Please note that we have stopped the regular imports of Gene Expression Omnibus (GEO) data into ArrayExpress. This may not be the latest version of this experiment.
E-GEOD-31606 - Hippocampal gene network analysis to determine the effects of coral calcium hydride in an experimental model of accelerated senescence
Released on 22 September 2011, last updated on 12 October 2011
Recent studies strongly support the hypothesis that antioxidant diet inhibits the pathological aging process as shown in senescence-accelerated mouse prone 8 (SAM/P-8). In our previous study, we reported that a diet rich in antioxidants inhibits the pathological aging process, as shown coral calcium hydride (CCH) increased the endogenous antioxidant ability and contributed to prolonging the life-span of SAM/P-8. In order to test the hypothesis that antioxidant CCH supplementation to SAM/P-8 mice would change the gene expression and understand how CCH reverses the acceleration of aging in SAM/P-8 mice, in the current study, we used a DNA array to compare the expression levels in the hippocampus of the brains from 16-week-old SAM/P-8 mice treated or not treated with CCH. The most significant up regulated changes in the gene network of SAM/P-8 mice were free radical scavenging and molecular transport, and genes associated with cell death, cancer, and cell cycle were downregulated. Our findings about changes in these mRNA might be associated with that inhibition of the acceleration of aging is observed in SAM/P-8 mice fed a CCH-diet. Eight-week-old male SAM/P-8 and SAM/R-1 mice were assigned to two groups: the CCH-fed group (fed with CCH for 8 weeks with CE-2 (rodent diet, Clea Japan, Inc., Tokyo, Japan) containing 0.1% CCH) and the control group (fed with CE-2 for 8 weeks).
transcription profiling by array
Toshio Kojima <firstname.lastname@example.org>, Taneaki Oikawa, Toshio Kojima, Yuto Ueda