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Changes in expressions of proinflammatory cytokines IL-1β, TNF-α and IL-6 in the brain of senescence accelerated mouse (SAM) P8
Authors:Kyi Kyi Tha   Yasunobu Okuma   Hiroyuki Miyazaki   Toshihiko Murayama   Takashi Uehara   Rieko Hatakeyama   Yuka Hayashi  Yasuyuki Nomura  
Affiliation:a Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo 060-0812, Japan;b Hokkaido Foundation for Promotion of Scientific and Industrial Technology, Sapporo, Japan
Abstract: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.
Keywords:Senescence-accelerated mouse (SAM)   Aging   Interleukin-1β   (IL-1β  )   Tumor necrosis factor (TNF-β  )   Interleukin-6 (IL-6)   Hippocampus   Cerebral cortex   Hypothalamus   Learning and memory
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