We examined the effect of astaxanthin (AST) on suppression of renal injury by improvement in intestinal flora in adenine-induced renal injury model. Histopathologically, moderate tubular damage and inflammatory cell infiltration were observed in 0.1% adenine-administrated group, and these changes were ameliorated by AST co-administration. In 0.2% adenine-administered group, renal injury became severer than 0.1% adenine-administered group and this was slightly ameliorated by AST co-administration. Positive reaction for HNF4α in the nuclei of tubular epithelial cells decreased in injured tubules which was recovered by AST co-administration. The number of CD3- and F4/80-positive cells increased by adenine administration and decreased by AST co-administration in both dose groups. Intestinal flora did not change by AST co-administration. The mRNA expression of inflammatory cytokines did not change by AST co-administration. In the present study, AST had some role in the anti-inflammatory effect, but not in the intestinal environment. Moreover, recovery of HNF4α in injured tubules indicated the amelioration of tubular injury by AST and the utility of HNF4α as a tubular injury marker. Based on the results of this experiment and other reports it was suggested that amelioration effect of AST on renal injury might be different according to the degree and quality of injury.
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