Skip to content

Study · Animal study (in vivo) · rat · 2026

20 results

AICAR attenuates ischemia-reperfusion-induced AKI by modulating AMPK-TXNIP-NLRP3 pathway and energy metabolism.

Gan L, Li W, Zhang Y, Zeng J, Xu B

Cellular and molecular life sciences : CMLS5 Feb 2026Cited by 6 (Europe PMC)

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: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study20

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In a study of rats and HK-2 cells with renal injury, AICAR activated AMPK.

    In plain wordsIn rats studied alongside cells with kidney injury, AICAR activated AMPK.

    Outcome
    IncreaseAMPK activation
    Study

    ratn: not reported in source

    IRI-AKI
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    we demonstrated that AICAR activates AMPK,
  2. 02AnimalAnimal study (in vivo)Mechanism

    In a study of rats and HK-2 cells with renal injury, AICAR significantly downregulated TXNIP.

    In plain wordsIn rats studied alongside cells with kidney injury, AICAR reduced TXNIP.

    Outcome
    DecreaseTXNIP downregulation
    Study

    ratn: not reported in source

    IRI-AKI
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    we demonstrated that AICAR activates AMPK, leading to the significant downregulation of TXNIP and NLRP3,
  3. 03AnimalAnimal study (in vivo)Mechanism

    In a study of rats and HK-2 cells with renal injury, AICAR significantly downregulated NLRP3.

    In plain wordsIn rats studied alongside cells with kidney injury, AICAR reduced NLRP3.

    Outcome
    DecreaseNLRP3 downregulation
    Study

    ratn: not reported in source

    IRI-AKI
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    we demonstrated that AICAR activates AMPK, leading to the significant downregulation of TXNIP and NLRP3,
  4. 04AnimalAnimal study (in vivo)Mechanism

    In a study of rats and HK-2 cells with renal injury, AICAR blocked Caspase-1-dependent IL-1β release.

    In plain wordsIn rats studied alongside cells with kidney injury, AICAR blocked release of the inflammatory signal IL-1β.

    Outcome
    DecreaseIL-1β release
    Study

    ratn: not reported in source

    IRI-AKI
    Outcome group
    Inflammation markers · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    blocks Caspase-1-dependent release of IL-1β and IL-18,
  5. 05AnimalAnimal study (in vivo)Mechanism

    In a study of rats and HK-2 cells with renal injury, AICAR blocked Caspase-1-dependent IL-18 release.

    In plain wordsIn rats studied alongside cells with kidney injury, AICAR blocked release of the inflammatory signal IL-18.

    Outcome
    DecreaseIL-18 release
    Study

    ratn: not reported in source

    IRI-AKI
    Outcome group
    Inflammation markers · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    blocks Caspase-1-dependent release of IL-1β and IL-18,
  6. 06AnimalAnimal study (in vivo)Mechanism

    In a study of rats and HK-2 cells with renal injury, AICAR suppressed pyroptosis.

    In plain wordsIn rats studied alongside cells with kidney injury, AICAR suppressed inflammatory cell death.

    Outcome
    DecreasePyroptosis
    Study

    ratn: not reported in source

    IRI-AKI
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and ultimately suppresses pyroptosis, thereby alleviating renal inflammatory injury.
  7. 07AnimalAnimal study (in vivo)Mechanism

    In a study of rats and HK-2 cells with renal injury, AICAR alleviated renal inflammatory injury.

    In plain wordsIn rats studied alongside cells with kidney injury, AICAR reduced inflammatory injury.

    Outcome
    DecreaseInflammatory injury
    Study

    ratn: not reported in source

    IRI-AKI
    Outcome group
    Inflammation markers · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and ultimately suppresses pyroptosis, thereby alleviating renal inflammatory injury.
  8. 08AnimalAnimal study (in vivo)Mechanism

    In rats with IRI-AKI, AICAR reduced reactive oxygen species production in renal tissues.

    In plain wordsIn rats with kidney injury, AICAR reduced reactive oxygen species in kidney tissue.

    Outcome
    DecreaseRenal reactive oxygen species
    Study

    ratn: not reported in source

    IRI-AKI
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, AICAR restored mitochondrial membrane potential and ATP levels in H/R-treated HK-2 cells, reduced reactive oxygen species production in renal tissues of IRI-AKI rats, and elevated levels of antioxidant enzymes.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In rats with IRI-AKI, AICAR elevated antioxidant enzyme levels.

    In plain wordsIn rats with kidney injury, AICAR increased antioxidant enzyme levels.

    Outcome
    IncreaseAntioxidant enzymes
    Study

    ratn: not reported in source

    IRI-AKI
    Outcome group
    Oxidative stress · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, AICAR restored mitochondrial membrane potential and ATP levels in H/R-treated HK-2 cells, reduced reactive oxygen species production in renal tissues of IRI-AKI rats, and elevated levels of antioxidant enzymes.
  10. 10AnimalAnimal study (in vivo)Mechanism

    In the IRI-AKI study, AICAR restored multiple metabolites associated with glycolysis, the TCA cycle, the urea cycle, and tryptophan metabolism.

    In plain wordsIn rats studied alongside cells with kidney injury, AICAR restored multiple metabolites associated with several metabolic pathways.

    Outcome
    Direction not reportedMetabolite levels
    Study

    ratn: not reported in source

    IRI-AKI
    Outcome group
    Energy expenditure and thermogenesis · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Concurrently, utilizing targeted metabolomics technology, we discovered that AICAR effectively restores the levels of multiple metabolites associated with glycolysis, the TCA cycle, the urea cycle, and tryptophan metabolism and alleviates lipid deposition in IRI-AKI.
  11. 11AnimalAnimal study (in vivo)Mechanism

    In the IRI-AKI study, AICAR alleviated lipid deposition.

