Protections Of EGCG Attenuating Focal Cerebral Ischemia And Reperfusion Injury In Rats

Stroke is considered as one of the leading causes of death and disability around the world and ischemic stroke accounts for about 80%. Studies showed that cerebral ischemia triggered massive physiopathologic processes including oxidative stress, inflammatory responses, energy metabolism, increased release of excitatory amion acids, etc., which direct/indirect resulting in neurological deficit and brain edema formation. Among those, oxidative stress and inflammatory responses are the most important mechanisms. To date, few therapeutic options are available to treat stroke. To explore effevtive methods to protect nerve cells, prevent and cure cerebral ischemia effectively is the research hotspot and difficulty.(-)-epigallocatechin-3-gallate(EGCG), a natural polyphenol and a main constituent of green tea extract, has neuroprotective effects in autoimmune encephalomyelitis, spinal cord injury and Alzheimer’s disease, through its anti-oxidation and anti-inflammation properties. Many experimental studies have shown that the administration of EGCG is neuroprotective. It is a promising method for the treatment of ischemic brain disease. However, all previous studies mostly focused on the antioxidant activity of EGCG, the precise mechanisms of the neuroprotective effect of EGCG, such as anti-inflammatory mechanisms, are not entirely known. As far as we know, few studies focused on the anti-inflammatory of EGCG for the treatment of ischemic brain disease. As mentioned, EGCG has a neuroprotective effect, through its anti-inflammatory properties, and inflammation plays a critical role in cerebral ischemia. Therefore, this study was undertaken to demonstrate our hypothesis that EGCG can prevent cerebral ischemia/reperfusion injury in an experimental t MCAO rat model through attenuation of oxidative stress and inflammation. The results as below:(1) The administration of EGCG is effective which can ameliorate the neurological deficit, decrease the infarct size and regulate the expression of Nrf2 and HO-1 in m RNA and protein levels. EGCG significantly increased the levels of GSH, decreased the levels of MDA. The underlying mechanism of this neuroprotection may be involved in increasing the levels of GSH, decreasing the levels of MDA and regulating Nrf2 and HO-1 expression.(2) The inflammation-related molecules TNF-α, IL-1β, IL-6 levels usually caused by ischemia/reperfusion were significantly ameliorated by EGCG. EGCG also inhibited the upregulation of nuclear factor-kappa B/p65(NF-κB/p65), and induction of cyclooxygenase 2(COX-2) and inducible nitric oxide synthase(i NOS), compared with vehicle. The present study indicates that EGCG may be a promising therapeutic agent for cerebral ischemia/reperfusion injury through attenuation of inflammation.In conclusion, cerebral ischemia/reperfusion induces multiple injury pathways including oxidative stress and inflammatory reactions, which then trigger the secondary brain damage cascade leading to neurological deficits. The neuroprotective effects of EGCG appear to be associated with regulation of Nrf2 and NF-κB activation.