Journal
NEUROCHEMICAL RESEARCH
Volume 38, Issue 4, Pages 815-825Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11064-013-0984-5
Keywords
Cerebral ischemia; Ischemic postconditioning; RGM proteins; Rat; Inflammatory factor; Axonal injury
Categories
Funding
- National Science Foundation of China (NSFC) [30770762, 30970987]
- Medical Science Foundation of the First Affiliated Hospital of Chongqing Medical University [YXJJ2009-02, YXJJ2009-14]
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Whether ischemic postconditioning (IPC) can significantly alleviate ischemic injury hinges on the appropriate measure. In this study, the expression RGMa and IL-1 beta, 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-1 beta 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.
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