title: Effective neuroprotection by ischemic postconditioning is associated with a decreased expression of RGMa and inflammation mediators in ischemic rats.
abstract: Whether ischemic postconditioning (IPC) can significantly alleviate ischemic injury hinges on the appropriate measure. In this study, the expression RGMa and IL-1β, IL-6 are investigated to estimate the therapeutic benefits of various postconditioning strategies after cerebral ischemia/reperfusion. The study consists of the sham-operated group and five treatment groups: ischemia/reperfusion (I/R), two proximate ischemic postconditioning (IPC-S and IPC-M), remote postconditioning (RIPC) and delayed postconditioning (DIPC) groups. We find that rats in IPC and RIPC groups exhibit significantly less neural deficit and lower infarct volume than that in I/R and DIPC groups after ischemia/reperfusion. Moreover, in ischemic cortex and hippocampus, the mRNA level of RGMa is much lower in IPC and RIPC groups. Immunohistochemical analysis indicates that the expression of RGMa, IL-1β and IL-6 are reduced in IPC and RIPC groups (especially in IPC-S group). Furthermore, neurofilament staining reveals that the rats in IPC and RIPC groups have less axonal injury than that in I/R and DIPC groups. Our studies suggest that the optimal strategy to attenuate cerebral ischemia/reperfusion is achieved by early, short-term, and multiple cycles of proximal IPC. The cerebral protective effect of IPC may be associated with the decreased expression of RGMa and inflammation mediators.
authors: Department of Neurology and Chongqing Key Laboratory of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
authors: Yuhan
authors: Y
authors: Kong
authors: Mary R
authors: MR
authors: Rogers
authors: Xinyue
authors: X
authors: Qin
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000628:therapy*; D058851:GPI-Linked Proteins; D020244:Infarction, Middle Cerebral Artery / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism*; D057775:Ischemic Postconditioning / Q000379:methods; D008565:Membrane Proteins / Q000096:biosynthesis*; D009419:Nerve Tissue Proteins / Q000096:biosynthesis*; D051381:Rats; D015427:Reperfusion Injury / Q000503:physiopathology*
chemical_list: D058851:GPI-Linked Proteins; D018836:Inflammation Mediators; D008565:Membrane Proteins; D009419:Nerve Tissue Proteins; C551856:RGMA protein, rat
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