glycyrrhizic acid/infarction

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

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

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

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

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