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Study · In vitro (cells) · 2019

10 results

Thymosin beta 4 attenuates oxidative stress-induced injury of spinal cord-derived neural stem/progenitor cells through the TLR4/MyD88 pathway.

Li H, Wang Y, Hu X, Ma B, Zhang H

Gene1 May 2019Cited by 19 (Europe PMC)

PMID31054361 (opens in a new tab)DOI10.1016/j.gene.2019.04.083 (opens in a new tab)PepBankPUB-31054361
Publisher pagePubMedAsk about this study
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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

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In H2O2-injured neural stem/progenitor cells, Tβ4 dose dependently increased cell viability in an MTT assay.

    In plain wordsIn cells, thymosin beta‑4 increased the survival of injured neural stem cells in a dose-dependent way.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseViability of H2O2-injured NSPCs
    Study

    n: not reported in source

    spinal cord-derived neural stem/progenitor cells (NSPCs) injured with H2O2
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Using an MTT assay, we found that Tβ4 dose dependently increased viability of the injured NSPCs.
    1 context sentence
    Summary · context
    We exposed NSPCs to oxidative stress and found reduced expression of Tβ4 in H2O2-injured NSPCs.
  2. 02LabIn vitro (cells)Mechanism

    In H2O2-injured neural stem/progenitor cells, Tβ4 reversed the H2O2-induced decrease of intracellular Ca2+ concentration.

    In plain wordsIn cells, thymosin beta‑4 reversed the drop in intracellular calcium caused by oxidative injury.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseIntracellular Ca2+ concentration
    Study

    n: not reported in source

    spinal cord-derived neural stem/progenitor cells (NSPCs) injured with H2O2
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ4 also reversed the decreases of intracellular Ca2+ concentration and increases of lactate dehydrogenase in NSPCs induced by H2O2 treatment.
    1 context sentence
    Summary · context
    We exposed NSPCs to oxidative stress and found reduced expression of Tβ4 in H2O2-injured NSPCs.
  3. 03LabIn vitro (cells)Mechanism

    In H2O2-injured neural stem/progenitor cells, Tβ4 reversed the H2O2-induced increase of lactate dehydrogenase.

    In plain wordsIn cells, thymosin beta‑4 reversed the rise in the cell damage marker lactate dehydrogenase caused by oxidative injury.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseLactate dehydrogenase level
    Study

    n: not reported in source

    spinal cord-derived neural stem/progenitor cells (NSPCs) injured with H2O2
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ4 also reversed the decreases of intracellular Ca2+ concentration and increases of lactate dehydrogenase in NSPCs induced by H2O2 treatment.
    1 context sentence
    Summary · context
    We exposed NSPCs to oxidative stress and found reduced expression of Tβ4 in H2O2-injured NSPCs.
  4. 04LabIn vitro (cells)Efficacy outcome

    In neural stem/progenitor cells, Tβ4 decreased the apoptosis that H2O2 exposure increased.

    In plain wordsIn cells, thymosin beta‑4 reduced the cell death caused by oxidative injury.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseApoptosis of NSPCs
    Study

    n: not reported in source

    spinal cord-derived neural stem/progenitor cells (NSPCs) injured with H2O2
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    H2O2 exposure increased NSPC apoptosis, which Tβ4 decreased.
    1 context sentence
    Summary · context
    We exposed NSPCs to oxidative stress and found reduced expression of Tβ4 in H2O2-injured NSPCs.
  5. 05LabIn vitro (cells)Mechanism

    In H2O2-induced neural stem/progenitor cells, Tβ4 reversed the increase in ROS production.

    In plain wordsIn cells, thymosin beta‑4 reversed the rise in reactive oxygen species caused by oxidative injury.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseROS production
    Study

    n: not reported in source

    spinal cord-derived neural stem/progenitor cells (NSPCs) injured with H2O2
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In H2O2-induced NSPCs, ROS production and pro-inflammatory cytokines increased, and again, Tβ4 reversed these effects.
    1 context sentence
    Summary · context
    We exposed NSPCs to oxidative stress and found reduced expression of Tβ4 in H2O2-injured NSPCs.
  6. 06LabIn vitro (cells)Mechanism

    In H2O2-induced neural stem/progenitor cells, Tβ4 reversed the increase in pro-inflammatory cytokines.

    In plain wordsIn cells, thymosin beta‑4 reversed the rise in inflammatory signals caused by oxidative injury.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreasePro-inflammatory cytokines
    Study

    n: not reported in source

    spinal cord-derived neural stem/progenitor cells (NSPCs) injured with H2O2
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In H2O2-induced NSPCs, ROS production and pro-inflammatory cytokines increased, and again, Tβ4 reversed these effects.
    1 context sentence
    Summary · context
    We exposed NSPCs to oxidative stress and found reduced expression of Tβ4 in H2O2-injured NSPCs.
  7. 07LabIn vitro (cells)Mechanism

    In H2O2-exposed neural stem/progenitor cells, Tβ4 reduced expression of TLR4.

    In plain wordsIn cells, thymosin beta‑4 lowered the level of the receptor TLR4.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseTLR4 expression
    Study

    n: not reported in source

    spinal cord-derived neural stem/progenitor cells (NSPCs) injured with H2O2
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our results showed that Tβ4 reduced expression of TLR4 and MyD88.
    1 context sentence
    Summary · context
    We exposed NSPCs to oxidative stress and found reduced expression of Tβ4 in H2O2-injured NSPCs.
  8. 08LabIn vitro (cells)Mechanism

    In H2O2-exposed neural stem/progenitor cells, Tβ4 reduced expression of MyD88.

    In plain wordsIn cells, thymosin beta‑4 lowered the level of the signalling protein MyD88.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseMyD88 expression
    Study

    n: not reported in source

    spinal cord-derived neural stem/progenitor cells (NSPCs) injured with H2O2
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Our results showed that Tβ4 reduced expression of TLR4 and MyD88.
    1 context sentence
    Summary · context
    We exposed NSPCs to oxidative stress and found reduced expression of Tβ4 in H2O2-injured NSPCs.

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. 09LabEndogenous levelIn vitro (cells)Mechanism

    In spinal cord-derived neural stem/progenitor cells, oxidative stress with H2O2 reduced the expression of Tβ4.

    In plain wordsIn cells, oxidative stress lowered the body's own thymosin beta‑4 expression in neural stem cells.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseTβ4 expression in H2O2-injured NSPCs
    Study

    n: not reported in source

    spinal cord-derived neural stem/progenitor cells (NSPCs) injured with H2O2
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    We exposed NSPCs to oxidative stress and found reduced expression of Tβ4 in H2O2-injured NSPCs.

    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 alone1

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. 10LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In H2O2-exposed neural stem/progenitor cells, a TLR4/MyD88 pathway inhibitor reversed the effects caused by H2O2, similar to the effects of Tβ4.

    In plain wordsIn cells, a drug that blocks the TLR4/MyD88 pathway reversed oxidative injury effects in a way similar to thymosin beta‑4.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableEffect of TLR4/MyD88 pathway inhibitor on H2O2 injury
    Study

    n: not reported in source

    spinal cord-derived neural stem/progenitor cells (NSPCs) injured with H2O2
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition

    Source sentences

    Summary
    Moreover, H2O2-exposed NSPCs that were treated with the TLR4/MyD88 pathway inhibitor showed a reversal of all the effects caused by H2O2, similar to Tβ4's effects.
    1 context sentence
    Summary · context
    We exposed NSPCs to oxidative stress and found reduced expression of Tβ4 in H2O2-injured NSPCs.

    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.

Publication types

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