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Study · Animal study (in vivo) · mouse · 2023

26 results

Thymosin β4 Exerts a Cytoprotective Function and Attenuates Liver Injury in Murine Hepatic Sinusoidal Obstruction Syndrome after Hematopoietic Stem Cell Transplantation.

Wang X, Zhou Y, Sun Q, Zhang Q, Zhou H, Zhang J, Du Y, Wang Y, Yuan K, Xu L, Zhang M, Yan D, Zeng L, Xu K, Sang W

Transplantation and cellular therapy14 May 2023Cited by 2 (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: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study26

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In a murine HSOS model, circulating alanine aminotransferase was significantly reduced after Tβ4 peptide administration.

    In plain wordsIn mice with a liver blood-vessel injury model, thymosin β4 lowered the liver enzyme ALT.

    Outcome
    DecreaseCirculating alanine aminotransferase
    Study

    mousen: not reported in source

    HSOS model
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In a murine HSOS model, levels of circulating alanine aminotransferase, aspartate aminotransferase, total bilirubin, and pro-inflammatory cytokines IL-6, IL-1β, and TNF-α were significantly reduced after administration of Tβ4 peptide; furthermore, Tβ4 treatment successfully ameliorated HSEC injury,…
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In a murine HSOS model, circulating aspartate aminotransferase was significantly reduced after Tβ4 peptide administration.

    In plain wordsIn mice with a liver blood-vessel injury model, thymosin β4 lowered the liver enzyme AST.

    Outcome
    DecreaseCirculating aspartate aminotransferase
    Study

    mousen: not reported in source

    HSOS model
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In a murine HSOS model, levels of circulating alanine aminotransferase, aspartate aminotransferase, total bilirubin, and pro-inflammatory cytokines IL-6, IL-1β, and TNF-α were significantly reduced after administration of Tβ4 peptide; furthermore, Tβ4 treatment successfully ameliorated HSEC injury,…
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In a murine HSOS model, total bilirubin was significantly reduced after Tβ4 peptide administration.

    In plain wordsIn mice with a liver blood-vessel injury model, thymosin β4 lowered bilirubin.

    Outcome
    DecreaseTotal bilirubin
    Study

    mousen: not reported in source

    HSOS model
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In a murine HSOS model, levels of circulating alanine aminotransferase, aspartate aminotransferase, total bilirubin, and pro-inflammatory cytokines IL-6, IL-1β, and TNF-α were significantly reduced after administration of Tβ4 peptide; furthermore, Tβ4 treatment successfully ameliorated HSEC injury,…
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In a murine HSOS model, circulating IL-6 was significantly reduced after Tβ4 peptide administration.

    In plain wordsIn mice with a liver blood-vessel injury model, thymosin β4 lowered the inflammation marker IL-6.

    Outcome
    DecreaseCirculating IL-6
    Study

    mousen: not reported in source

    HSOS model
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In a murine HSOS model, levels of circulating alanine aminotransferase, aspartate aminotransferase, total bilirubin, and pro-inflammatory cytokines IL-6, IL-1β, and TNF-α were significantly reduced after administration of Tβ4 peptide; furthermore, Tβ4 treatment successfully ameliorated HSEC injury,…
  5. 05AnimalAnimal study (in vivo)Efficacy outcome

    In a murine HSOS model, circulating IL-1β was significantly reduced after Tβ4 peptide administration.

    In plain wordsIn mice with a liver blood-vessel injury model, thymosin β4 lowered the inflammation marker IL-1β.

    Outcome
    DecreaseCirculating IL-1β
    Study

    mousen: not reported in source

    HSOS model
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In a murine HSOS model, levels of circulating alanine aminotransferase, aspartate aminotransferase, total bilirubin, and pro-inflammatory cytokines IL-6, IL-1β, and TNF-α were significantly reduced after administration of Tβ4 peptide; furthermore, Tβ4 treatment successfully ameliorated HSEC injury,…
  6. 06AnimalAnimal study (in vivo)Efficacy outcome

    In a murine HSOS model, circulating TNF-α was significantly reduced after Tβ4 peptide administration.

