| BACKGROUND: Cerebral ischemia/reperfusion-induced injury is a complex pathophysiological process, the mechanisms were not well known. At present, oxygen-derived free radical (OFR) injury, neurotoxic effects of exciting amino acid (EAA), overloading of intracellular calcium and the role of inflammation and cell apoptosis are considered as prominent factors. The roles of these factors are not independent, but interact with each other. Currently, many neuroprotective agents have been developed, including NMDA receptor antagonists, calcium antagonists, free radical scavenger, neurotrophic factors and other anti-inflammatory drugs. However, most of them have severe side-effects or/and poor efficacies on brain ischemia clinically. Therefore, it is necessary to search new types of therapeutic drugs for the treatment of cerebral ischemia. Baicalin is an effective composition from traditional Chinese medicines, which possesses anti-inflammatory, anti-oxidant, anti-infection effects as well as protective effect on cerebral ischemic injury. In the present study, we aimed to investigate the properties of baicalin's effect on the ischemic injury in vitro.PURPOSE: To determine the effect of baicalein on ischemic injury, we established and improved in vitro injury models of oxygen glucose deprivation (OGD)and reperfusion (RP) in the brain slices from mice and the primary cultured rat cortical neurons. Then we investigate the protective effect of baicalin on OGD/RP-induced ischemic injury and possible mechanism in mouse brain slices and rat cortical neurons.METHODS: In mouse brain slices, the viability after OGD/RP was assessed by formation of formazan, a red product of 2,3,5-trihenylterzolium chloride (TTC). In primary cultured rat cortical neurons, the neuronal viability and damage after OGD/RP were assessed by MTT reduction and LDH release;the intracellular free radicals were measured with 2,7-dichlorofluorescein diacetate (DCF-DA). The concentration-dependent effect of baicalin added at different times (before, during or after OGD) on OGD/RP injury was evaluated.RESULTS: In mouse brain slices, baicalin significantly attenuated OGD/RP injury at 0.01 ~ 1 jumol/L when added throughout the experiment or during OGD, and at 0.1 ~ 1 jMmol/L when added during reperfusion. In rat cortical neurons, baicalin protected the neurons from OGD/RP injury, and inhibited the elevation of intracellular free radicals at 0.01 ~ 1 ^mol/Lwhen added throughout the experiment.CONCLUSION: Baicalin has concentration-dependent protective effect on OGD/RP injury in vitro even when administrated during reperfusion;this effect may be, at least partly, mediated by inhibition of intracellular free radicals.
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