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Study · Animal study (in vivo) · mouse · 2021

3 results

Catalpol ameliorates depressive-like behaviors in CUMS mice via oxidative stress-mediated NLRP3 inflammasome and neuroinflammation.

Wang YL, Wu HR, Zhang SS, Xiao HL, Yu J, Ma YY, Zhang YD, Liu Q, Liu Q

Translational psychiatry8 Jun 2021Cited by 123 (Europe PMC)

PMID34103482 (opens in a new tab)PMCIDPMC8187638 (opens in a new tab)DOI10.1038/s41398-021-01468-7 (opens in a new tab)PepBankPUB-34103482
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Summary

The purpose of the present study was to investigate whether catalpol exhibited neuroprotective effects in chronic unpredictable mild stress (CUMS) mice through oxidative stress-mediated nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin-domain-containing 3 (NLRP3) inflammasome and neuroinflammation. Deficits in behavioral tests, including open field test (OFT), forced swim test (FST), and elevated plus-maze test (EPM), were ameliorated following catalpol administration. To study the potential mechanism, western blots, quantitative real-time PCR (qRT-PCR) analysis and immunofluorescence imaging were performed on the hippocampus samples. We found that the defects of behavioral tests induced by CUMS could be reversed by the absence of NLRP3 and NLRP3 inflammasome might be involved in the antidepressant effects of catalpol on CUMS mice. Similar to the NLRP3 inflammasome, the expression of interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and inducible nitride oxide synthase (iNOS) were increased after CUMS. The current study demonstrated that catalpol possessed anti-inflammatory effect on CUMS mice and inhibited microglial polarization to the M1 phenotype. In addition, the activity of mitochondrial oxidative stress might be involved in the NLRP3 activation, which was proved by the downregulation of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and cleaved IL-1β, after the administration of mitochondrion-targeted antioxidant peptide SS31. Taken together, we provided evidence that catalpol exhibited antidepressive effects on CUMS mice possibly via the oxidative stress-mediated regulation of NLRP3 and neuroinflammation.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In CUMS mice, administration of the mitochondrion-targeted antioxidant peptide SS31 was followed by downregulation of NLRP3.

    In plain wordsIn mice under chronic stress, SS31 was followed by lower levels of the inflammation protein NLRP3.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseNLRP3 expression
    Study

    mousen: not reported in source

    Chronic unpredictable mild stress (CUMS)
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    downregulation of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and cleaved IL-1β, after the administration of mitochondrion-targeted antioxidant peptide SS31
  2. 02AnimalAnimal study (in vivo)Mechanism

    In CUMS mice, administration of the mitochondrion-targeted antioxidant peptide SS31 was followed by downregulation of ASC.

    In plain wordsIn mice under chronic stress, SS31 was followed by lower levels of the inflammation protein ASC.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseASC expression
    Study

    mousen: not reported in source

    Chronic unpredictable mild stress (CUMS)
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    downregulation of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and cleaved IL-1β, after the administration of mitochondrion-targeted antioxidant peptide SS31
  3. 03AnimalAnimal study (in vivo)Mechanism

    In CUMS mice, administration of the mitochondrion-targeted antioxidant peptide SS31 was followed by downregulation of cleaved IL-1β.

    In plain wordsIn mice under chronic stress, SS31 was followed by lower levels of the inflammation signal cleaved IL-1β.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseCleaved IL-1β expression
    Study

    mousen: not reported in source

    Chronic unpredictable mild stress (CUMS)
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    downregulation of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and cleaved IL-1β, after the administration of mitochondrion-targeted antioxidant peptide SS31

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

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

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