Maintenance of anti-inflammatory cytokines and reduction of glial activation in the ischemic hippocampal CA1 region preconditioned with lipopolysaccharide.
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 CA1 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.
Yu
Jia Tian
JT
Department of Anatomy and Neurobiology, and Institute of Neurodegeneration and Neuroregeneration, College of Medicine, Hallym University, Chuncheon 200-702, Republic of Korea.
Lee
Choong Hyun
CH
Yoo
Ki-Yeon
KY
Choi
Jung Hoon
JH
Li
Hua
H
Park
Ok Kyu
OK
Yan
Bingchun
B
Hwang
In Koo
IK
Kwon
Young-Guen
YG
Kim
Young-Myeong
YM
Won
Moo-Ho
MH
D000818:Animals; D015153:Blotting, Western; D002545:Brain Ischemia / Q000276:immunology* / Q000378:metabolism* / Q000473:pathology; D056547:CA1 Region, Hippocampal / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D016207:Cytokines / Q000378:metabolism*; D005456:Fluorescent Dyes; D005849:Gerbillinae; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry; D018793:Interleukin-13 / Q000378:metabolism; D002546:Ischemic Attack, Transient / Q000276:immunology / Q000378:metabolism; D019194:Ischemic Preconditioning; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008262:Macrophage Activation / Q000502:physiology*; D008297:Male; D009043:Motor Activity / Q000502:physiology; D009419:Nerve Tissue Proteins / Q000096:biosynthesis; D009457:Neuroglia / Q000502:physiology*
D016207:Cytokines; D005456:Fluorescent Dyes; D005904:Glial Fibrillary Acidic Protein; D018793:Interleukin-13; D008070:Lipopolysaccharides; D009419:Nerve Tissue Proteins