the chronic protective effects of limb remote preconditioning and the underlying mechanisms involved in inflammatory factors in rat stroke慢性肢体远程预处理的保护作用和潜在机制参与炎性因子在大鼠中风.pdfVIP

the chronic protective effects of limb remote preconditioning and the underlying mechanisms involved in inflammatory factors in rat stroke慢性肢体远程预处理的保护作用和潜在机制参与炎性因子在大鼠中风.pdf

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the chronic protective effects of limb remote preconditioning and the underlying mechanisms involved in inflammatory factors in rat stroke慢性肢体远程预处理的保护作用和潜在机制参与炎性因子在大鼠中风

The Chronic Protective Effects of Limb Remote Preconditioning and the Underlying Mechanisms Involved in Inflammatory Factors in Rat Stroke 1,2,3,4. 1,2,5. 6 1,2 Dingtai Wei , Chuancheng Ren , Xiaoyuan Chen , Heng Zhao * 1 Department of Neurosurgery, Stanford University, Stanford, California, United States of America, 2 Stroke Center, Stanford University, Stanford, California, United States of America, 3 Department of Radiology, Tianjin Medical University General Hospital, Tianjin, China, 4 Department of Radiology, Fujian Medical University Ningde Hospital, Fujian, China, 5 Shanghai No.5 Hospital, Fudan University, Shanghai, China, 6 Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Bethesda, Maryland, United States of America Abstract We recently demonstrated that limb remote preconditioning (LRP) protects against focal ischemia measured 2 days post- stroke. Here, we studied whether LRP provides long-term protection and improves neurological function. We also investigated whether LRP transmits its protective signaling via the afferent nerve pathways from the preconditioned limb to the ischemic brain and whether inflammatory factors are involved in LRP, including the novel galectin-9/Tim-3 inflammatory cell signaling pathway, which induces cell death in lymphocytes. LRP in the left hind femoral artery was performed immediately before stroke. LRP reduced brain injury size both at 2 days and 60 days post-stroke and improved behavioral outcomes for up to 2 months. The sensory nerve inhibitors capsaicin and hexamethonium, a ganglion blocker, abolished the protective effects of

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