerebral ischemia is caused by various disorders, such as stroke, myocardial infarction or peripheral vascular disease. The purpose of this paper was to investigate the effects of glycyrrhizic acid (GA) on cerebral ischemia/reperfusion (I/R) injury. Middle cerebral artery occlusion (MCAO) was

Cardioprotective effects of glycyrrhizic acid against isoproterenol-induced myocardial ischemia in rats.

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The aim of the present study was to look into the possible protective effects of glycyrrhizic acid (GA) against isoproterenol-induced acute myocardial infarction in Sprague-Dawley rats. The effect of three doses of glycyrrhizic acid in response to isoproterenol (ISO)-induced changes in

Glycyrrhizic acid affords robust neuroprotection in the postischemic brain via anti-inflammatory effect by inhibiting HMGB1 phosphorylation and secretion.

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High mobility group box 1 (HMGB1) is an endogenous danger signal molecule. In a previous report, we showed that HMGB1 is massively released during NMDA-induced acute damaging process in the postischemic brain and triggers inflammatory processes, like microglial activation. siRNA-mediated HMGB1

Neuroprotective effect of Trichosanthes kirilowii cassia twig on cerebral ischemia-reperfusion injury in rats.

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In this study, in-depth observation and investigation of blood-brain barrier permeability and neuroprotective effect of Trichosanthes kirilowii cassia twig particles on rats with cerebral ischemia-reperfusion injury were performed. Focal cerebral ischemia-reperfusion injury model was established by

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