Study summary · research use only
5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranoside-attenuates LPS/D-Gal-induced acute hepatitis in mice
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this study using a mouse model of LPS/D-galactosamine-induced acute hepatitis, the authors investigated the AMP-activated protein kinase (AMPK) activator AICAR (5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside). The abstract reports that AICAR treatment suppressed elevation of plasma aminotransferases, alleviated histopathological abnormalities, and inhibited LPS/D-Gal-induced up-regulation of TNF-alpha, nitric oxide and myeloperoxidase. It states AICAR also suppressed pro-apoptotic Bax, caspase-3 cleavage, elevation of hepatic caspase-3, -8 and -9 activities, and TUNEL-positive cells. The authors suggest AICAR could attenuate LPS/D-Gal-induced acute hepatitis and that AMPK might be a target for inflammation-based liver disorders.
Abstract
The AMP-activated protein kinase (AMPK)-mediated energy-sensing signals play important roles in reprogramming the expression of inflammatory genes. In the present study, the potential effects of the AMPK activator 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR) were investigated in a mouse model with LPS/D-Gal-induced acute hepatitis. Our experimental data indicated that treatment with AICAR suppressed the elevation of plasma aminotransferases and alleviated the histopathological abnormalities in mice exposed to LPS/D-Gal. Treatment with AICAR also inhibited the LPS/D-Gal-induced up-regulation of TNF-α, NO and myeloperoxidase. In addition, the LPS/D-Gal-induced expression of pro-apoptotic factor Bax, cleavage of caspase-3, elevation of hepatic caspase-3, caspase-8, caspase-9 activities and induction of terminal deoxynucleotidyl transferase-mediated nucleotide nick-end labeling-positive cells were all suppressed by AICAR. These results suggested that the AMPK activator AICAR could attenuate LPS/D-Gal-induced acute hepatitis, which implies that AMPK might become a novel target for the treatment of inflammation-based liver disorders.
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