Scorpion Venom Heat-Resistant Peptide is Neuroprotective against Cerebral Ischemia-Reperfusion Injury in Association with the NMDA-MAPK Pathway

被引:0
|
作者
Xu-Gang Wang [1 ,2 ,3 ]
Dan-Dan Zhu [1 ,3 ]
Na Li [4 ]
Yue-Lin Huang [1 ]
Ying-Zi Wang [1 ,3 ]
Ting Zhang [1 ]
Chen-Mei Wang [1 ]
Bin Wang [1 ]
Yan Peng [1 ]
Bi-Ying Ge [1 ]
Shao Li [1 ,2 ]
Jie Zhao [1 ,2 ]
机构
[1] Liaoning Provincial Key Laboratory of Cerebral Diseases,Department of Physiology, College of Basic Medical Sciences, Dalian Medical University
[2] National-Local Joint Engineering Research Center for Drug-Research and Development of Neurodegenerative Diseases,Dalian Medical University
[3] The Second Hospital of Dalian Medical University
[4] National-Local Joint Engineering Research Center for DrugResearch and Development of Neurodegenerative Diseases,Dalian Medical University
基金
中国国家自然科学基金;
关键词
Scorpion venom heat-resistant peptide; Cerebral ischemia/reperfusion injury; Neuroprotection; NMDARs; p38; MAPK;
D O I
暂无
中图分类号
R743 [脑血管疾病];
学科分类号
摘要
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.
引用
收藏
页码:243 / 253
页数:11
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