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

6 results

AMPK activation attenuates inflammatory pain through inhibiting NF-κB activation and IL-1β expression.

Xiang HC, Lin LX, Hu XF, Zhu H, Li HP, Zhang RY, Hu L, Liu WT, Zhao YL, Shu Y, Pan HL, Li M

Journal of neuroinflammation12 Feb 2019Cited by 209 (Europe PMC)

Summary

BackgroundChronic pain is a major clinical problem with limited treatment options. Previous studies have demonstrated that activation of adenosine monophosphate-activated protein kinase (AMPK) can attenuate neuropathic pain. Inflammation/immune response at the site of complete Freund's adjuvant (CFA) injection is known to be a critical trigger of the pathological changes that produce inflammatory pain. However, whether activation of AMPK produces an analgesic effect through inhibiting the proinflammatory cytokines, including interleukin-1β (IL-1β), in inflammatory pain remains unknown.MethodsInflammatory pain was induced in mice injected with CFA. The effects of AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside, an AMPK activator), Compound C (an AMPK inhibitor), and IL-1ra (an IL-1 receptor antagonist) were tested at day 4 after CFA injection. Inflammatory pain was assessed with von Frey filaments and hot plate. Immunoblotting, hematoxylin and eosin (H&E) staining, and immunofluorescence were used to assess inflammation-induced biochemical changes.ResultsThe AMPK activator AICAR produced an analgesic effect and inhibited the level of proinflammatory cytokine IL-1β in the inflamed skin in mice. Moreover, activation of AMPK suppressed CFA-induced NF-κB p65 translocation from the cytosol to the nucleus in activated macrophages (CD68+ and CX3CR1+) of inflamed skin tissues. Subcutaneous injection of IL-1ra attenuated CFA-induced inflammatory pain. The AMPK inhibitor Compound C and AMPKα shRNA reversed the analgesic effect of AICAR and the effects of AICAR on IL-1β and NF-κB activation in inflamed skin tissues.ConclusionsOur study provides new information that AMPK activation produces the analgesic effect by inhibiting NF-κB activation and reducing the expression of IL-1β in inflammatory pain.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In mice with CFA-induced inflammation, AICAR produced an analgesic effect.

    In plain wordsIn mice with CFA-induced inflammation, AICAR reduced pain.

    Outcome
    DecreaseInflammatory pain
    Study

    mousen: not reported in source

    CFA-induced inflammatory pain
    Outcome group
    Pain · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The AMPK activator AICAR produced an analgesic effect and inhibited the level of proinflammatory cytokine IL-1β in the inflamed skin in mice.
    2 context sentences
    Summary · context
    Inflammatory pain was induced in mice injected with CFA.
    Summary · context
    The effects of AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside, an AMPK activator), Compound C (an AMPK inhibitor), and IL-1ra (an IL-1 receptor antagonist) were tested at day 4 after CFA injection.
  2. 02AnimalAnimal study (in vivo)Mechanism

    In mice with CFA-induced inflammation, AICAR reduced IL-1β in inflamed skin.

    In plain wordsIn mice with CFA-induced inflammation, AICAR reduced IL-1β in inflamed skin.

    Outcome
    DecreaseSkin IL-1β level
    Study

    mousen: not reported in source

    CFA-induced inflammatory pain
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The AMPK activator AICAR produced an analgesic effect and inhibited the level of proinflammatory cytokine IL-1β in the inflamed skin in mice.
    2 context sentences
    Summary · context
    Inflammatory pain was induced in mice injected with CFA.
    Summary · context
    The effects of AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside, an AMPK activator), Compound C (an AMPK inhibitor), and IL-1ra (an IL-1 receptor antagonist) were tested at day 4 after CFA injection.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In inflamed mouse skin, AMPK activation suppressed CFA-induced NF-κB p65 nuclear translocation in activated macrophages.

    In plain wordsIn mice, AMPK activation reduced NF-κB movement into macrophage nuclei in inflamed skin.

