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Study · Animal study (in vivo) · rat · 2019

13 results

AMPK agonist AICAR ameliorates portal hypertension and liver cirrhosis via NO pathway in the BDL rat model.

Hu L, Su L, Dong Z, Wu Y, Lv Y, George J, Wang J

Journal of molecular medicine (Berlin, Germany)5 Feb 2019Cited by 29 (Europe PMC)

PMID30721324 (opens in a new tab)PMCIDPMC6394556 (opens in a new tab)DOI10.1007/s00109-019-01746-4 (opens in a new tab)PepBankPUB-30721324
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Summary

Recent studies have indicated that the Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) pathway is closely involved in liver fibrosis and other fibrotic diseases. However, whether targeting the AMPK pathway can rescue liver fibrosis and its complications, such as portal hypertension, is unknown. This study aimed to explore the therapeutic value of AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside), an agonist of the AMPK pathway, on liver fibrosis and portal hypertension in bile duct ligation (BDL) rats. In vitro experiments showed that the gene expression levels of TGF-b, a-SMA, and collagen 1 in primary rat hepatic stellate cells (HSCs) were significantly decreased after AICAR treatment. The p-eNOS expression and nitric oxide (NO) production were increased by AICAR administration in sinusoidal endothelial cells (SECs). For in vivo animal studies, AICAR acutely decreased portal pressure in the BDL and CCL4 fibrotic rats, but not in the partial portal vein ligation (PVL) rats, without changes in systemic hemodynamics. It was also observed by using intravital fluorescence microscopy that AICAR led to sinusoidal vasodilation in situ experiment. We propose that the relevant mechanisms may be related to the activation of the AMPK/NO pathway in SECs and that this activation promoted NO production in the liver, thereby promoting hepatic sinusoid microcirculation and decreased intrahepatic resistance. The results were verified using the NO inhibitor L-NAME. Chronic AICAR treatment also showed profound beneficial effects on the BDL model rats. The hemodynamic condition was greatly improved, but the positive effect could be partially blocked by L-NAME. Moreover, AICAR also decreased hepatic fibrogenesis in the BDL rats. KEY MESSAGES: Acute and chronic use of AICAR could alleviate portal pressure without changing systemic hemodynamics. AICAR induced sinusoidal vasodilation by improving NO bioavailability and ameliorating endothelial dysfunction in vivo and in vitro. AICAR could alleviate liver cirrhosis in the BDL model rats.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study13

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In BDL rats, acute AICAR treatment decreased portal pressure.

    In plain wordsIn rats with bile duct ligation, AICAR reduced portal pressure after acute treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseAcute portal pressure in BDL rats
    Study

    ratn: not reported in source

    Bile duct ligation
    Outcome group
    Blood pressure · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    For in vivo animal studies, AICAR acutely decreased portal pressure in the BDL and CCL4 fibrotic rats, but not in the partial portal vein ligation (PVL) rats, without changes in systemic hemodynamics.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In CCL4 fibrotic rats, acute AICAR treatment decreased portal pressure.

    In plain wordsIn rats with CCL4-induced liver fibrosis, AICAR reduced portal pressure after acute treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseAcute portal pressure in CCL4 rats
    Study

    ratn: not reported in source

    CCL4-induced liver fibrosis
    Outcome group
    Blood pressure · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    For in vivo animal studies, AICAR acutely decreased portal pressure in the BDL and CCL4 fibrotic rats, but not in the partial portal vein ligation (PVL) rats, without changes in systemic hemodynamics.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In partial portal vein ligation rats, acute AICAR treatment did not decrease portal pressure.

    In plain wordsIn rats with partial portal vein ligation, AICAR did not reduce portal pressure.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeAcute portal pressure in PVL rats
    Study

    ratn: not reported in source

    Partial portal vein ligation
    Outcome group
    Blood pressure · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    For in vivo animal studies, AICAR acutely decreased portal pressure in the BDL and CCL4 fibrotic rats, but not in the partial portal vein ligation (PVL) rats, without changes in systemic hemodynamics.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In the reported rat portal hypertension models, acute AICAR treatment did not change systemic hemodynamics.

    In plain wordsIn rat portal hypertension models, acute AICAR treatment did not change systemic blood circulation measurements.

    Peptide
    AICAR (acadesine)
    Outcome
    No significant changeSystemic hemodynamics
    Study

    ratn: not reported in source

    BDL, CCL4 fibrosis and PVL models
    Outcome group
    Blood pressure · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    For in vivo animal studies, AICAR acutely decreased portal pressure in the BDL and CCL4 fibrotic rats, but not in the partial portal vein ligation (PVL) rats, without changes in systemic hemodynamics.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In rats, AICAR caused sinusoidal vasodilation observed by intravital fluorescence microscopy.