    In plain wordsIn rats studied alongside cells with kidney injury, AICAR reduced fat deposition.

    Outcome
    DecreaseLipid deposition
    Study

    ratn: not reported in source

    IRI-AKI
    Outcome group
    Lipids · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Concurrently, utilizing targeted metabolomics technology, we discovered that AICAR effectively restores the levels of multiple metabolites associated with glycolysis, the TCA cycle, the urea cycle, and tryptophan metabolism and alleviates lipid deposition in IRI-AKI.
  12. 12LabIn vitro (cells)Mechanism

    In a study of HK-2 cells and rats with renal injury, AICAR activated AMPK.

    In plain wordsIn cells studied alongside rats with kidney injury, AICAR activated AMPK.

    Outcome
    IncreaseAMPK activation
    Study

    humann: not reported in source

    H/R-treated HK-2 cells
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    we demonstrated that AICAR activates AMPK,
  13. 13LabIn vitro (cells)Mechanism

    In a study of HK-2 cells and rats with renal injury, AICAR significantly downregulated TXNIP.

    In plain wordsIn cells studied alongside rats with kidney injury, AICAR reduced TXNIP.

    Outcome
    DecreaseTXNIP downregulation
    Study

    humann: not reported in source

    H/R-treated HK-2 cells
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    we demonstrated that AICAR activates AMPK, leading to the significant downregulation of TXNIP and NLRP3,
  14. 14LabIn vitro (cells)Mechanism

    In a study of HK-2 cells and rats with renal injury, AICAR significantly downregulated NLRP3.

    In plain wordsIn cells studied alongside rats with kidney injury, AICAR reduced NLRP3.

    Outcome
    DecreaseNLRP3 downregulation
    Study

    humann: not reported in source

    H/R-treated HK-2 cells
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    we demonstrated that AICAR activates AMPK, leading to the significant downregulation of TXNIP and NLRP3,
  15. 15LabIn vitro (cells)Mechanism

    In a study of HK-2 cells and rats with renal injury, AICAR blocked Caspase-1-dependent IL-1β release.

    In plain wordsIn cells studied alongside rats with kidney injury, AICAR blocked release of the inflammatory signal IL-1β.

    Outcome
    DecreaseIL-1β release
    Study

    humann: not reported in source

    H/R-treated HK-2 cells
    Outcome group
    Inflammation markers · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    blocks Caspase-1-dependent release of IL-1β and IL-18,
  16. 16LabIn vitro (cells)Mechanism

    In a study of HK-2 cells and rats with renal injury, AICAR blocked Caspase-1-dependent IL-18 release.

    In plain wordsIn cells studied alongside rats with kidney injury, AICAR blocked release of the inflammatory signal IL-18.

    Outcome
    DecreaseIL-18 release
    Study

    humann: not reported in source

    H/R-treated HK-2 cells
    Outcome group
    Inflammation markers · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    blocks Caspase-1-dependent release of IL-1β and IL-18,
  17. 17LabIn vitro (cells)Mechanism

    In a study of HK-2 cells and rats with renal injury, AICAR suppressed pyroptosis.

    In plain wordsIn cells studied alongside rats with kidney injury, AICAR suppressed inflammatory cell death.

    Outcome
    DecreasePyroptosis
    Study

    humann: not reported in source

    H/R-treated HK-2 cells
    Outcome group
    Receptor activity and mechanism · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and ultimately suppresses pyroptosis, thereby alleviating renal inflammatory injury.
  18. 18LabIn vitro (cells)Mechanism

    In a study of HK-2 cells and rats with renal injury, AICAR alleviated renal inflammatory injury.

    In plain wordsIn cells studied alongside rats with kidney injury, AICAR reduced inflammatory injury.

    Outcome
    DecreaseInflammatory injury
    Study

    humann: not reported in source

    H/R-treated HK-2 cells
    Outcome group
    Inflammation markers · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and ultimately suppresses pyroptosis, thereby alleviating renal inflammatory injury.
  19. 19LabIn vitro (cells)Mechanism

    In H/R-treated HK-2 cells, AICAR restored mitochondrial membrane potential.

    In plain wordsIn cells with low-oxygen and reoxygenation injury, AICAR restored mitochondrial membrane potential.

    Outcome
    Direction not reportedMitochondrial membrane potential
    Study

    humann: not reported in source

    H/R-treated HK-2 cells
    Outcome group
    Mitochondrial function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, AICAR restored mitochondrial membrane potential and ATP levels in H/R-treated HK-2 cells, reduced reactive oxygen species production in renal tissues of IRI-AKI rats, and elevated levels of antioxidant enzymes.
  20. 20LabIn vitro (cells)Mechanism

    In H/R-treated HK-2 cells, AICAR restored ATP levels.

    In plain wordsIn cells with low-oxygen and reoxygenation injury, AICAR restored levels of the energy molecule ATP.

    Outcome
    Direction not reportedATP levels
    Study

    humann: not reported in source

    H/R-treated HK-2 cells
    Outcome group
    Mitochondrial function · Kidney and urinary
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, AICAR restored mitochondrial membrane potential and ATP levels in H/R-treated HK-2 cells, reduced reactive oxygen species production in renal tissues of IRI-AKI rats, and elevated levels of antioxidant enzymes.

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.