Scorpion venom heat-resistant peptide(SVHRP)is a component purified from Buthus martensii Karsch scorpion venom. Our previous studies have shown that SVHRP is neuroprotective in models of Alzheimer’s disease and Park...Scorpion venom heat-resistant peptide(SVHRP)is a component purified from Buthus martensii Karsch scorpion venom. Our previous studies have shown that SVHRP is neuroprotective in models of Alzheimer’s disease and Parkinson’s disease. The present study aimed to explore the potential neuroprotective effects of SVHRP on cerebral ischemia/reperfusion(I/R) injury, using a mouse model of middle cerebral artery occlusion/reperfusion(MCAO/R) and a cellular model of oxygen-glucose deprivation/reoxygenation(OGD/R). Our results showed that SVHRP treatment decreased the neurological deficit scores, edema formation, infarct volume and neuronal loss in the MCAO/R mice, and protected primary neurons against OGD/R insult. SVHRP pretreatment suppressed the alterations in protein levels of N-methyl-D-aspartate receptors(NMDARs) and phosphorylated p38 MAPK as well as some proinflammatory factors in both the animal and cellular models. These results suggest that SVHRP has neuroprotective effects against cerebral I/R injury, which might be associated with inhibition of the NMDA-MAPKmediated excitotoxicity.展开更多
基金by grants from National Natural Science Foundation of China(81571061 and 81671061)the Scientific Study Project for Institutes of Higher Learning,Ministry of Education,Liaoning Province,China(LZ2017001)+1 种基金Liaoning Provincial Key R&D Program(2019JH2/10300043)the Liaoning Revitalization Talents Program(XLYC1808031).
文摘Scorpion venom heat-resistant peptide(SVHRP)is a component purified from Buthus martensii Karsch scorpion venom. Our previous studies have shown that SVHRP is neuroprotective in models of Alzheimer’s disease and Parkinson’s disease. The present study aimed to explore the potential neuroprotective effects of SVHRP on cerebral ischemia/reperfusion(I/R) injury, using a mouse model of middle cerebral artery occlusion/reperfusion(MCAO/R) and a cellular model of oxygen-glucose deprivation/reoxygenation(OGD/R). Our results showed that SVHRP treatment decreased the neurological deficit scores, edema formation, infarct volume and neuronal loss in the MCAO/R mice, and protected primary neurons against OGD/R insult. SVHRP pretreatment suppressed the alterations in protein levels of N-methyl-D-aspartate receptors(NMDARs) and phosphorylated p38 MAPK as well as some proinflammatory factors in both the animal and cellular models. These results suggest that SVHRP has neuroprotective effects against cerebral I/R injury, which might be associated with inhibition of the NMDA-MAPKmediated excitotoxicity.
