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Study · In vitro (cells) · 2023

6 results

Thymosin Beta 4 Inhibits LPS and ATP-Induced Hepatic Stellate Cells via the Regulation of Multiple Signaling Pathways.

Choi J, Cho Y, Choi H, Lee S, Han H, Lee J, Kwon J

International journal of molecular sciences8 Feb 2023Cited by 11 (Europe PMC)

PMID36834849 (opens in a new tab)PMCIDPMC9959661 (opens in a new tab)DOI10.3390/ijms24043439 (opens in a new tab)PepBankPUB-36834849
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Summary

Risk signals are characteristic of many common inflammatory diseases and can function to activate nucleotide-binding oligomerization (NLR) family pyrin domain-containing 3 (NLRP3), the innate immune signal receptor in cytoplasm. The NLRP3 inflammasome plays an important role in the development of liver fibrosis. Activated NLRP3 nucleates the assembly of inflammasomes, leading to the secretion of interleukin (IL)-1β and IL-18, the activation of caspase-1, and the initiation of the inflammatory process. Therefore, it is essential to inhibit the activation of the NLRP3 inflammasome, which plays a vital role in the immune response and in initiating inflammation. RAW 264.7 and LX-2 cells were primed with lipopolysaccharide (LPS) for 4 h and subsequently stimulated for 30 min with 5 mM of adenosine 5'-triphosphate (ATP) to activate the NLRP3 inflammasome. Thymosin beta 4 (Tβ4) was supplemented to RAW264.7 and LX-2 cells 30 min before ATP was added. As a result, we investigated the effects of Tβ4 on the NLRP3 inflammasome. Tβ4 prevented LPS-induced NLRP3 priming by inhibiting NF-kB and JNK/p38 MAPK expression and the LPS and ATP-induced production of reactive oxygen species. Moreover, Tβ4 induced autophagy by controlling autophagy markers (LC3A/B and p62) through the inhibition of the PI3K/AKT/mTOR pathway. LPS combined with ATP significantly increased thee protein expression of inflammatory mediators and NLRP3 inflammasome markers. These events were remarkably suppressed by Tβ4. In conclusion, Tβ4 attenuated NLRP3 inflammasomes by inhibiting NLRP3 inflammasome-related proteins (NLRP3, ASC, IL-1β, and caspase-1). Our results indicate that Tβ4 attenuated the NLRP3 inflammasome through multiple signaling pathway regulations in macrophage and hepatic stellate cells. Therefore, based on the above findings, it is hypothesized that Tβ4 could be a potential inflammatory therapeutic agent targeting the NLRP3 inflammasome in hepatic fibrosis regulation.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

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

  1. 01LabIn vitro (cells)Mechanism

    In macrophage and hepatic stellate cell lines, Tβ4 prevented LPS-induced NLRP3 priming by inhibiting NF-kB and JNK/p38 MAPK expression.

    In plain wordsIn cells, Tβ4 blocked the first inflammation signal from LPS by lowering NF-kB and JNK/p38 MAPK.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseLPS-induced NLRP3 priming, NF-kB and JNK/p38 MAPK expression
    Study

    n: not reported in source

    RAW 264.7 macrophages and LX-2 hepatic stellate cells with LPS and ATP
    Comparator
    LPS and ATP without Tβ4
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Tβ4 prevented LPS-induced NLRP3 priming by inhibiting NF-kB and JNK/p38 MAPK expression
    2 context sentences
    Summary · context
    RAW 264.7 and LX-2 cells were primed with lipopolysaccharide (LPS) for 4 h and subsequently stimulated for 30 min with 5 mM of adenosine 5'-triphosphate (ATP) to activate the NLRP3 inflammasome.
    Summary · context
    Thymosin beta 4 (Tβ4) was supplemented to RAW264.7 and LX-2 cells 30 min before ATP was added.
  2. 02LabIn vitro (cells)Mechanism

    In macrophage and hepatic stellate cell lines, Tβ4 inhibited the LPS and ATP-induced production of reactive oxygen species.

    In plain wordsIn cells, Tβ4 lowered the reactive oxygen species made after LPS and ATP.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseLPS and ATP-induced reactive oxygen species
    Study

    n: not reported in source

    RAW 264.7 macrophages and LX-2 hepatic stellate cells with LPS and ATP
    Comparator
    LPS and ATP without Tβ4
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    and the LPS and ATP-induced production of reactive oxygen species.
    2 context sentences
    Summary · context
    RAW 264.7 and LX-2 cells were primed with lipopolysaccharide (LPS) for 4 h and subsequently stimulated for 30 min with 5 mM of adenosine 5'-triphosphate (ATP) to activate the NLRP3 inflammasome.
    Summary · context
    Thymosin beta 4 (Tβ4) was supplemented to RAW264.7 and LX-2 cells 30 min before ATP was added.
  3. 03LabIn vitro (cells)Mechanism

    In cell lines, Tβ4 induced autophagy by controlling the autophagy markers LC3A/B and p62.

