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

Posted on:2012-07-05Degree:MasterType:Thesis
Country:ChinaCandidate:S M GaoFull Text:PDF
GTID:2214330362457322Subject:Anesthesia
Abstract/Summary:PDF Full Text Request
【Objective】To establish intraluminal suture right middle cerebral artery occlusion(MCAO) model and observe the protective effects and mechanisms of epigallocatechin gallate (EGCG) on focal cerebral ischemia and reperfusion injury in rats.【Methods】The model of focal cerebral ischemia and reperfusion injury was established by inserting thread into middle cerebral artery for 2 h followed by reperfusion. Fifty-four adult male Sprague-Dawley rats (200 to 250 g) were randomly divided into three groups: sham-operated group(sham group), ischemia reperfusion group(I/R) and EGCG group (E group). EGCG 0.1 mg was intracerebroventricularlly administrated to E group after ischemia, and saline was administrated to shame and I/R group. The neurological deficts, infarct volume, morphologic injury, apoptosis neuronal were evaluated at 24 h reperfusion. The expression of cytokines TNF-αand IL-1βin brain tissue were measured by ELISA assay. The activity of MPO and SOD and the levels of the lipid peroxidation in brain tissue were measured after 24 h reperfusion. The expression of Bcl-2 and Bax were assessed by immunohistochemistry assay.【Results】Administration of EGCG ameliorated neurological deficts and pathological damage, attenuated infarction volume, extenuated neuronal apoptosis. The content of MDA and the activity of MPO were decreased, while the activity of SOD were increased. Pretreated with EGCG, the levels of cytokines TNF-αand IL-1βwere downregulated, and the expression of Bcl-2 increased while Bax decreased. 【Discussion】Many studies have proved that the generation and development of cerebral ischemia and reperfusion injury are relative with oxidative stress, inflammation response and cell apoptosis. There also are evidence that attenuating oxidative stress and inflammation as well as decreasing cell apoptosis could protect cerebral injury from ischemia and reperfusion. This study discovered that EGCG could extenuate oxidative stress and inflammation response and decrease cell apoptosis after cerebral ischemia and reperfusion. The cerebral protection effects of EGCG for ameliorating neurological deficts and pathological damage as well as attenuating infarction volume could be relative with the mechanisms depicted above.【Conclusions】These results demonstrate that pretreat of EGCG remarkably attenuated cerebral ischemia and reperfusion injury by its anti-inflammatory and anti-oxidant effects which can reduce neuronal apoptosis.
Keywords/Search Tags:Epigallocatechin gallate (EGCG), Cerebral ischemia and reperfusion injury, Inflammation factors, Oxidative stress, Apoptosis
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