Effect Of Epigllocatechin Gallate On Synaptic Transmission In Hippocampus In Normal Rats And Cerebral Ischemia-Reperfusion Rats

To investigate the effect and underlying mechanisms of EGCG on rat cerebral ischemia in vivo and in vitro. Method: 1. The effect of EGCG on normal rats and cerebral ischemia-reperfusion rats in vivo: Male SD rats were divided into NS and the EGCG (12.5ug, 25ug, 50ug, 100ug) treated groups. After EGCG was administrated by i.c.v. in treated groups,we used in vivo field potential recording to observe the amplitude change of population spikes(PS) in area CA1 of hippocampus; Male SD rats were divided into four groups (sham-operated, ischemic and treated group (lower dose and higher dose)). Middle cerebral artery occlusion (MCAO) was introduced as an in vivo ischemic model. After EGCG was administrated by i.v. in treated groups, we also used in vivo field potential recording to observe the amplitude change of population spikes(PS) in area CA1 of hippocampus.2. Study of EGCG on cultured rat hippocampal neurons suffered from oxygen-glucose deprivation (OGD): OGD was served as an in vitro ischemia model. Primary cultures of cortical and hippocampal neurons were exposed to 4 h OGD. EGCG(25μmol/L,50μmol/L,100μmol/L) was added 12 h before OGD initiated. Cell injury was measured by lactate dehydrogenase (LDH) release and cell viability by reduction of 3-[4,5-dimethylthia -2-yl]-2,5-diphenyl- tetrazolium bromide (MTT). Results:1.EGCG can facilitate long-term potentiation (LTP) on normal rats in vivo.2.EGCG can not only improve depression of synaptic transmission efficiency induced by MCAO in vivo, but also improve cell validity in cultures suffered from OGD. 3.EGCG decrease LDH level in cultures suffered from OGD. Conclusion: EGCG can ameliorate ischemic impairment induced by MCAO and OGD. The neuroprotective effect is partly due to its functions as follow: anti-free radical injury; reducing glutamate acid excitotoxicity.