    In plain wordsIn cells, Tβ4 changed the autophagy markers LC3A/B and p62 in a way that switched on autophagy.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    MixedAutophagy markers LC3A/B and p62
    Study

    n: not reported in source

    RAW 264.7 macrophages and LX-2 hepatic stellate cells with LPS and ATP
    Comparator
    LPS and ATP without Tβ4
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Moreover, Tβ4 induced autophagy by controlling autophagy markers (LC3A/B and p62)
    2 context sentences
    Summary · context
    RAW 264.7 and LX-2 cells were primed with lipopolysaccharide (LPS) for 4 h and subsequently stimulated for 30 min with 5 mM of adenosine 5'-triphosphate (ATP) to activate the NLRP3 inflammasome.
    Summary · context
    Thymosin beta 4 (Tβ4) was supplemented to RAW264.7 and LX-2 cells 30 min before ATP was added.
  4. 04LabIn vitro (cells)Mechanism

    In cell lines, Tβ4 inhibited the PI3K/AKT/mTOR pathway.

    In plain wordsIn cells, Tβ4 lowered activity of the PI3K/AKT/mTOR pathway.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreasePI3K/AKT/mTOR pathway
    Study

    n: not reported in source

    RAW 264.7 macrophages and LX-2 hepatic stellate cells with LPS and ATP
    Comparator
    LPS and ATP without Tβ4
    Outcome group
    Receptor activity and mechanism · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    through the inhibition of the PI3K/AKT/mTOR pathway.
    2 context sentences
    Summary · context
    RAW 264.7 and LX-2 cells were primed with lipopolysaccharide (LPS) for 4 h and subsequently stimulated for 30 min with 5 mM of adenosine 5'-triphosphate (ATP) to activate the NLRP3 inflammasome.
    Summary · context
    Thymosin beta 4 (Tβ4) was supplemented to RAW264.7 and LX-2 cells 30 min before ATP was added.
  5. 05LabIn vitro (cells)Mechanism

    LPS and ATP together increased protein expression of inflammatory mediators and NLRP3 inflammasome markers, and Tβ4 remarkably suppressed these events.

    In plain wordsIn cells, Tβ4 strongly reduced the rise in inflammation proteins caused by LPS and ATP.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseInflammatory mediators and NLRP3 inflammasome markers after LPS and ATP
    Study

    n: not reported in source

    RAW 264.7 macrophages and LX-2 hepatic stellate cells with LPS and ATP
    Comparator
    LPS and ATP without Tβ4
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    LPS combined with ATP significantly increased thee protein expression of inflammatory mediators and NLRP3 inflammasome markers. These events were remarkably suppressed by Tβ4.
    2 context sentences
    Summary · context
    RAW 264.7 and LX-2 cells were primed with lipopolysaccharide (LPS) for 4 h and subsequently stimulated for 30 min with 5 mM of adenosine 5'-triphosphate (ATP) to activate the NLRP3 inflammasome.
    Summary · context
    Thymosin beta 4 (Tβ4) was supplemented to RAW264.7 and LX-2 cells 30 min before ATP was added.
  6. 06LabIn vitro (cells)Mechanism

    Tβ4 attenuated NLRP3 inflammasomes by inhibiting NLRP3, ASC, IL-1β and caspase-1 proteins.

    In plain wordsIn cells, Tβ4 lowered the NLRP3, ASC, IL-1β and caspase-1 proteins of the inflammasome.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    DecreaseNLRP3, ASC, IL-1β and caspase-1 proteins
    Study

    n: not reported in source

    RAW 264.7 macrophages and LX-2 hepatic stellate cells with LPS and ATP
    Comparator
    LPS and ATP without Tβ4
    Outcome group
    Inflammation markers · Liver
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In conclusion, Tβ4 attenuated NLRP3 inflammasomes by inhibiting NLRP3 inflammasome-related proteins (NLRP3, ASC, IL-1β, and caspase-1).
    2 context sentences
    Summary · context
    RAW 264.7 and LX-2 cells were primed with lipopolysaccharide (LPS) for 4 h and subsequently stimulated for 30 min with 5 mM of adenosine 5'-triphosphate (ATP) to activate the NLRP3 inflammasome.
    Summary · context
    Thymosin beta 4 (Tβ4) was supplemented to RAW264.7 and LX-2 cells 30 min before ATP was added.

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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