TY - JOUR
T1 - Changes in expressions of proinflammatory cytokines IL-1β, TNF-α and IL-6 in the brain of senescence accelerated mouse (SAM) P8
AU - Tha, Kyi Kyi
AU - Okuma, Yasunobu
AU - Miyazaki, Hiroyuki
AU - Murayama, Toshihiko
AU - Uehara, Takashi
AU - Hatakeyama, Rieko
AU - Hayashi, Yuka
AU - Nomura, Yasuyuki
N1 - Funding Information:
The authors would like to thank Dr T. Takeda (Kyoto University) for the original provision of SAM. This study was supported in part by Grants-in-Aid from the Ministry of Education, Science, Sports and Culture, Japan and by Joint-Research Project for Regional Intensive from Japan Science and Technology Corporation.
PY - 2000/12/1
Y1 - 2000/12/1
N2 - The senescence-accelerated mouse (SAM) is known to be a murine model for accelerated aging. The SAMP8 strain shows age-related deterioration of learning and memory at an earlier age than control mice (SAMR1). In the present study, we investigated the changes in expressions of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the brain of SAMP8. In the hippocampus of 10 months old SAMP8, the expression of IL-1 mRNA was significantly elevated in comparison with that of SAMR1. In both strains of SAMs, increases in IL-1β protein in the brain were observed at 10 months of age compared with 2 and 5 months. The only differences found between the strain in protein levels were at 10 months and were elevations in IL-1β in the hippocampus and hypothalamus, and in TNF-α and IL-6 in the cerebral cortex and the hippocampus in SAMP8 as compared with SAMR1. However, lipopolysaccharide-induced increases in the expression of these cytokines in brain did not differ between SAMP8 and SAMR1. Increases in expression of proinflammatory cytokines in the brain may be involved in the age-related neural dysfunction and/or learning deficiency in SAMP8. Copyright (C) 2000 Elsevier Science B.V.
AB - The senescence-accelerated mouse (SAM) is known to be a murine model for accelerated aging. The SAMP8 strain shows age-related deterioration of learning and memory at an earlier age than control mice (SAMR1). In the present study, we investigated the changes in expressions of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the brain of SAMP8. In the hippocampus of 10 months old SAMP8, the expression of IL-1 mRNA was significantly elevated in comparison with that of SAMR1. In both strains of SAMs, increases in IL-1β protein in the brain were observed at 10 months of age compared with 2 and 5 months. The only differences found between the strain in protein levels were at 10 months and were elevations in IL-1β in the hippocampus and hypothalamus, and in TNF-α and IL-6 in the cerebral cortex and the hippocampus in SAMP8 as compared with SAMR1. However, lipopolysaccharide-induced increases in the expression of these cytokines in brain did not differ between SAMP8 and SAMR1. Increases in expression of proinflammatory cytokines in the brain may be involved in the age-related neural dysfunction and/or learning deficiency in SAMP8. Copyright (C) 2000 Elsevier Science B.V.
KW - Aging
KW - Cerebral cortex
KW - Hippocampus
KW - Hypothalamus
KW - Interleukin-1β (IL-1β)
KW - Interleukin-6 (IL-6)
KW - Learning and memory
KW - Senescence-accelerated mouse (SAM)
KW - Tumor necrosis factor (TNF-β)
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U2 - 10.1016/S0006-8993(00)02883-3
DO - 10.1016/S0006-8993(00)02883-3
M3 - Article
C2 - 11121526
AN - SCOPUS:0034564998
VL - 885
SP - 25
EP - 31
JO - Molecular Brain Research
JF - Molecular Brain Research
SN - 0006-8993
IS - 1
ER -