Skip to content

Study · Animal study (in vivo) · mouse · 2015

11 results

5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranoside-attenuates LPS/D-Gal-induced acute hepatitis in mice.

Zhou D, Ai Q, Lin L, Gong X, Ge P, Che Q, Wan J, Wen A, Zhang L

Innate immunity15 May 2015Cited by 9 (Europe PMC)

PMID25979627 (opens in a new tab)DOI10.1177/1753425915586231 (opens in a new tab)PepBankPUB-25979627
Publisher pagePubMedAsk about this study
Jump to 11 results

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study11

11 results from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to LPS/D-Gal, AICAR suppressed elevated plasma aminotransferases.

    In plain wordsIn mice with induced hepatitis, AICAR reduced elevated blood aminotransferases.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreasePlasma aminotransferases
    Study

    mousen: not reported in source

    LPS/D-Gal-induced acute hepatitis
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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.
    1 context sentence
    Summary · context
    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.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to LPS/D-Gal, AICAR alleviated histopathological abnormalities.

    In plain wordsIn mice with induced hepatitis, AICAR reduced abnormal tissue changes.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseLiver histopathology
    Study

    mousen: not reported in source

    LPS/D-Gal-induced acute hepatitis
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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.
    1 context sentence
    Summary · context
    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.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to LPS/D-Gal, AICAR inhibited TNF-alpha upregulation.

    In plain wordsIn mice with induced hepatitis, AICAR reduced the rise in TNF-alpha.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseTNF-alpha
    Study

    mousen: not reported in source

    LPS/D-Gal-induced acute hepatitis
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment with AICAR also inhibited the LPS/D-Gal-induced up-regulation of TNF-α, NO and myeloperoxidase.
    1 context sentence
    Summary · context
    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.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to LPS/D-Gal, AICAR inhibited nitric oxide upregulation.

    In plain wordsIn mice with induced hepatitis, AICAR reduced the rise in nitric oxide.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseNitric oxide
    Study

    mousen: not reported in source

    LPS/D-Gal-induced acute hepatitis
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment with AICAR also inhibited the LPS/D-Gal-induced up-regulation of TNF-α, NO and myeloperoxidase.
    1 context sentence
    Summary · context
    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.
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to LPS/D-Gal, AICAR inhibited myeloperoxidase upregulation.

    In plain wordsIn mice with induced hepatitis, AICAR reduced the rise in myeloperoxidase.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseMyeloperoxidase
    Study

    mousen: not reported in source

    LPS/D-Gal-induced acute hepatitis
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Treatment with AICAR also inhibited the LPS/D-Gal-induced up-regulation of TNF-α, NO and myeloperoxidase.
    1 context sentence
    Summary · context
    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.
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to LPS/D-Gal, AICAR suppressed pro-apoptotic Bax expression.

    In plain wordsIn mice with induced hepatitis, AICAR reduced Bax expression.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseBax expression
    Study

    mousen: not reported in source

    LPS/D-Gal-induced acute hepatitis
    Outcome group
    Cell viability and death · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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.
    1 context sentence
    Summary · context
    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.
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to LPS/D-Gal, AICAR suppressed caspase-3 cleavage.

    In plain wordsIn mice with induced hepatitis, AICAR reduced caspase-3 cleavage.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCaspase-3 cleavage
    Study

    mousen: not reported in source

    LPS/D-Gal-induced acute hepatitis
    Outcome group
    Cell viability and death · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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.
    1 context sentence
    Summary · context
    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.
  8. 08AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to LPS/D-Gal, AICAR suppressed elevated hepatic caspase-3 activity.

    In plain wordsIn mice with induced hepatitis, AICAR reduced liver caspase-3 activity.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseHepatic caspase-3 activity
    Study

    mousen: not reported in source

    LPS/D-Gal-induced acute hepatitis
    Outcome group
    Cell viability and death · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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.
    1 context sentence
    Summary · context
    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.
  9. 09AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to LPS/D-Gal, AICAR suppressed elevated hepatic caspase-8 activity.

    In plain wordsIn mice with induced hepatitis, AICAR reduced liver caspase-8 activity.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseHepatic caspase-8 activity
    Study

    mousen: not reported in source

    LPS/D-Gal-induced acute hepatitis
    Outcome group
    Cell viability and death · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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.
    1 context sentence
    Summary · context
    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.
  10. 10AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to LPS/D-Gal, AICAR suppressed elevated hepatic caspase-9 activity.

    In plain wordsIn mice with induced hepatitis, AICAR reduced liver caspase-9 activity.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseHepatic caspase-9 activity
    Study

    mousen: not reported in source

    LPS/D-Gal-induced acute hepatitis
    Outcome group
    Cell viability and death · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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.
    1 context sentence
    Summary · context
    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.
  11. 11AnimalAnimal study (in vivo)Efficacy outcome

    In mice exposed to LPS/D-Gal, AICAR suppressed induction of TUNEL-positive cells.

    In plain wordsIn mice with induced hepatitis, AICAR reduced cells with DNA fragmentation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseTUNEL-positive cells
    Study

    mousen: not reported in source

    LPS/D-Gal-induced acute hepatitis
    Outcome group
    Cell viability and death · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    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.
    1 context sentence
    Summary · context
    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.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    21 Oct 2026, 15:58 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 12:50 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

PepBank is a research reference. Talk to a doctor before you use any peptide.