    In plain wordsIn rats, AICAR widened liver sinusoids during microscopy.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseSinusoidal vasodilation
    Study

    ratn: not reported in source

    In situ hepatic microscopy
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    It was also observed by using intravital fluorescence microscopy that AICAR led to sinusoidal vasodilation in situ experiment.
    1 context sentence
    Summary · context
    For in vivo animal studies, AICAR acutely decreased portal pressure in the BDL and CCL4 fibrotic rats, but not in the partial portal vein ligation (PVL) rats, without changes in systemic hemodynamics.
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    In BDL rats, chronic AICAR treatment improved the hemodynamic condition.

    In plain wordsIn rats with bile duct ligation, chronic AICAR treatment improved blood circulation measurements.

    Peptide
    AICAR (acadesine)
    Outcome
    Direction not reportedChronic hemodynamic condition
    Study

    ratn: not reported in source

    Bile duct ligation
    Outcome group
    Blood pressure · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The hemodynamic condition was greatly improved, but the positive effect could be partially blocked by L-NAME.
    1 context sentence
    Summary · context
    Chronic AICAR treatment also showed profound beneficial effects on the BDL model rats.
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    In BDL rats, AICAR decreased hepatic fibrogenesis.

    In plain wordsIn rats with bile duct ligation, AICAR reduced liver scar formation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseHepatic fibrogenesis
    Study

    ratn: not reported in source

    Bile duct ligation
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, AICAR also decreased hepatic fibrogenesis in the BDL rats.
  8. 08LabIn vitro (cells)Mechanism

    In primary rat hepatic stellate cells, AICAR significantly decreased TGF-b gene expression.

    In plain wordsIn cells from rat livers, AICAR reduced TGF-b gene expression.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseTGF-b gene expression
    Study

    ratn: not reported in source

    Primary hepatic stellate cells
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro experiments showed that the gene expression levels of TGF-b, a-SMA, and collagen 1 in primary rat hepatic stellate cells (HSCs) were significantly decreased after AICAR treatment.
  9. 09LabIn vitro (cells)Mechanism

    In primary rat hepatic stellate cells, AICAR significantly decreased a-SMA gene expression.

    In plain wordsIn cells from rat livers, AICAR reduced a-SMA gene expression.

    Peptide
    AICAR (acadesine)
    Outcome
    Decreasea-SMA gene expression
    Study

    ratn: not reported in source

    Primary hepatic stellate cells
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro experiments showed that the gene expression levels of TGF-b, a-SMA, and collagen 1 in primary rat hepatic stellate cells (HSCs) were significantly decreased after AICAR treatment.
  10. 10LabIn vitro (cells)Mechanism

    In primary rat hepatic stellate cells, AICAR significantly decreased collagen 1 gene expression.

    In plain wordsIn cells from rat livers, AICAR reduced collagen 1 gene expression.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseCollagen 1 gene expression
    Study

    ratn: not reported in source

    Primary hepatic stellate cells
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In vitro experiments showed that the gene expression levels of TGF-b, a-SMA, and collagen 1 in primary rat hepatic stellate cells (HSCs) were significantly decreased after AICAR treatment.
  11. 11LabIn vitro (cells)Mechanism

    In sinusoidal endothelial cells, AICAR increased p-eNOS expression.

    In plain wordsIn lab tests, AICAR increased p-eNOS in sinusoidal endothelial cells.

    Peptide
    AICAR (acadesine)
    Outcome
    Increasep-eNOS expression
    Study

    n: not reported in source

    Sinusoidal endothelial cells
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The p-eNOS expression and nitric oxide (NO) production were increased by AICAR administration in sinusoidal endothelial cells (SECs).
  12. 12LabIn vitro (cells)Mechanism

    In sinusoidal endothelial cells, AICAR increased nitric oxide production.

    In plain wordsIn lab tests, AICAR increased nitric oxide production in sinusoidal endothelial cells.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseNitric oxide production
    Study

    n: not reported in source

    Sinusoidal endothelial cells
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The p-eNOS expression and nitric oxide (NO) production were increased by AICAR administration in sinusoidal endothelial cells (SECs).

Studies that did not test the peptide alone1

In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking AICAR (acadesine).

  1. 13AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In BDL rats, L-NAME partially blocked the hemodynamic benefit of chronic AICAR treatment.

    In plain wordsIn rats with bile duct ligation, L-NAME partly blocked AICAR's benefit to blood circulation.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseL-NAME blockade of hemodynamic benefit
    Study

    ratn: not reported in source

    Bile duct ligation
    Outcome group
    Blood pressure · Liver

    Source sentences

    Summary
    The hemodynamic condition was greatly improved, but the positive effect could be partially blocked by L-NAME.
    1 context sentence
    Summary · context
    Chronic AICAR treatment also showed profound beneficial effects on the BDL model rats.

    In this study, AICAR (acadesine) was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking AICAR (acadesine).

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.

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