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Study · In vitro (cells) · rat · 2012

7 results

Thymosin beta 4 protects cardiomyocytes from oxidative stress by targeting anti-oxidative enzymes and anti-apoptotic genes.

Wei C, Kumar S, Kim IK, Gupta S

PloS one3 Aug 2012Cited by 38 (Europe PMC)

PMID22880044 (opens in a new tab)PMCIDPMC3411836 (opens in a new tab)DOI10.1371/journal.pone.0042586 (opens in a new tab)PepBankPUB-22880044
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Summary

BackgroundThymosin beta-4 (Tβ4) is a ubiquitous protein with many properties relating to cell proliferation and differentiation that promotes wound healing and modulates inflammatory mediators. The mechanism by which Tβ4 modulates cardiac protection under oxidative stress is not known. The purpose of this study is to dissect the cardioprotective mechanism of Tβ4 on H(2)O(2) induced cardiac damage.MethodsRat neonatal cardiomyocytes with or without Tβ4 pretreatment were exposed to H(2)O(2) and expression of antioxidant, apoptotic, and anti-inflammatory genes was evaluated by quantitative real-time PCR and western blotting. ROS levels were estimated by DCF-DA using fluorescent microscopy and fluorimetry. Selected antioxidant, anti-inflammatory and antiapoptotic genes were silenced by siRNA transfections in neonatal cardiomyocytes and effect of Tβ4 on H(2)O(2)-induced cardiac damage was evaluated.ResultsPre-treatment of Tβ4 resulted in reduction of the intracellular ROS levels induced by H(2)O(2) in cardiomyocytes. Tβ4 pretreatment also resulted in an increase in the expression of antiapoptotic proteins and reduction of Bax/BCl(2) ratio in the cardiomyocytes. Pretreatment with Tβ4 resulted in stimulating the expression of antioxidant enzymes copper/zinc SOD and catalase in cardiomyocytes at both transcription and translation levels. Tβ4 treatment resulted in the increased expression of anti-apoptotic and anti-inflammatory genes. Silencing of Cu/Zn SOD and catalase gene resulted in apoptotic cell death in the cardiomyocytes which was prevented by treatment with Tβ4.ConclusionThis is the first report that demonstrates the effect of Tβ4 on cardiomyocytes and its capability to selectively upregulate anti-oxidative enzymes, anti-inflammatory genes, and antiapoptotic enzymes in the neonatal cardiomyocytes thus preventing cell death thereby protecting the myocardium. Tβ4 treatment resulted in decreased oxidative stress and inflammation in the myocardium under oxidative stress.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study7

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

  1. 01LabIn vitro (cells)Mechanism

    In rat neonatal cardiomyocytes, Tβ4 pretreatment reduced intracellular ROS induced by H2O2.

    In plain wordsIn rat heart cells, thymosin β4 pretreatment lowered the reactive oxygen molecules caused by hydrogen peroxide.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseIntracellular ROS after H2O2
    Study

    ratn: not reported in source

    neonatal cardiomyocytes under H2O2 oxidative stress
    Comparator
    H2O2 without Tβ4 pretreatment
    Outcome group
    Myocardial injury · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pre-treatment of Tβ4 resulted in reduction of the intracellular ROS levels induced by H(2)O(2) in cardiomyocytes.
    1 context sentence
    Summary · context
    Rat neonatal cardiomyocytes with or without Tβ4 pretreatment were exposed to H(2)O(2) and expression of antioxidant, apoptotic, and anti-inflammatory genes was evaluated by quantitative real-time PCR and western blotting.
  2. 02LabIn vitro (cells)Mechanism

    In rat neonatal cardiomyocytes, Tβ4 pretreatment increased the expression of antiapoptotic proteins.

    In plain wordsIn rat heart cells, thymosin β4 pretreatment increased proteins that protect against cell death.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseExpression of antiapoptotic proteins
    Study

    ratn: not reported in source

    neonatal cardiomyocytes under H2O2 oxidative stress
    Comparator
    H2O2 without Tβ4 pretreatment
    Outcome group
    Myocardial injury · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ4 pretreatment also resulted in an increase in the expression of antiapoptotic proteins and reduction of Bax/BCl(2) ratio in the cardiomyocytes.
    1 context sentence
    Summary · context
    Rat neonatal cardiomyocytes with or without Tβ4 pretreatment were exposed to H(2)O(2) and expression of antioxidant, apoptotic, and anti-inflammatory genes was evaluated by quantitative real-time PCR and western blotting.
  3. 03LabIn vitro (cells)Mechanism

    In rat neonatal cardiomyocytes, Tβ4 pretreatment reduced the Bax/Bcl-2 ratio.

