Single low-dose lipopolysaccharide preconditioning:neuroprotective against axonal injury and modulates glial cells

作     者：Ryan C.Turner Zachary J.Naser Brandon P.Lucke-Wold Aric F.Logsdon Reyna L.Vangilder Rae R.Matsumoto Jason D.Huber Charles L.Rosen 

作者机构：Department of NeurosurgeryWest Virginia UniversitySchool of MedicineMorgantownWV26506USA Center for NeuroscienceWest Virginia UniversitySchool of MedicineMorgantownWV 26506USA Department of Basic Pharmaceutical SciencesWest Virginia UniversitySchool of PharmacyMorgantownWV 26506USA Center for Health RestorationWest Virginia UniversitySchool of NursingMorgantownWV 26506USA 

出 版 物：《Neuroimmunology and Neuroinflammation》 (神经免疫与神经炎症（英文版）)

年 卷 期：2017年第4卷第1期

页      面：6-15页

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

主　　题：Lipopolysaccharide preconditioning oncostatin M receptor diffuse axonal injury gliosis neuroprotection 

摘      要：Aim:Over 7 million traumatic brain injuries (TBI) are reported each year in the United ***,treatments and neuroprotection following TBI are limited because secondary injury cascades are poorly *** (LPS) administration before controlled cortical impact can contribute to ***,the underlying mechanisms and whether LPS preconditioning confers neuroprotection against closed-head injuries remains ***:The authors hypothesized that preconditioning with a low dose of LPS (0.2 mg/kg) would regulate glial reactivity and protect against diffuse axonal injury induced by weight *** was administered 7 days prior to *** administration reduced locomotion,which recovered completely by time of ***:LPS preconditioning significantly reduced the post-injury gliosis response near the corpus callosum,possibly by downregulating the oncostatin M *** novel findings demonstrate a protective role of LPS preconditioning against diffuse axonal *** preconditioning successfully prevented neurodegeneration near the corpus callosum,as measured by fluorojade ***:Further work is required to elucidate whether LPS preconditioning confers long-term protection against behavioral deficits and to elucidate the biochemical mechanisms responsible for LPS-induced neuroprotective effects.