Antioxioxidant and antiapoptotic effects of Thymosin β4 in Aβ-induced SH-SY5Y cells via the 5-HTR1A/ERK axis.

Zhang GH, Chin KL, Yan SY, Pare R

PloS one3 Oct 2023Cited by 5 (Europe PMC)

PMID37788276PMCIDPMC10547165DOI10.1371/journal.pone.0287817PepBankPUB-37788276

Summary

Alzheimer's disease (AD) is a common amnestic cognitive impairment characterised by β-amyloid (Aβ) plaques deposit in the brain of the elderly. AD is a yet incurable disease due to its unknown exact pathogenesis and unavailability of effective remedies in clinical application. Thymosin β4 (Tβ4) is a housekeeping protein that plays important role in cell proliferation, migration and differentiation. It has the ability to protect and repair neurons however it is still unclear involvement in AD. Therefore, the aim of this study is to elucidate the role and mechanism of Tβ4 in mediating the improvement of AD. AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ. Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection. We performed western blot and flow cytometry to study the apoptosis and standard kits to measure the oxidative stress-associated biomarkers. There is significant increased in viability and decreased apoptosis in Tβ4 overexpression group compared to control. Furthermore, overexpression of Tβ4 suppressed the expression of pro-apoptotic markers such as Caspase-3, Caspase-8, and Bax meanwhile upregulated the expression of anti-apoptotic gene Bcl-2. Tβ4 alleviated oxidative damage by reducing MDA, LDH and ROS and increasing SOD and GSH-PX in Aβ-treated SH-SY5Y cells. We found that Tβ4 inhibit ERK/p38 MAPK pathway and intensify the expression of 5-HTR1A. Additionally, we showed that upregulation of 5-HTR1A dampened the Tβ4 to activate ERK signalling. In conclusion, our study revealed the neuroprotective role of Tβ4 in AD which may open up new therapeutic applications in AD treatment.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study13

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone13

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).

01LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Efficacy outcome
In Aβ-treated SH-SY5Y cells, Tβ4 overexpression significantly increased viability compared with control.
In plain wordsIn cells modeling Alzheimer's disease, raising Tβ4 levels increased cell survival compared with control.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseCell viability
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
There is significant increased in viability and decreased apoptosis in Tβ4 overexpression group compared to control.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827601
02LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Efficacy outcome
In Aβ-treated SH-SY5Y cells, Tβ4 overexpression significantly decreased apoptosis compared with control.
In plain wordsIn cells modeling Alzheimer's disease, raising Tβ4 levels reduced cell death compared with control.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseApoptosis
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
There is significant increased in viability and decreased apoptosis in Tβ4 overexpression group compared to control.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827602
03LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In Aβ-treated SH-SY5Y cells, Tβ4 overexpression suppressed expression of the pro-apoptotic marker Caspase-3.
In plain wordsIn cells modeling Alzheimer's disease, raising Tβ4 levels lowered a cell death marker, Caspase-3.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseCaspase-3 expression
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Furthermore, overexpression of Tβ4 suppressed the expression of pro-apoptotic markers such as Caspase-3, Caspase-8, and Bax meanwhile upregulated the expression of anti-apoptotic gene Bcl-2.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827603
04LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In Aβ-treated SH-SY5Y cells, Tβ4 overexpression suppressed expression of the pro-apoptotic marker Caspase-8.
In plain wordsIn cells modeling Alzheimer's disease, raising Tβ4 levels lowered a cell death marker, Caspase-8.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseCaspase-8 expression
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Furthermore, overexpression of Tβ4 suppressed the expression of pro-apoptotic markers such as Caspase-3, Caspase-8, and Bax meanwhile upregulated the expression of anti-apoptotic gene Bcl-2.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827604
05LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In Aβ-treated SH-SY5Y cells, Tβ4 overexpression suppressed expression of the pro-apoptotic marker Bax.
In plain wordsIn cells modeling Alzheimer's disease, raising Tβ4 levels lowered a cell death marker, Bax.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseBax expression
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Furthermore, overexpression of Tβ4 suppressed the expression of pro-apoptotic markers such as Caspase-3, Caspase-8, and Bax meanwhile upregulated the expression of anti-apoptotic gene Bcl-2.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827605
06LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In Aβ-treated SH-SY5Y cells, Tβ4 overexpression upregulated expression of the anti-apoptotic gene Bcl-2.
In plain wordsIn cells modeling Alzheimer's disease, raising Tβ4 levels increased a cell survival gene, Bcl-2.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseBcl-2 expression
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Neuroprotection · Nervous system and cognition
Source sentences
Summary
Furthermore, overexpression of Tβ4 suppressed the expression of pro-apoptotic markers such as Caspase-3, Caspase-8, and Bax meanwhile upregulated the expression of anti-apoptotic gene Bcl-2.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827606
07LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Efficacy outcome
In Aβ-treated SH-SY5Y cells, Tβ4 reduced MDA.
In plain wordsIn cells modeling Alzheimer's disease, Tβ4 reduced the oxidative damage marker MDA.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseMalondialdehyde (MDA)
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Oxidative stress · Nervous system and cognition
Source sentences
Summary
Tβ4 alleviated oxidative damage by reducing MDA, LDH and ROS and increasing SOD and GSH-PX in Aβ-treated SH-SY5Y cells.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827607
08LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Efficacy outcome
In Aβ-treated SH-SY5Y cells, Tβ4 reduced LDH.
In plain wordsIn cells modeling Alzheimer's disease, Tβ4 reduced the cell damage marker LDH.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseLactate dehydrogenase (LDH)
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Oxidative stress · Nervous system and cognition
Source sentences
Summary
Tβ4 alleviated oxidative damage by reducing MDA, LDH and ROS and increasing SOD and GSH-PX in Aβ-treated SH-SY5Y cells.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827608
09LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Efficacy outcome
In Aβ-treated SH-SY5Y cells, Tβ4 reduced ROS.
In plain wordsIn cells modeling Alzheimer's disease, Tβ4 reduced reactive oxygen species.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseReactive oxygen species (ROS)
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Oxidative stress · Nervous system and cognition
Source sentences
Summary
Tβ4 alleviated oxidative damage by reducing MDA, LDH and ROS and increasing SOD and GSH-PX in Aβ-treated SH-SY5Y cells.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827609
10LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Efficacy outcome
In Aβ-treated SH-SY5Y cells, Tβ4 increased SOD.
In plain wordsIn cells modeling Alzheimer's disease, Tβ4 increased the antioxidant enzyme SOD.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseSuperoxide dismutase (SOD)
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Oxidative stress · Nervous system and cognition
Source sentences
Summary
Tβ4 alleviated oxidative damage by reducing MDA, LDH and ROS and increasing SOD and GSH-PX in Aβ-treated SH-SY5Y cells.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827610
11LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Efficacy outcome
In Aβ-treated SH-SY5Y cells, Tβ4 increased GSH-PX.
In plain wordsIn cells modeling Alzheimer's disease, Tβ4 increased the antioxidant enzyme GSH-PX.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseGlutathione peroxidase (GSH-PX)
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Oxidative stress · Nervous system and cognition
Source sentences
Summary
Tβ4 alleviated oxidative damage by reducing MDA, LDH and ROS and increasing SOD and GSH-PX in Aβ-treated SH-SY5Y cells.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827611
12LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In Aβ-treated SH-SY5Y cells, Tβ4 inhibited the ERK/p38 MAPK pathway.
In plain wordsIn cells modeling Alzheimer's disease, Tβ4 inhibited the ERK/p38 MAPK signaling pathway.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseERK/p38 MAPK pathway
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Source sentences
Summary
We found that Tβ4 inhibit ERK/p38 MAPK pathway and intensify the expression of 5-HTR1A.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827612
13LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In Aβ-treated SH-SY5Y cells, Tβ4 intensified the expression of 5-HTR1A.
In plain wordsIn cells modeling Alzheimer's disease, Tβ4 increased expression of the receptor 5-HTR1A.
Peptide
Thymosin beta-4 (human)
Outcome
Increase5-HTR1A expression
Study
n: not reported in source
SH-SY5Y neuroblastoma cells treated with Aβ
Comparator
Control
Outcome group
Receptor activity and mechanism · Nervous system and cognition
Source sentences
Summary
We found that Tβ4 inhibit ERK/p38 MAPK pathway and intensify the expression of 5-HTR1A.
2 context sentences(design, population, supporting numbers)
Summary · context
AD-like cell model was constructed in neuroblastoma cell line SH-SY5Y treated with Aβ.
Summary · context
Overexpression of Tβ4 were done using lentivirus infection and downregulation through siRNA transfection.
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).
Show in the study text Report a problemFND-3778827613

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

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MeSH terms

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