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Neuroprotective Effect on Cerebral Ischemiainjury in Animal Models by Intravenous Injection of Tea Polyphenol and Its Possible Mechanisms

Author: YangLiSong
Tutor: LiWeiPing
School: Dalian Medical University
Course: Pharmacology
Keywords: tea polyphenol ischemia reperfusion SOD activity nNOS
CLC: R285
Type: Master's thesis
Year: 2005
Downloads: 72
Quote: 0
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Abstract


Purpose: Tea polyphenols(TP) are polyphenolic components extracted fromcamellia sinenesis. Previous studies have demonstrated that they have thebiological functions of anti-oxidation and scavenging free radicals.Theyplay an important role in anticancer,decreasing blood pressure and bloodglucose,etc.This experiment aims to study the neuroprotective effect of TPon cerebral ischemia reperfusion injury and further to explore its possiblemechanisms. Method: 1.Mice were given TP intravenously at several different doses andmortality of mice was detected.The LD50 of TP was calculated. 2.Incomplete global ischemia reperfusion model was made byrepeated ligation releasing of bilateral common carotid artery in mice.Thehistopathological changes and SOD activity in brain tissue were measured. 3.The rat model of middle cerebral ischemia reperfusion injury wasestablished with suture method.Effects of TP on survival time within24h,neurologic deficit,brain infarcted area and nNOS positive neurons inperi-infarcted area were investigated. Results: 1.The calculation of LD50 of TPLD50 = 0.33 g.kg-1±0.025 g.kg-1 95% confidence intervals:0.305 g.kg-1,0.357 g.kg-1 2.Effect of TP on incomplete global ischemia reperfusion injury inmice. TP iv improved SOD activity as well as histopathological changes atthe doses of 100 mg.kg-1 and 50 mg.kg-1 respectively(P<0.01) comparedwith control group. 3.Effect of TP on focal cerebral ischemia reperfusion injury in rats TP iv significantly prolonged survival time and increased survival ratewithin 24h (90%,P<0.001 ; 22%,P<0.01);decreased neurologic deficitscore(3.57±1.81,P<0.001;4.71±1.38,P<0.05), reduced infarcted area by78.56% and 53.46%(P<0.001)and lowered the number of nNOS positiveneurons as well as alleviated histopathological changes. Conclusions: The above results suggest that TP play an important role in ischemiareperfusion injury probably by improving the antioxidant capacity of theischemic tissue and by decreasing the releasing of NO produced by nNOS.

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