El Khashab I.H.Abdelsalam R.M.Elbrairy A.I.Attia A.S.Department of Pharmacology and ToxicologyFaculty of PharmacyModern Sciences and Arts University (MSA)GizaEgypt; Department of Pharmacology and ToxicologyFaculty of PharmacyCairo UniversityEgypt2020-01-092020-01-0920197533322https://doi.org/10.1016/j.biopha.2019.108619PubMed ID 30797156https://t.ly/rx7kxScopusGlobal cerebral ischemia is a leading cause of mortality worldwide. Several biomechanisms play a role in the pathology of cerebral ischemia reperfusion damage, such as oxidative stress, inflammation, apoptosis and excitotoxicity. Chrysin, a natural flavonoid with many important biological activities, was investigated in the present study for its possible neuroprotective properties in a rat model of global ischemia reperfusion. Male Wistar rats were allocated into three groups: sham-operated, ischemia/reperfusion, and chrysin (30 mg/kg) groups. All animals were subjected to ischemia for 15 min followed by reperfusion for 60 min, except for the sham-operated group. Rats were decapitated, then both hippocampi were rapidly excised to evaluate several biomarkers that reflect ischemic injury. The obtained results showed that pre-treatment with chrysin attenuated ischemia-induced oxidative stress by: (i) restoring the glutathione level; and (ii) depressing the levels/activities of thiobarbituric acid reactive substances, the hippocampal NADPH, as well as the xanthine oxidase. Exposure to chrysin also suppressed the inflammation accompanying the ischemia/reperfusion (I/R) damage, through increasing the interleukin-10 level, while decreasing the levels of both interleukin-6 and tumour necrosis factor-alpha. Moreover, an increase in Bcl2 and a decrease in both BAX and Hsp90 levels were recorded following chrysin exposure, which was also accompanied with elevated glutamate and aspartate levels. In conclusion, chrysin has demonstrated an anti-ischemic potential, through attenuation of the mechanisms underlying I/R injury. These data add to the knowledge on the significance of natural flavonoids as neuroprotective agents. � 2019 The AuthorsEnglishAntioxidantApoptosisChrysinInflammationIschemia-reperfusionNeuroprotectionchrysininterleukin 10interleukin 6neurotransmitterprotein bcl 2tumor necrosis factorchrysinflavonoidneuroprotective agentanimal experimentanimal modelapoptosisArticleblood brain barrierbrain ischemiacommon carotid arterycomparative studycontrolled studydecapitationenzyme activationinflammationmalenonhumanoxidation reduction reactionoxidative stresspriority journalratreperfusion injuryanimalapoptosisbrain ischemiadrug effectinflammationmetabolismoxidative stresspathologyphysiologyWistar ratAnimalsApoptosisBrain IschemiaFlavonoidsInflammationMaleNeuroprotective AgentsOxidative StressRatsRats, WistarArticlehttps://doi.org/10.1016/j.biopha.2019.108619PubMed ID 30797156