Function of Thymosin Beta-4 in Ethanol-Induced Microglial Activation.

Zhang J, Wu J, Zeng W, Yao K, Zu H, Zhao Y

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology19 May 2016Cited by 9 (Europe PMC)

PMID27189760DOI10.1159/000445578PepBankPUB-27189760

Publisher page PubMedAsk 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: CC BY-NC-ND. Results still quote short attributed sentences.

Results from this study11

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

01AnimalAnimal study (in vivo)Efficacy outcome
In a neonatal mouse model of fetal alcohol spectrum disorders, Tβ4 treatment blocked the ethanol-induced increase in inflammatory mediators to the level in vehicle-treated controls.
In plain wordsIn newborn mice exposed to alcohol, Tβ4 treatment blocked the rise in inflammation markers.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseEthanol-induced inflammatory mediators in FASD model
Study
mousen: not reported in source
neonatal mouse FASD model
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
A neonatal mouse fetal alcohol spectrum disorders (FASD) model showed that Tβ4 expression in the microglia of the hippocampus was markedly enhanced, while Tβ4 treatment effectively blocked the ethanol-induced increase in inflammatory mediators, to the level expressed in vehicle-treated control animals.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to investigate the function of Tβ4 in ethanol-induced microglia activation.
Report a problemFND-2718976011
02LabIn vitro (cells)Activity measurement
In BV-2 cells, exogenous Tβ4 significantly inhibited ethanol-induced TNF-α expression and secretion.
In plain wordsIn cells, added Tβ4 reduced TNF-α made after ethanol exposure.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseTNF-α expression and secretion with exogenous Tβ4
Study
n: not reported in source
BV-2 microglial cells
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Exogenous Tβ4 treatment significantly inhibited expression and secretion of these inflammatory mediators.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to investigate the function of Tβ4 in ethanol-induced microglia activation.
Report a problemFND-2718976005
03LabIn vitro (cells)Activity measurement
In BV-2 cells, exogenous Tβ4 significantly inhibited ethanol-induced IL-1β expression and secretion.
In plain wordsIn cells, added Tβ4 reduced IL-1β made after ethanol exposure.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseIL-1β expression and secretion with exogenous Tβ4
Study
n: not reported in source
BV-2 microglial cells
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Exogenous Tβ4 treatment significantly inhibited expression and secretion of these inflammatory mediators.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to investigate the function of Tβ4 in ethanol-induced microglia activation.
Report a problemFND-2718976006
04LabIn vitro (cells)Activity measurement
In BV-2 cells, exogenous Tβ4 significantly inhibited ethanol-induced nitric oxide.
In plain wordsIn cells, added Tβ4 reduced nitric oxide made after ethanol exposure.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseNO expression and secretion with exogenous Tβ4
Study
n: not reported in source
BV-2 microglial cells
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Exogenous Tβ4 treatment significantly inhibited expression and secretion of these inflammatory mediators.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to investigate the function of Tβ4 in ethanol-induced microglia activation.
Report a problemFND-2718976007
05LabIn vitro (cells)Mechanism
In ethanol-exposed microglia, Tβ4 treatment attenuated p38 and ERK MAPK and NF-κB pathway activation.
In plain wordsIn cells, Tβ4 reduced inflammatory signalling switched on by ethanol.
Peptide
Thymosin beta-4 (human)
Outcome
Decreasep38, ERK MAPK and NF-κB pathway activation
Study
n: not reported in source
BV-2 microglial cells
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Tβ4 treatment attenuated p38, ERK MAPKs, and nuclear factor-kappa B (NF-x03BA;B) pathway activation, and enhanced miR-339-5p expression induced by ethanol exposure in microglia.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to investigate the function of Tβ4 in ethanol-induced microglia activation.
Report a problemFND-2718976008
06LabIn vitro (cells)Mechanism
In ethanol-exposed microglia, Tβ4 treatment enhanced miR-339-5p expression.
In plain wordsIn cells, Tβ4 raised the level of a small regulatory RNA, miR-339-5p, after ethanol exposure.
Peptide
Thymosin beta-4 (human)
Outcome
IncreasemiR-339-5p expression
Study
n: not reported in source
BV-2 microglial cells
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Tβ4 treatment attenuated p38, ERK MAPKs, and nuclear factor-kappa B (NF-x03BA;B) pathway activation, and enhanced miR-339-5p expression induced by ethanol exposure in microglia.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to investigate the function of Tβ4 in ethanol-induced microglia activation.
Report a problemFND-2718976009

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.

