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Study · In vitro (cells) · 2022

10 results

Thymosin β4 Suppresses LPS-Induced Murine Lung Fibrosis by Attenuating Oxidative Injury and Alleviating Inflammation.

Tian Z, Yao N, Wang F, Ruan L

Inflammation19 Aug 2021Cited by 21 (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: Publisher copyright. Results still quote short attributed sentences.

Results from this study10

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

  1. 01LabIn vitro (cells)Mechanism

    In HPAEpiC cells, Tβ4 significantly attenuated the LPS-induced inhibition of mitophagy.

    In plain wordsIn cells, Tβ4 reduced the block of mitophagy caused by LPS.

    Outcome
    IncreaseLPS-induced mitophagy inhibition
    Study

    humann: not reported in source

    HPAEpiC cells with LPS
    Outcome group
    Mitochondrial function · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our in vitro experiments also showed that LPS inhibited mitophagy and promoted inflammation via oxidative stress in HPAEpiC, and Tβ4 significantly attenuated LPS-induced mitophagy inhibition, inflammasome activation, and transforming growth factor-β (TGF)-β1-induced epithelial-mesenchymal transition (EMT) in HPAEpiC.
    1 context sentence
    Summary · context
    In vitro tests with HPAEpiC and HLF-1 cells were performed to confirm the effects of Tβ4.
  2. 02LabIn vitro (cells)Mechanism

    In HPAEpiC cells, Tβ4 significantly attenuated LPS-induced inflammasome activation.

    In plain wordsIn cells, Tβ4 reduced inflammasome activation caused by LPS.

    Outcome
    DecreaseLPS-induced inflammasome activation
    Study

    humann: not reported in source

    HPAEpiC cells with LPS
    Outcome group
    Inflammation markers · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our in vitro experiments also showed that LPS inhibited mitophagy and promoted inflammation via oxidative stress in HPAEpiC, and Tβ4 significantly attenuated LPS-induced mitophagy inhibition, inflammasome activation, and transforming growth factor-β (TGF)-β1-induced epithelial-mesenchymal transition (EMT) in HPAEpiC.
    1 context sentence
    Summary · context
    In vitro tests with HPAEpiC and HLF-1 cells were performed to confirm the effects of Tβ4.
  3. 03LabIn vitro (cells)Mechanism

    In HPAEpiC cells, Tβ4 significantly attenuated TGF-β1-induced epithelial-mesenchymal transition.

    In plain wordsIn cells, Tβ4 reduced the TGF-β1-induced change of lung cells toward a fibrotic type.

    Outcome
    DecreaseTGF-β1-induced epithelial-mesenchymal transition
    Study

    humann: not reported in source

    HPAEpiC cells with TGF-β1
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our in vitro experiments also showed that LPS inhibited mitophagy and promoted inflammation via oxidative stress in HPAEpiC, and Tβ4 significantly attenuated LPS-induced mitophagy inhibition, inflammasome activation, and transforming growth factor-β (TGF)-β1-induced epithelial-mesenchymal transition (EMT) in HPAEpiC.
    1 context sentence
    Summary · context
    In vitro tests with HPAEpiC and HLF-1 cells were performed to confirm the effects of Tβ4.
  4. 04LabIn vitro (cells)Mechanism

    Tβ4 suppressed the proliferation of HLF-1 cells.

    In plain wordsIn cells, Tβ4 slowed the growth of lung fibroblast cells.

    Outcome
    DecreaseHLF-1 cell proliferation
    Study

    humann: not reported in source

    HLF-1 cells
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, Tβ4 suppressed the proliferation and attenuated the TGF-β1-induced activation of HLF-1 cells.
    1 context sentence
    Summary · context
    In vitro tests with HPAEpiC and HLF-1 cells were performed to confirm the effects of Tβ4.
  5. 05LabIn vitro (cells)Mechanism

    Tβ4 attenuated the TGF-β1-induced activation of HLF-1 cells.

    In plain wordsIn cells, Tβ4 reduced the TGF-β1-induced activation of lung fibroblast cells.

    Outcome
    DecreaseTGF-β1-induced activation of HLF-1 cells
    Study

    humann: not reported in source

    HLF-1 cells with TGF-β1
    Outcome group
    Lung injury and fibrosis · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, Tβ4 suppressed the proliferation and attenuated the TGF-β1-induced activation of HLF-1 cells.
    1 context sentence
    Summary · context
    In vitro tests with HPAEpiC and HLF-1 cells were performed to confirm the effects of Tβ4.