    Outcome
    DecreaseMacrophage NF-κB p65 nuclear translocation
    Study

    mousen: not reported in source

    CFA-induced inflammatory pain
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, activation of AMPK suppressed CFA-induced NF-κB p65 translocation from the cytosol to the nucleus in activated macrophages (CD68+ and CX3CR1+) of inflamed skin tissues.
    3 context sentences
    Summary · context
    The AMPK activator AICAR produced an analgesic effect and inhibited the level of proinflammatory cytokine IL-1β in the inflamed skin in mice.
    Summary · context
    Inflammatory pain was induced in mice injected with CFA.
    Summary · context
    The effects of AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside, an AMPK activator), Compound C (an AMPK inhibitor), and IL-1ra (an IL-1 receptor antagonist) were tested at day 4 after CFA injection.

Studies that did not test the peptide alone3

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. 04AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In mice with inflamed skin, Compound C and AMPKα shRNA reversed AICAR's analgesic effect.

    In plain wordsIn mice with inflamed skin, Compound C and AMPKα shRNA reversed AICAR's pain relief.

    Outcome
    DecreaseReversal of AICAR analgesia
    Study

    mousen: not reported in source

    CFA-induced inflammatory pain
    Outcome group
    Pain · Nervous system and cognition

    Source sentences

    Summary
    The AMPK inhibitor Compound C and AMPKα shRNA reversed the analgesic effect of AICAR and the effects of AICAR on IL-1β and NF-κB activation in inflamed skin tissues.
    2 context sentences
    Summary · context
    Inflammatory pain was induced in mice injected with CFA.
    Summary · context
    The effects of AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside, an AMPK activator), Compound C (an AMPK inhibitor), and IL-1ra (an IL-1 receptor antagonist) were tested at day 4 after CFA injection.

    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).

  2. 05AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In inflamed mouse skin, Compound C and AMPKα shRNA reversed AICAR's effect on IL-1β.

    In plain wordsIn mice with inflamed skin, Compound C and AMPKα shRNA reversed AICAR's effect on IL-1β.

    Outcome
    IncreaseReversal of AICAR effect on IL-1β
    Study

    mousen: not reported in source

    CFA-induced inflammatory pain
    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    The AMPK inhibitor Compound C and AMPKα shRNA reversed the analgesic effect of AICAR and the effects of AICAR on IL-1β and NF-κB activation in inflamed skin tissues.
    2 context sentences
    Summary · context
    Inflammatory pain was induced in mice injected with CFA.
    Summary · context
    The effects of AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside, an AMPK activator), Compound C (an AMPK inhibitor), and IL-1ra (an IL-1 receptor antagonist) were tested at day 4 after CFA injection.

    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).

  3. 06AnimalNot a test of AICAR (acadesine) aloneAnimal study (in vivo)Mechanism

    In inflamed mouse skin, Compound C and AMPKα shRNA reversed AICAR's effect on NF-κB activation.

    In plain wordsIn mice with inflamed skin, Compound C and AMPKα shRNA reversed AICAR's effect on NF-κB activation.

    Outcome
    IncreaseReversal of AICAR effect on NF-κB activation
    Study

    mousen: not reported in source

    CFA-induced inflammatory pain
    Outcome group
    Inflammation markers · Immune and inflammation

    Source sentences

    Summary
    The AMPK inhibitor Compound C and AMPKα shRNA reversed the analgesic effect of AICAR and the effects of AICAR on IL-1β and NF-κB activation in inflamed skin tissues.
    2 context sentences
    Summary · context
    Inflammatory pain was induced in mice injected with CFA.
    Summary · context
    The effects of AICAR (5-aminoimidazole-4-carboxyamide ribonucleoside, an AMPK activator), Compound C (an AMPK inhibitor), and IL-1ra (an IL-1 receptor antagonist) were tested at day 4 after CFA injection.

    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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