    In plain wordsIn mice with a liver blood-vessel injury model, thymosin β4 lowered the inflammation marker TNF-α.

    Outcome
    DecreaseCirculating TNF-α
    Study

    mousen: not reported in source

    HSOS model
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In a murine HSOS model, levels of circulating alanine aminotransferase, aspartate aminotransferase, total bilirubin, and pro-inflammatory cytokines IL-6, IL-1β, and TNF-α were significantly reduced after administration of Tβ4 peptide; furthermore, Tβ4 treatment successfully ameliorated HSEC injury,…
  7. 07AnimalAnimal study (in vivo)Efficacy outcome

    In a murine HSOS model, Tβ4 treatment ameliorated HSEC injury.

    In plain wordsIn mice with a liver blood-vessel injury model, thymosin β4 reduced damage to liver blood-vessel lining cells.

    Outcome
    DecreaseHSEC injury
    Study

    mousen: not reported in source

    HSOS model
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ4 treatment successfully ameliorated HSEC injury, inflammatory damage, and fibrosis of the murine liver.
  8. 08AnimalAnimal study (in vivo)Efficacy outcome

    In a murine HSOS model, Tβ4 treatment ameliorated inflammatory damage of the liver.

    In plain wordsIn mice with a liver blood-vessel injury model, thymosin β4 reduced inflammatory liver damage.

    Outcome
    DecreaseInflammatory liver damage
    Study

    mousen: not reported in source

    HSOS model
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ4 treatment successfully ameliorated HSEC injury, inflammatory damage, and fibrosis of the murine liver.
  9. 09AnimalAnimal study (in vivo)Efficacy outcome

    In a murine HSOS model, Tβ4 treatment ameliorated fibrosis of the murine liver.

    In plain wordsIn mice with a liver blood-vessel injury model, thymosin β4 reduced liver scarring.

    Outcome
    DecreaseLiver fibrosis
    Study

    mousen: not reported in source

    HSOS model
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ4 treatment successfully ameliorated HSEC injury, inflammatory damage, and fibrosis of the murine liver.
  10. 10LabIn vitro (cells)Efficacy outcome

    In hepatic sinusoidal endothelial cells in vitro, Tβ4 stimulated proliferation.

    In plain wordsIn cells, thymosin β4 made liver blood-vessel lining cells multiply.

    Outcome
    IncreaseHSEC proliferation
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Angiogenesis · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In this study, we found that Tβ4 can stimulate HSEC proliferation, migration, and tube formation in vitro via activation of pro-survival signaling AKT (protein kinase B).
  11. 11LabIn vitro (cells)Efficacy outcome

    In hepatic sinusoidal endothelial cells in vitro, Tβ4 stimulated migration.

    In plain wordsIn cells, thymosin β4 made liver blood-vessel lining cells move more.

    Outcome
    IncreaseHSEC migration
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Angiogenesis · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In this study, we found that Tβ4 can stimulate HSEC proliferation, migration, and tube formation in vitro via activation of pro-survival signaling AKT (protein kinase B).
  12. 12LabIn vitro (cells)Efficacy outcome

    In hepatic sinusoidal endothelial cells in vitro, Tβ4 stimulated tube formation.

    In plain wordsIn cells, thymosin β4 helped liver blood-vessel lining cells form tube-like structures.

    Outcome
    IncreaseHSEC tube formation
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Angiogenesis · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In this study, we found that Tβ4 can stimulate HSEC proliferation, migration, and tube formation in vitro via activation of pro-survival signaling AKT (protein kinase B).
  13. 13LabIn vitro (cells)Mechanism

    In hepatic sinusoidal endothelial cells in vitro, Tβ4 activated the pro-survival signaling protein AKT.

