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Study · Animal study (in vivo) · rat · 2023

6 results

AICAR Ameliorates Non-Alcoholic Fatty Liver Disease via Modulation of the HGF/NF-κB/SNARK Signaling Pathway and Restores Mitochondrial and Endoplasmic Reticular Impairments in High-Fat Diet-Fed Rats.

Zineldeen DH, Tahoon NM, Sarhan NI

International journal of molecular sciences8 Feb 2023Cited by 18 (Europe PMC)

PMID36834782 (opens in a new tab)PMCIDPMC9959470 (opens in a new tab)DOI10.3390/ijms24043367 (opens in a new tab)PepBankPUB-36834782
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Summary

Non-alcoholic fatty liver disease (NAFLD) is a global health problem characterized by altered lipid and redox homeostasis, mitochondrial dysfunction, and endoplasmic reticulum (ER) stress. The AMP-dependent kinase (AMPK) agonist 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) has been shown to improve the outcome of NAFLD in the context of AMPK activation, yet the underlying molecular mechanism remains obscure. This study investigated the potential mechanism(s) of AICAR to attenuate NAFLD by exploring AICAR's effects on the HGF/NF-κB/SNARK axis and downstream effectors as well as mitochondrial and ER derangements. High-fat diet (HFD)-fed male Wistar rats were given intraperitoneal AICAR at 0.7 mg/g body weight or left untreated for 8 weeks. In vitro steatosis was also examined. ELISA, Western blotting, immunohistochemistry and RT-PCR were used to explore AICAR's effects. NAFLD was confirmed by steatosis score, dyslipidemia, altered glycemic, and redox status. HGF/NF-κB/SNARK was downregulated in HFD-fed rats receiving AICAR with improved hepatic steatosis and reduced inflammatory cytokines and oxidative stress. Aside from AMPK dominance, AICAR improved hepatic fatty acid oxidation and alleviated the ER stress response. In addition, it restored mitochondrial homeostasis by modulating Sirtuin 2 and mitochondrial quality gene expression. Our results provide a new mechanistic insight into the prophylactic role of AICAR in the prevention of NAFLD and its complications.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In HFD-fed rats, AICAR downregulated HGF/NF-κB/SNARK signaling compared with untreated rats.

    In plain wordsIn rats fed a high-fat diet, AICAR reduced HGF/NF-κB/SNARK signaling compared with no treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseHGF/NF-κB/SNARK signaling
    Study

    ratn: not reported in source

    high-fat diet-fed male Wistar rats
    Comparator
    untreated high-fat diet-fed rats
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    0.7 mg/g body weight · intraperitoneal · 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    HGF/NF-κB/SNARK was downregulated in HFD-fed rats receiving AICAR with improved hepatic steatosis and reduced inflammatory cytokines and oxidative stress.
    1 context sentence
    Summary · context
    High-fat diet (HFD)-fed male Wistar rats were given intraperitoneal AICAR at 0.7 mg/g body weight or left untreated for 8 weeks.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In HFD-fed rats, AICAR improved hepatic steatosis compared with untreated rats.

    In plain wordsIn rats fed a high-fat diet, AICAR reduced liver fat accumulation compared with no treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseHepatic steatosis
    Study

    ratn: not reported in source

    high-fat diet-fed male Wistar rats
    Comparator
    untreated high-fat diet-fed rats
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    0.7 mg/g body weight · intraperitoneal · 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    HGF/NF-κB/SNARK was downregulated in HFD-fed rats receiving AICAR with improved hepatic steatosis and reduced inflammatory cytokines and oxidative stress.
    1 context sentence
    Summary · context
    High-fat diet (HFD)-fed male Wistar rats were given intraperitoneal AICAR at 0.7 mg/g body weight or left untreated for 8 weeks.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In HFD-fed rats, AICAR reduced inflammatory cytokines compared with untreated rats.

    In plain wordsIn rats fed a high-fat diet, AICAR reduced inflammatory cytokines compared with no treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseInflammatory cytokines
    Study

    ratn: not reported in source

    high-fat diet-fed male Wistar rats
    Comparator
    untreated high-fat diet-fed rats
    Outcome group
    Inflammation markers · Liver
    Studied dose
    0.7 mg/g body weight · intraperitoneal · 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    HGF/NF-κB/SNARK was downregulated in HFD-fed rats receiving AICAR with improved hepatic steatosis and reduced inflammatory cytokines and oxidative stress.
    1 context sentence
    Summary · context
    High-fat diet (HFD)-fed male Wistar rats were given intraperitoneal AICAR at 0.7 mg/g body weight or left untreated for 8 weeks.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In HFD-fed rats, AICAR reduced oxidative stress compared with untreated rats.

    In plain wordsIn rats fed a high-fat diet, AICAR reduced oxidative stress compared with no treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseOxidative stress
    Study

    ratn: not reported in source

    high-fat diet-fed male Wistar rats
    Comparator
    untreated high-fat diet-fed rats
    Outcome group
    Oxidative stress · Liver
    Studied dose
    0.7 mg/g body weight · intraperitoneal · 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    HGF/NF-κB/SNARK was downregulated in HFD-fed rats receiving AICAR with improved hepatic steatosis and reduced inflammatory cytokines and oxidative stress.
    1 context sentence
    Summary · context
    High-fat diet (HFD)-fed male Wistar rats were given intraperitoneal AICAR at 0.7 mg/g body weight or left untreated for 8 weeks.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In HFD-fed rats, AICAR improved hepatic fatty acid oxidation compared with untreated rats.

    In plain wordsIn rats fed a high-fat diet, AICAR improved liver fat oxidation compared with no treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    IncreaseHepatic fatty acid oxidation
    Study

    ratn: not reported in source

    high-fat diet-fed male Wistar rats
    Comparator
    untreated high-fat diet-fed rats
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    0.7 mg/g body weight · intraperitoneal · 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    Aside from AMPK dominance, AICAR improved hepatic fatty acid oxidation and alleviated the ER stress response.
    1 context sentence
    Summary · context
    High-fat diet (HFD)-fed male Wistar rats were given intraperitoneal AICAR at 0.7 mg/g body weight or left untreated for 8 weeks.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In HFD-fed rats, AICAR alleviated the endoplasmic reticulum stress response compared with untreated rats.

    In plain wordsIn rats fed a high-fat diet, AICAR reduced endoplasmic reticulum stress compared with no treatment.

    Peptide
    AICAR (acadesine)
    Outcome
    DecreaseEndoplasmic reticulum stress response
    Study

    ratn: not reported in source

    high-fat diet-fed male Wistar rats
    Comparator
    untreated high-fat diet-fed rats
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    0.7 mg/g body weight · intraperitoneal · 8 weeksAs given in this study (rat).

    Source sentences

    Summary
    Aside from AMPK dominance, AICAR improved hepatic fatty acid oxidation and alleviated the ER stress response.
    1 context sentence
    Summary · context
    High-fat diet (HFD)-fed male Wistar rats were given intraperitoneal AICAR at 0.7 mg/g body weight or left untreated for 8 weeks.

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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