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Study · In vitro (cells) · 2017

5 results

Thymosin-β4 inhibits proliferation and induces apoptosis of hepatic stellate cells through PI3K/AKT pathway.

Zhu L, Cheng M, Liu Y, Yao Y, Zhu Z, Zhang B, Mou Q, Cheng Y

Oncotarget28 Jun 2017Cited by 8 (Europe PMC)

Summary

Liver fibrosis is a necessary stage for chronic liver diseases, and serious threat to human health. Hepatic fibrosis is a necessary stage for chronic liver diseases. Hepatic stellate cells (HSCs) are the primary cell type responsible for fibrosis. Thymosin beta 4 (Tβ4) has a potential role in the pathogenesis of liver fibrosis and that it is especially associated with the activation of HSCs, however, the underlying mechanisms are not fully elucidated. Herein, we investigated the potential role of Tβ4 in liver fibrosis by describing the effects of Tβ4, and we discuss the possible signaling pathway regulated by Tβ4. The expression of Tβ4 was significantly decreased in human HSC cell line LX-2 and CCl4-treated mouse liver. The depletion of Tβ4 significantly associated with the activation of HSCs via the enhanced expression of α-SMA and vimentin. Tβ4 significantly suppressed the viability and migration of HSCs. Understanding the potential effects and regulatory mechanism of Tβ4 in liver fibrosis might help to provide a novel treatment for patients with liver fibrosis.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study5

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

  1. 01LabIn vitro (cells)Efficacy outcome

    Tβ4 significantly suppressed the viability of hepatic stellate cells.

    In plain wordsIn lab cells, thymosin beta‑4 lowered the viability of liver stellate cells.

    Outcome
    DecreaseHSC viability
    Study

    n: not reported in source

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

    Source sentences

    Summary
    Tβ4 significantly suppressed the viability and migration of HSCs.
  2. 02LabIn vitro (cells)Efficacy outcome

    Tβ4 significantly suppressed the migration of hepatic stellate cells.

    In plain wordsIn lab cells, thymosin beta‑4 lowered migration of liver stellate cells.

    Outcome
    DecreaseHSC migration
    Study

    n: not reported in source

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

    Source sentences

    Summary
    Tβ4 significantly suppressed the viability and migration of HSCs.

Natural levels measured2

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. 03AnimalEndogenous levelAnimal study (in vivo)Other

    Tβ4 expression was significantly decreased in the liver of CCl4-treated mice.

    In plain wordsIn mice with toxin-induced liver damage, the body's own thymosin beta‑4 level in the liver was lower.

    Outcome
    DecreaseTβ4 expression in CCl4-treated mouse liver
    Study

    mousen: not reported in source

    CCl4-treated mouse liver
    Outcome group
    Liver fat and liver function · Liver

    Source sentences

    Summary
    The expression of Tβ4 was significantly decreased in human HSC cell line LX-2 and CCl4-treated mouse liver.

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

  2. 04LabEndogenous levelIn vitro (cells)Other

    Tβ4 expression was significantly decreased in the human hepatic stellate cell line LX-2.

    In plain wordsIn human liver stellate cells in the lab, the body's own thymosin beta‑4 level was lower.

    Outcome
    DecreaseTβ4 expression in LX-2 cells
    Study

    humann: not reported in source

    Hepatic stellate cell line LX-2
    Outcome group
    Liver fat and liver function · Liver

    Source sentences

    Summary
    The expression of Tβ4 was significantly decreased in human HSC cell line LX-2 and CCl4-treated mouse liver.

    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. 05LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    Depletion of Tβ4 was significantly associated with hepatic stellate cell activation, with enhanced expression of α-SMA and vimentin.

    In plain wordsIn lab cells, removing thymosin beta‑4 was linked to activation of liver stellate cells and higher scarring markers.

    Outcome
    IncreaseHSC activation markers after Tβ4 depletion
    Study

    n: not reported in source

    Outcome group
    Liver fat and liver function · Liver

    Source sentences

    Summary
    The depletion of Tβ4 significantly associated with the activation of HSCs via the enhanced expression of α-SMA and vimentin.

    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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