    In plain wordsIn cells, thymosin β4 switched on a survival signal called AKT.

    Outcome
    IncreaseAKT pro-survival signaling
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In this study, we found that Tβ4 can stimulate HSEC proliferation, migration, and tube formation in vitro via activation of pro-survival signaling AKT (protein kinase B).
  14. 14LabIn vitro (cells)Efficacy outcome

    In hepatic sinusoidal endothelial cells in vitro, Tβ4 resisted γ irradiation-induced growth arrest.

    In plain wordsIn cells, thymosin β4 protected liver blood-vessel lining cells from radiation-induced growth arrest.

    Outcome
    DecreaseIrradiation-induced HSEC growth arrest
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Angiogenesis · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, Tβ4 resisted γ irradiation-induced HSEC growth arrest and apoptosis in parallel with upregulation of anti-apoptotic protein B cell lymphoma extra-large (Bcl-xL) and B cell lymphoma-2 (Bcl-2), which may be associated with activation of AKT.
  15. 15LabIn vitro (cells)Efficacy outcome

    In hepatic sinusoidal endothelial cells in vitro, Tβ4 resisted γ irradiation-induced apoptosis.

    In plain wordsIn cells, thymosin β4 protected liver blood-vessel lining cells from radiation-induced cell death.

    Outcome
    DecreaseIrradiation-induced HSEC apoptosis
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Angiogenesis · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, Tβ4 resisted γ irradiation-induced HSEC growth arrest and apoptosis in parallel with upregulation of anti-apoptotic protein B cell lymphoma extra-large (Bcl-xL) and B cell lymphoma-2 (Bcl-2), which may be associated with activation of AKT.
  16. 16LabIn vitro (cells)Mechanism

    In irradiated hepatic sinusoidal endothelial cells, Tβ4 upregulated the anti-apoptotic protein Bcl-xL.

    In plain wordsIn cells, thymosin β4 raised a protein that blocks cell death after radiation.

    Outcome
    IncreaseBcl-xL expression
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, Tβ4 resisted γ irradiation-induced HSEC growth arrest and apoptosis in parallel with upregulation of anti-apoptotic protein B cell lymphoma extra-large (Bcl-xL) and B cell lymphoma-2 (Bcl-2), which may be associated with activation of AKT.
  17. 17LabIn vitro (cells)Mechanism

    In irradiated hepatic sinusoidal endothelial cells, Tβ4 upregulated the anti-apoptotic protein Bcl-2.

    In plain wordsIn cells, thymosin β4 raised a second protein that blocks cell death after radiation.

    Outcome
    IncreaseBcl-2 expression
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In addition, Tβ4 resisted γ irradiation-induced HSEC growth arrest and apoptosis in parallel with upregulation of anti-apoptotic protein B cell lymphoma extra-large (Bcl-xL) and B cell lymphoma-2 (Bcl-2), which may be associated with activation of AKT.
  18. 18LabIn vitro (cells)Efficacy outcome

    In irradiated hepatic sinusoidal endothelial cells, Tβ4 significantly inhibited pro-inflammatory cytokines.

    In plain wordsIn cells, thymosin β4 lowered inflammatory signals caused by radiation.

    Outcome
    DecreaseIrradiation-induced pro-inflammatory cytokines
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    More importantly, Tβ4 significantly inhibited irradiation-induced pro-inflammatory cytokines in parallel with negative regulation of TLR4/MyD88/NF-κB and MAPK p38.
  19. 19LabIn vitro (cells)Mechanism

    In irradiated hepatic sinusoidal endothelial cells, Tβ4 negatively regulated TLR4/MyD88/NF-κB signaling.

    In plain wordsIn cells, thymosin β4 turned down an inflammation signal pathway after radiation.

