4.5 Article

Maintenance of anti-inflammatory cytokines and reduction of glial activation in the ischemic hippocampal CA1 region preconditioned with lipopolysaccharide

期刊

JOURNAL OF THE NEUROLOGICAL SCIENCES
卷 296, 期 1-2, 页码 69-78

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.jns.2010.06.004

关键词

Lipopolysaccharide; Ischemia; Hippocampus; Neuroprotection; Anti-inflammatory cytokine; Glial activation

资金

  1. Ministry of Education, Science and Technology [2010-0009165]
  2. Korea Ministry of Education, Science and Technology (Medical & Bio-material Research Center)
  3. National Research Foundation of Korea [2010-0009165, 2009-50378] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Lipopolysaccharide (LPS) induces a strong immune response, and pretreatment with low dose of LPS suppresses the production of proinflammatory mediators. In the present study, we investigated the effect of LPS preconditioning on the delayed neuronal death in the gerbil hippocampal CA1 region after 5 min of transient cerebral ischemia. LPS preconditioning showed neuroprotective effects against ischemic damage in the hippocampal CA1 region after ischemic insult: About 92% of neurons in the CA1 region survived in the LPS-treated ischemia group. LPS preconditioning maintained anti-inflammatory cytokines, such as interleukin (IL)-4 and IL-13, in pyramidal neurons in the CA1 region after ischemia/reperfusion. In addition, IL-4 and IL-13 protein levels in the CM region of the LPS-treated ischemia group were similar to the vehicle-treated sham group. We found that reactive gliosis was markedly attenuated in the CA1 region of the LPS-treated ischemia group compared to the vehicle-treated ischemia group using immunohistochemistry of glial fibrillary acidic protein for astrocytes, and ionized calcium-binding adapter molecule 1 and isolectin B4 for microglia. These results indicate that LPS preconditioning may provide neuroprotection in the ischemic hippocampal CA1 region via maintenance of anti-inflammatory cytokines and suppression of glial activation. (C) 2010 Elsevier B.V. All rights reserved.

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