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The Therapeutic Effect And Mechanism Of Mu-xiang-you-formulation On Cerebral Ischemia-reperfusion Injury In Rats

Posted on:2018-08-19Degree:MasterType:Thesis
Country:ChinaCandidate:S F WangFull Text:PDF
GTID:2334330536469605Subject:Pharmacology
Abstract/Summary:PDF Full Text Request
Objective: The model of cerebral ischemia-reperfusion injury was established by middle cerebral artery occlusion(MCAO).The therapeutic effects of Mu-Xiang-YouFormulation(MXYF)on cerebral ischemia-reperfusion injury rats were observed by means of neuroethology index and molecular biology,and the mechanism in oxidative stress and apoptosis was investigated.Methods: We used 300 ± 20 g male SD rats and established the MCAO model by Zea-Longa suture method.After 2 hours of ischemia,the rats were randomly divided into 6 groups according to the principle of uniform nerve function score: sham operation group,model control group,nimodipine control group(12mg/kg),low dose group(4g/kg),medium dose group(8g/kg),and high dose group(16g/kg).After the rats were re-instilled and conscious,the symptoms of neurological deficits were assessed by Zea Longa grade 5 score,and then scored 8 am daily after ischemia.The rats were given MXYF at 4h after reperfusion for the first,then given it daily at 9am for 7 days,the sham and model control groups were given vehicle(0.5% CMC-Na)(1 mL/100 g),and at the 7 day,collected the blood,and the brain,then detected the related indicators.The levels of SOD,LDH,CAT,MDA,T-AOC and GSH-PX in the serum were detected by kit method.Then used TTC staining to detect the area of cerebral infarction,and the expression of Cyt-c,Bax,Bcl-2,Caspase-3,Caspase-7 and Caspase-9 were detected by Western-blot.Results: We found that MXYF could significantly reduced the neurological score,and effectively decreased the cerebral infarct size.The levels of SOD,GSH-PX,T-AOC and CAT in the serum were significantly increased in MXYF group compared with the model group,and the levels of MDA and LDH were decreased after MXYF treatment.Western-blot showed that MXYF could increased the expression of Bcl-2,and decreased the levels of Bax,Cyt-c,Caspase-7,Caspase-9,and Caspase-3.Conclusions: MXYF could attenuated the cerebral ischemia-reperfusion injury in rats by regulated Bcl-2 family protein expression,inhibited of pro-apoptotic protein expression,and eliminated free radicals to decrease the oxidative stress injury.
Keywords/Search Tags:Cerebral ischemia-reperfusion injury, MXYF, Oxidative stress, Apoptosis, Therapeutic
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