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

10 results

Recombinant Human Thymosin β4 Attenuates Endotoxemia-Induced ALI and EAE by Suppressing Inflammatory and Oxidative Responses.

Ye Y, Yang X, Liu Y, Zhao J, Chen T, Xing Y, Zuo H, Hao Y, Li Y

Biomolecules22 May 2026

PMID42352234 (opens in a new tab)DOI10.3390/biom16060766 (opens in a new tab)PepBankPUB-42352234
Publisher pagePubMedAsk about this study
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Summary

Endotoxemia represents a life-threatening clinical disorder driven by an aberrant host immune response to pathogenic infection, often resulting in severe multiple organ dysfunction. Among its most devastating complications are acute lung injury (ALI) and endotoxemia-associated encephalopathy (EAE), both of which are associated with elevated mortality and currently lack effective targeted interventions. This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia. Our results showed that treatment with rhTβ4 markedly enhanced survival rates and diminished the systemic overproduction of diverse proinflammatory cytokines and chemokines in endotoxemic mice. These systemic protective actions were achieved through the inhibition of the TLR4/NF-κB signaling cascade, the reduction in M1 macrophage polarization, and the simultaneous alleviation of mitochondrial impairment and oxidative stress. Moreover, rhTβ4 treatment significantly rescued EAE-related cognitive deficits and attenuated neuronal damage, primarily through the suppression of neuroinflammation and microglial overactivation. Integrative transcriptomic profiling and functional assays identified lysophosphatidic acid receptor 3 (LPAR3) as an important contributor, suggesting that rhTβ4 suppresses microglial-mediated neurotoxicity at least in part through LPAR3 downregulation. In conclusion, rhTβ4 confers robust multi-organ protection against endotoxemic injury by orchestrating the inhibition of systemic and central neuroinflammatory cascades, positioning it as a promising candidate for the treatment of endotoxemia-induced ALI and EAE.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study10

10 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 LPS-induced endotoxemia, rhTβ4 treatment markedly enhanced survival rates.

    In plain wordsIn mice with endotoxemia, recombinant thymosin β4 improved survival.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseSurvival
    Study

    mousen: not reported in source

    LPS-induced endotoxemia
    Outcome group
    Mortality · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    treatment with rhTβ4 markedly enhanced survival rates and diminished the systemic overproduction of diverse proinflammatory cytokines and chemokines in endotoxemic mice.
    1 context sentence
    Summary · context
    This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In mice with LPS-induced endotoxemia, rhTβ4 diminished the systemic overproduction of diverse proinflammatory cytokines and chemokines.

    In plain wordsIn mice with endotoxemia, recombinant thymosin β4 lowered the blood levels of several inflammatory signals.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseSystemic proinflammatory cytokines and chemokines
    Study

    mousen: not reported in source

    LPS-induced endotoxemia
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    diminished the systemic overproduction of diverse proinflammatory cytokines and chemokines in endotoxemic mice.
    1 context sentence
    Summary · context
    This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced endotoxemia, rhTβ4 inhibited the TLR4/NF-κB signaling cascade.

    In plain wordsIn mice with endotoxemia, recombinant thymosin β4 blocked an inflammatory signalling pathway.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseTLR4/NF-κB signaling
    Study

    mousen: not reported in source

    LPS-induced endotoxemia
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    These systemic protective actions were achieved through the inhibition of the TLR4/NF-κB signaling cascade, the reduction in M1 macrophage polarization, and the simultaneous alleviation of mitochondrial impairment and oxidative stress.
    1 context sentence
    Summary · context
    This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced endotoxemia, rhTβ4 reduced M1 macrophage polarization.

    In plain wordsIn mice with endotoxemia, recombinant thymosin β4 reduced inflammatory macrophage activation.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseM1 macrophage polarization
    Study

    mousen: not reported in source

    LPS-induced endotoxemia
    Outcome group
    Immune response · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    These systemic protective actions were achieved through the inhibition of the TLR4/NF-κB signaling cascade, the reduction in M1 macrophage polarization, and the simultaneous alleviation of mitochondrial impairment and oxidative stress.
    1 context sentence
    Summary · context
    This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced endotoxemia, rhTβ4 alleviated mitochondrial impairment.