    In plain wordsIn rat heart cells, thymosin β4 pretreatment lowered a marker ratio linked to cell death.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseBax/Bcl-2 ratio
    Study

    ratn: not reported in source

    neonatal cardiomyocytes under H2O2 oxidative stress
    Comparator
    H2O2 without Tβ4 pretreatment
    Outcome group
    Myocardial injury · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ4 pretreatment also resulted in an increase in the expression of antiapoptotic proteins and reduction of Bax/BCl(2) ratio in the cardiomyocytes.
    1 context sentence
    Summary · context
    Rat neonatal cardiomyocytes with or without Tβ4 pretreatment were exposed to H(2)O(2) and expression of antioxidant, apoptotic, and anti-inflammatory genes was evaluated by quantitative real-time PCR and western blotting.
  4. 04LabIn vitro (cells)Mechanism

    In rat neonatal cardiomyocytes, Tβ4 pretreatment increased copper/zinc SOD expression at transcription and translation levels.

    In plain wordsIn rat heart cells, thymosin β4 pretreatment raised an antioxidant enzyme, copper/zinc SOD.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseCu/Zn SOD expression
    Study

    ratn: not reported in source

    neonatal cardiomyocytes under H2O2 oxidative stress
    Comparator
    H2O2 without Tβ4 pretreatment
    Outcome group
    Myocardial injury · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with Tβ4 resulted in stimulating the expression of antioxidant enzymes copper/zinc SOD and catalase in cardiomyocytes at both transcription and translation levels.
    1 context sentence
    Summary · context
    Rat neonatal cardiomyocytes with or without Tβ4 pretreatment were exposed to H(2)O(2) and expression of antioxidant, apoptotic, and anti-inflammatory genes was evaluated by quantitative real-time PCR and western blotting.
  5. 05LabIn vitro (cells)Mechanism

    In rat neonatal cardiomyocytes, Tβ4 pretreatment increased catalase expression at transcription and translation levels.

    In plain wordsIn rat heart cells, thymosin β4 pretreatment raised an antioxidant enzyme, catalase.

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

    ratn: not reported in source

    neonatal cardiomyocytes under H2O2 oxidative stress
    Comparator
    H2O2 without Tβ4 pretreatment
    Outcome group
    Myocardial injury · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Pretreatment with Tβ4 resulted in stimulating the expression of antioxidant enzymes copper/zinc SOD and catalase in cardiomyocytes at both transcription and translation levels.
    1 context sentence
    Summary · context
    Rat neonatal cardiomyocytes with or without Tβ4 pretreatment were exposed to H(2)O(2) and expression of antioxidant, apoptotic, and anti-inflammatory genes was evaluated by quantitative real-time PCR and western blotting.
  6. 06LabIn vitro (cells)Mechanism

    In rat neonatal cardiomyocytes, Tβ4 treatment increased the expression of anti-inflammatory genes.

    In plain wordsIn rat heart cells, thymosin β4 raised the activity of genes that reduce inflammation.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseAnti-inflammatory gene expression
    Study

    ratn: not reported in source

    neonatal cardiomyocytes under H2O2 oxidative stress
    Comparator
    H2O2 without Tβ4 pretreatment
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ4 treatment resulted in the increased expression of anti-apoptotic and anti-inflammatory genes.
    1 context sentence
    Summary · context
    Rat neonatal cardiomyocytes with or without Tβ4 pretreatment were exposed to H(2)O(2) and expression of antioxidant, apoptotic, and anti-inflammatory genes was evaluated by quantitative real-time PCR and western blotting.
  7. 07LabIn vitro (cells)Mechanism

    In rat neonatal cardiomyocytes with Cu/Zn SOD and catalase silenced, Tβ4 treatment prevented the apoptotic cell death.

    In plain wordsIn rat heart cells missing two antioxidant enzymes, thymosin β4 prevented cell death.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseApoptotic cell death after Cu/Zn SOD and catalase silencing
    Study

    ratn: not reported in source

    neonatal cardiomyocytes under H2O2 oxidative stress
    Comparator
    Silenced cells without Tβ4
    Outcome group
    Myocardial injury · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Silencing of Cu/Zn SOD and catalase gene resulted in apoptotic cell death in the cardiomyocytes which was prevented by treatment with Tβ4.
    2 context sentences
    Summary · context
    Selected antioxidant, anti-inflammatory and antiapoptotic genes were silenced by siRNA transfections in neonatal cardiomyocytes and effect of Tβ4 on H(2)O(2)-induced cardiac damage was evaluated.
    Summary · context
    Rat neonatal cardiomyocytes with or without Tβ4 pretreatment were exposed to H(2)O(2) and expression of antioxidant, apoptotic, and anti-inflammatory genes was evaluated by quantitative real-time PCR and western blotting.

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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