Natural levels measured1

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 06HumanEndogenous levelObservational studyOther

    Tβ4 expression was markedly higher in human or mouse fibrotic lung tissues.

    In plain wordsThe body's own Tβ4 was much higher in fibrotic lung tissue of people or mice.

    Outcome
    IncreaseTβ4 expression in fibrotic lung tissue
    Study

    human or mousen: not reported in source

    Outcome group
    Lung injury and fibrosis · Respiratory

    Source sentences

    Summary
    Tβ4 was markedly upregulated in human or mouse fibrotic lung tissues.
    1 context sentence
    Summary · context
    Expression of Tβ4 in fibrotic lung tissues was assessed by real-time quantitative reverse-transcription PCR (rt-PCR), immunohistochemistry (IHC), and western blotting.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

Studies that did not test the peptide alone4

In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

  1. 07AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome

    In mice with LPS-induced lung injury, AAV-Tβ4 markedly reduced oxidative damage.

    In plain wordsIn mice with lung injury, a virus that raises Tβ4 gene activity strongly reduced oxidative damage.

    Outcome
    DecreaseLPS-induced oxidative damage
    Study

    mousen: not reported in source

    LPS-induced lung injury and fibrosis
    Outcome group
    Oxidative stress · Respiratory

    Source sentences

    Summary
    AAV-Tβ4 markedly alleviated LPS-induced oxidative damage, lung injury, inflammation, and fibrosis in mice.
    1 context sentence
    Summary · context
    The effects of intraperitoneal adeno-associated virus-Tβ4 (AAV-Tβ4) on LPS-induced lung injury and fibrosis were observed through the evaluation of collagen deposition and α-smooth muscle actin (SMA) expression.

    In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

  2. 08AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome

    In mice with LPS-induced lung injury, AAV-Tβ4 markedly reduced lung injury.

    In plain wordsIn mice with lung injury, a virus that raises Tβ4 gene activity strongly reduced lung injury.

    Outcome
    DecreaseLPS-induced lung injury
    Study

    mousen: not reported in source

    LPS-induced lung injury and fibrosis
    Outcome group
    Lung injury and fibrosis · Respiratory

    Source sentences

    Summary
    AAV-Tβ4 markedly alleviated LPS-induced oxidative damage, lung injury, inflammation, and fibrosis in mice.
    1 context sentence
    Summary · context
    The effects of intraperitoneal adeno-associated virus-Tβ4 (AAV-Tβ4) on LPS-induced lung injury and fibrosis were observed through the evaluation of collagen deposition and α-smooth muscle actin (SMA) expression.

    In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

  3. 09AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome

    In mice with LPS-induced lung injury, AAV-Tβ4 markedly reduced inflammation.

    In plain wordsIn mice with lung injury, a virus that raises Tβ4 gene activity strongly reduced inflammation.

    Outcome
    DecreaseLPS-induced lung inflammation
    Study

    mousen: not reported in source

    LPS-induced lung injury and fibrosis
    Outcome group
    Inflammation markers · Respiratory

    Source sentences

    Summary
    AAV-Tβ4 markedly alleviated LPS-induced oxidative damage, lung injury, inflammation, and fibrosis in mice.
    1 context sentence
    Summary · context
    The effects of intraperitoneal adeno-associated virus-Tβ4 (AAV-Tβ4) on LPS-induced lung injury and fibrosis were observed through the evaluation of collagen deposition and α-smooth muscle actin (SMA) expression.

    In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

  4. 10AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome

    In mice with LPS-induced lung injury, AAV-Tβ4 markedly reduced fibrosis.

    In plain wordsIn mice with lung injury, a virus that raises Tβ4 gene activity strongly reduced scarring (fibrosis).

    Outcome
    DecreaseLPS-induced lung fibrosis
    Study

    mousen: not reported in source

    LPS-induced lung injury and fibrosis
    Outcome group
    Lung injury and fibrosis · Respiratory

    Source sentences

    Summary
    AAV-Tβ4 markedly alleviated LPS-induced oxidative damage, lung injury, inflammation, and fibrosis in mice.
    1 context sentence
    Summary · context
    The effects of intraperitoneal adeno-associated virus-Tβ4 (AAV-Tβ4) on LPS-induced lung injury and fibrosis were observed through the evaluation of collagen deposition and α-smooth muscle actin (SMA) expression.

    In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

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

Subjects

Terms as the source lists them.

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