    In plain wordsIn mice with endotoxemia, recombinant thymosin β4 reduced damage to mitochondria.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseMitochondrial impairment
    Study

    mousen: not reported in source

    LPS-induced endotoxemia
    Outcome group
    Mitochondrial function · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    These systemic protective actions were achieved through the inhibition of the TLR4/NF-κB signaling cascade, the reduction in M1 macrophage polarization, and the simultaneous alleviation of mitochondrial impairment and oxidative stress.
    1 context sentence
    Summary · context
    This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In mice with LPS-induced endotoxemia, rhTβ4 alleviated oxidative stress.

    In plain wordsIn mice with endotoxemia, recombinant thymosin β4 reduced oxidative stress.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseOxidative stress
    Study

    mousen: not reported in source

    LPS-induced endotoxemia
    Outcome group
    Inflammation markers · Whole body
    Studied dose
    Dose not stated

    Source sentences

    Summary
    These systemic protective actions were achieved through the inhibition of the TLR4/NF-κB signaling cascade, the reduction in M1 macrophage polarization, and the simultaneous alleviation of mitochondrial impairment and oxidative stress.
    1 context sentence
    Summary · context
    This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia.
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    In mice with endotoxemia-associated encephalopathy, rhTβ4 treatment significantly rescued cognitive deficits.

    In plain wordsIn mice with brain effects of endotoxemia, recombinant thymosin β4 reduced memory and thinking problems.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseCognitive deficits in endotoxemia-associated encephalopathy
    Study

    mousen: not reported in source

    LPS-induced endotoxemia
    Outcome group
    Cognition and memory · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, rhTβ4 treatment significantly rescued EAE-related cognitive deficits and attenuated neuronal damage, primarily through the suppression of neuroinflammation and microglial overactivation.
    1 context sentence
    Summary · context
    This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia.
  8. 08AnimalAnimal study (in vivo)Efficacy outcome

    In mice with endotoxemia-associated encephalopathy, rhTβ4 treatment attenuated neuronal damage.

    In plain wordsIn mice with brain effects of endotoxemia, recombinant thymosin β4 reduced damage to nerve cells.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseNeuronal damage
    Study

    mousen: not reported in source

    LPS-induced endotoxemia
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, rhTβ4 treatment significantly rescued EAE-related cognitive deficits and attenuated neuronal damage, primarily through the suppression of neuroinflammation and microglial overactivation.
    1 context sentence
    Summary · context
    This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia.
  9. 09AnimalAnimal study (in vivo)Mechanism

    In mice with endotoxemia-associated encephalopathy, rhTβ4 suppressed neuroinflammation and microglial overactivation.

    In plain wordsIn mice with brain effects of endotoxemia, recombinant thymosin β4 reduced brain inflammation and overactive immune cells.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseNeuroinflammation and microglial overactivation
    Study

    mousen: not reported in source

    LPS-induced endotoxemia
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, rhTβ4 treatment significantly rescued EAE-related cognitive deficits and attenuated neuronal damage, primarily through the suppression of neuroinflammation and microglial overactivation.
    1 context sentence
    Summary · context
    This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia.
  10. 10AnimalAnimal study (in vivo)Mechanism

    Transcriptomic profiling and functional assays identified LPAR3 as a contributor, suggesting rhTβ4 suppresses microglial-mediated neurotoxicity at least in part through LPAR3 downregulation.

    In plain wordsGene analysis suggested recombinant thymosin β4 reduces nerve-harming activity of brain immune cells partly by lowering the receptor LPAR3.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseLPAR3 downregulation and microglial neurotoxicity
    Study

    mousen: not reported in source

    LPS-induced endotoxemia
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Integrative transcriptomic profiling and functional assays identified lysophosphatidic acid receptor 3 (LPAR3) as an important contributor, suggesting that rhTβ4 suppresses microglial-mediated neurotoxicity at least in part through LPAR3 downregulation.
    1 context sentence
    Summary · context
    This study evaluated the therapeutic efficacy and underlying molecular mechanisms of recombinant human thymosin β4 (rhTβ4) in a murine model of lipopolysaccharide (LPS)-induced endotoxemia.

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

    13 Oct 2026, 01:52 UTC

    Study results updated

  2. Version 1

    12 Oct 2026, 18:17 UTC

    First added · source update from Europe PMC

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Terms as the source lists them.

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