Myricetin and Berberine Combination Ameliorates Brain Damage Induces by Cerebral Ischemia/Reperfusion Injury in Rats
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Abstract
Background: Cerebral ischemic/reperfusion (I/R)injurymayresultin considerable tissuedamageviainductionofinflammatorymediatorsandoxidativestressinbrain tissue.Theaimofthepresentstudy wastoinvestigatevalueofusingcombinedmyricetin plus berberinetreatmentinprotection againstshort-term globalcerebralI/Rinjuryin rats. MaterialandMethods:Thirty sixWistar-albinoratswereenrolledinthestudy,divided intofourgroupsincluding Shamgroup,I/Rgroup,I/R+(control-vehicle DMSO)andI/R+ myricetin 50 mg/kgplus berberine5 mg/kginjectedintraperitoneally1 hourbefore inductionof ischemia. Measurementof braintissueIL-1β,ICAM- 1, caspase-3, Notch 1 andJagged1wasdoneafteronehourofreperfusioninadditiontotheassessmentof brain infarcted areaand histopathologicaltissue analysis.
Results:MyricetinandberberinecombinationattenuatesthecerebralI/Rinjury induced increase in inflammatory cytokine (IL-1β), adhesion molecule (ICAM-1) and proapoptotic enzyme (caspase-3).Additionally,itreducesthe size of infarcted area and histopathologicaldamage.However,suchprotectiveeffectwasnotfoundtobe mediated by Notch1signalingpathwaybecausedrugstreatmentdidn’tshowanychangesinthe increased levels of Notch1 and Jagged 1 seen in brain withI/Rinjury.
Conclusions:Myricetinandberberine combinationhasa neurocytoprotectiveoutcome againstcerebralI/Rinjurywhichismanifestedasanti-inflammatory anti-apoptoticeffect thatpreservedcellstructure andviability,neverthelessthiseffectisnotmediatedthrough Notch 1 signalingpathway.