07AnimalEndogenous levelAnimal study (in vivo)Mechanism
In a neonatal mouse model of fetal alcohol spectrum disorders, Tβ4 expression in hippocampal microglia was markedly enhanced.
In plain wordsIn newborn mice exposed to alcohol, the animals' own Tβ4 rose in brain immune cells.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseTβ4 expression in hippocampal microglia in FASD model
Study
mousen: not reported in source
neonatal mouse FASD model
Outcome group
Inflammation markers · Immune and inflammation
Source sentences
Summary
A neonatal mouse fetal alcohol spectrum disorders (FASD) model showed that Tβ4 expression in the microglia of the hippocampus was markedly enhanced, while Tβ4 treatment effectively blocked the ethanol-induced increase in inflammatory mediators, to the level expressed in vehicle-treated control animals.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to investigate the function of Tβ4 in ethanol-induced microglia activation.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-2718976010
08LabEndogenous levelIn vitro (cells)Mechanism
Tβ4 expression was increased in ethanol-treated microglia.
In plain wordsIn cells, ethanol raised the cells' own Tβ4 levels.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseTβ4 expression in ethanol-treated microglia
Study
n: not reported in source
microglia
Outcome group
Inflammation markers · Immune and inflammation
Source sentences
Summary
Increased Tβ4 expression was observed in ethanol treated microglia.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to investigate the function of Tβ4 in ethanol-induced microglia activation.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-2718976001

Studies that did not test the peptide alone3

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).

09LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In BV-2 cells, knockdown of Tβ4 enhanced ethanol-induced TNF-α.
In plain wordsIn cells, removing Tβ4 made the ethanol-driven rise in TNF-α larger.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseTNF-α after Tβ4 knockdown with ethanol
Study
n: not reported in source
BV-2 microglial cells
Outcome group
Inflammation markers · Immune and inflammation
Source sentences
Summary
Knockdown of Tβ4 enhanced ethanol-induced inflammatory mediators tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and nitric oxide (NO) in BV-2 cells was performed.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to investigate the function of Tβ4 in ethanol-induced microglia activation.
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).
Report a problemFND-2718976002
10LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In BV-2 cells, knockdown of Tβ4 enhanced ethanol-induced IL-1β.
In plain wordsIn cells, removing Tβ4 made the ethanol-driven rise in IL-1β larger.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseIL-1β after Tβ4 knockdown with ethanol
Study
n: not reported in source
BV-2 microglial cells
Outcome group
Inflammation markers · Immune and inflammation
Source sentences
Summary
Knockdown of Tβ4 enhanced ethanol-induced inflammatory mediators tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and nitric oxide (NO) in BV-2 cells was performed.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to investigate the function of Tβ4 in ethanol-induced microglia activation.
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).
Report a problemFND-2718976003
11LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In BV-2 cells, knockdown of Tβ4 enhanced ethanol-induced nitric oxide.
In plain wordsIn cells, removing Tβ4 made the ethanol-driven rise in nitric oxide larger.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseNO after Tβ4 knockdown with ethanol
Study
n: not reported in source
BV-2 microglial cells
Outcome group
Inflammation markers · Immune and inflammation
Source sentences
Summary
Knockdown of Tβ4 enhanced ethanol-induced inflammatory mediators tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and nitric oxide (NO) in BV-2 cells was performed.
1 context sentence(design, population, supporting numbers)
Summary · context
The purpose of this study was to investigate the function of Tβ4 in ethanol-induced microglia activation.
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).
Report a problemFND-2718976004

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.

Version 2Current
13 Oct 2026, 01:52 UTC
Study results updated
Version 1
12 Oct 2026, 18:17 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

Publication types

Journal Article

MeSH terms

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