    Outcome
    DecreaseTLR4/MyD88/NF-κB signaling
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    More importantly, Tβ4 significantly inhibited irradiation-induced pro-inflammatory cytokines in parallel with negative regulation of TLR4/MyD88/NF-κB and MAPK p38.
  20. 20LabIn vitro (cells)Mechanism

    In irradiated hepatic sinusoidal endothelial cells, Tβ4 negatively regulated MAPK p38.

    In plain wordsIn cells, thymosin β4 turned down a stress signal protein called p38 after radiation.

    Outcome
    DecreaseMAPK p38 signaling
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    More importantly, Tβ4 significantly inhibited irradiation-induced pro-inflammatory cytokines in parallel with negative regulation of TLR4/MyD88/NF-κB and MAPK p38.
  21. 21LabIn vitro (cells)Efficacy outcome

    In hepatic sinusoidal endothelial cells, Tβ4 reduced intracellular reactive oxygen species production.

    In plain wordsIn cells, thymosin β4 lowered oxidative stress in liver blood-vessel lining cells.

    Outcome
    DecreaseIntracellular reactive oxygen species
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Meanwhile, Tβ4 reduced intracellular reactive oxygen species production and upregulated antioxidants in HSECs.
  22. 22LabIn vitro (cells)Mechanism

    In hepatic sinusoidal endothelial cells, Tβ4 upregulated antioxidants.

    In plain wordsIn cells, thymosin β4 raised protective antioxidant proteins.

    Outcome
    IncreaseAntioxidant expression
    Study

    n: not reported in source

    Hepatic sinusoidal endothelial cells (HSECs)
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Meanwhile, Tβ4 reduced intracellular reactive oxygen species production and upregulated antioxidants in HSECs.
  23. 23LabIn vitro (cells)Efficacy outcome

    In cell models, Tβ4 inhibited irradiation-induced activation of hepatic stellate cells.

    In plain wordsIn cells, thymosin β4 reduced radiation-induced activation of liver scar-forming cells.

    Outcome
    DecreaseIrradiation-induced hepatic stellate cell activation
    Study

    n: not reported in source

    Hepatic stellate cells
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Additionally, Tβ4 inhibited irradiation-induced activation of hepatic stellate cells by downregulating the expression of fibrogenic markers α-SMA, PAI-1, and TGF-β.
  24. 24LabIn vitro (cells)Mechanism

    In irradiated hepatic stellate cells, Tβ4 downregulated the fibrogenic marker α-SMA.

    In plain wordsIn cells, thymosin β4 lowered a scar-forming marker called α-SMA.

    Outcome
    Decreaseα-SMA expression
    Study

    n: not reported in source

    Hepatic stellate cells
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Additionally, Tβ4 inhibited irradiation-induced activation of hepatic stellate cells by downregulating the expression of fibrogenic markers α-SMA, PAI-1, and TGF-β.
  25. 25LabIn vitro (cells)Mechanism

    In irradiated hepatic stellate cells, Tβ4 downregulated the fibrogenic marker PAI-1.

    In plain wordsIn cells, thymosin β4 lowered a scar-forming marker called PAI-1.

    Outcome
    DecreasePAI-1 expression
    Study

    n: not reported in source

    Hepatic stellate cells
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Additionally, Tβ4 inhibited irradiation-induced activation of hepatic stellate cells by downregulating the expression of fibrogenic markers α-SMA, PAI-1, and TGF-β.
  26. 26LabIn vitro (cells)Mechanism

    In irradiated hepatic stellate cells, Tβ4 downregulated the fibrogenic marker TGF-β.

    In plain wordsIn cells, thymosin β4 lowered a scar-forming marker called TGF-β.

    Outcome
    DecreaseTGF-β expression
    Study

    n: not reported in source

    Hepatic stellate cells
    Outcome group
    Liver fat and liver function · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Additionally, Tβ4 inhibited irradiation-induced activation of hepatic stellate cells by downregulating the expression of fibrogenic markers α-SMA, PAI-1, and TGF-β.

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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