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Interleukin-10 endogenously expressed in microglia prevents lipopolysaccharide-induced neurodegeneration in the rat cerebral cortex in vivo.

Park, KW; Lee, HG; Jin, BK; Lee, YB
Experimental & molecular medicine, 39(6):812-819, 2007
Journal Title
Experimental & molecular medicine
A degree of brain inflammation is required for repair of damaged tissue, but excessive inflammation causes neuronal cell death. Here, we observe that IL-10 is expressed in LPS-injected rat cerebral cortex, contributing to neuronal survival. Cells immunopositive for IL-10 were detected as early as 8 h post-injection and persisted for up to 3 d, in parallel with the expression of IL-1beta, TNF-alpha, and iNOS. Double immunofluorescence staining showed that IL-10 expression was localized mainly in activated microglia. Next, we examined the neuroprotective effects of IL-10 using IL-10 neutralizing antibody (IL-10NA). Blockade of IL-10 action caused a significant loss of neurons both 3 d and 7 d after LPS injection. Further, the induction of mRNA species encoding IL-1beta, TNF-alpha, and iNOS, reactive oxygen species (ROS) production, and NADPH oxidase activation, increased after co-injection of LPS and IL-10NA, compared to the levels seen after injection of LPS alone. Taken together, these results clearly suggest that LPS-induced endogenous expression of IL-10 in microglia contributes to neuronal survival by inhibiting brain inflammation.
MeSH terms
AnimalsCerebral Cortex/drug effectsCerebral Cortex/pathology*Fluorescent Antibody TechniqueInterleukin-10/immunologyInterleukin-10/physiology*Lipopolysaccharides/pharmacology*Microglia/cytologyMicroglia/metabolism*Nerve Degeneration/pathologyNerve Degeneration/prevention & control*Neurons/cytologyNeurons/drug effectsNeurons/metabolism*Nitric Oxide Synthase/geneticsNitric Oxide Synthase/metabolismRatsRats, Sprague-DawleyReactive Oxygen Species/metabolism
Appears in Collections:
Journal Papers > Research Organization > Institute for Medical Sciences
AJOU Authors
진, 병관이, 용범
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