The Mitochondrial-Derived Peptide MOTS-c Attenuates Oxidative Stress Injury and the Inflammatory Response of H9c2 Cells Through the Nrf2/ARE and NF-κB Pathways.

Shen C, Wang J, Feng M, Peng J, Du X, Chu H, Chen X

Cardiovascular engineering and technology2 Dec 2021Cited by 28 (Europe PMC)

PMID34859377DOI10.1007/s13239-021-00589-wPepBankPUB-34859377

Publisher page PubMedAsk about this study

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: Publisher copyright. Results still quote short attributed sentences.

Results from this study11

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

01LabIn vitro (cells)Efficacy outcome
In rat H9c2 cardiomyocytes, MOTS‑c pretreatment reversed the loss of cell viability caused by hydrogen peroxide.
In plain wordsIn cells, MOTS‑c pretreatment reversed the loss of cell viability caused by hydrogen peroxide.
Peptide
MOTS-c
Outcome
IncreaseCell viability after hydrogen peroxide
Study
ratn: not reported in source
H9c2 cardiomyocytes
Outcome group
Cell viability and death · Cardiovascular
Studied dose
10, 20 or 50 μM · 24 h pretreatmentAs given in this study (rat).
Source sentences
Summary
However, pretreatment with MOTS-c significantly reversed H₂O₂-induced damage in H9c2 cells.
3 context sentences(design, population, supporting numbers)
Summary · context
decreased cell viability and the level of SOD
Summary · context
Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H₂O_2.
Summary · context
Then, the cell was treated with 100 μM H₂O₂ for 1 h to induce oxidative stress.
Report a problemFND-3485937701
02LabIn vitro (cells)Efficacy outcome
In rat H9c2 cardiomyocytes, MOTS‑c pretreatment reversed the fall in SOD level caused by hydrogen peroxide.
In plain wordsIn cells, MOTS‑c pretreatment reversed the fall in an antioxidant enzyme (SOD) caused by hydrogen peroxide.
Peptide
MOTS-c
Outcome
IncreaseSOD level after hydrogen peroxide
Study
ratn: not reported in source
H9c2 cardiomyocytes
Outcome group
Oxidative stress · Cardiovascular
Studied dose
10, 20 or 50 μM · 24 h pretreatmentAs given in this study (rat).
Source sentences
Summary
However, pretreatment with MOTS-c significantly reversed H₂O₂-induced damage in H9c2 cells.
3 context sentences(design, population, supporting numbers)
Summary · context
decreased cell viability and the level of SOD
Summary · context
Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H₂O_2.
Summary · context
Then, the cell was treated with 100 μM H₂O₂ for 1 h to induce oxidative stress.
Report a problemFND-3485937702
03LabIn vitro (cells)Efficacy outcome
In rat H9c2 cardiomyocytes, MOTS‑c pretreatment reversed the rise in reactive oxygen species (ROS) caused by hydrogen peroxide.
In plain wordsIn cells, MOTS‑c pretreatment reversed the rise in harmful reactive oxygen species caused by hydrogen peroxide.
Peptide
MOTS-c
Outcome
DecreaseROS level after hydrogen peroxide
Study
ratn: not reported in source
H9c2 cardiomyocytes
Outcome group
Oxidative stress · Cardiovascular
Studied dose
10, 20 or 50 μM · 24 h pretreatmentAs given in this study (rat).
Source sentences
Summary
However, pretreatment with MOTS-c significantly reversed H₂O₂-induced damage in H9c2 cells.
3 context sentences(design, population, supporting numbers)
Summary · context
increased the levels of ROS and MDA
Summary · context
Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H₂O_2.
Summary · context
Then, the cell was treated with 100 μM H₂O₂ for 1 h to induce oxidative stress.
Report a problemFND-3485937703
04LabIn vitro (cells)Efficacy outcome
In rat H9c2 cardiomyocytes, MOTS‑c pretreatment reversed the rise in MDA caused by hydrogen peroxide.
In plain wordsIn cells, MOTS‑c pretreatment reversed the rise in a marker of oxidative damage (MDA) caused by hydrogen peroxide.
Peptide
MOTS-c
Outcome
DecreaseMDA level after hydrogen peroxide
Study
ratn: not reported in source
H9c2 cardiomyocytes
Outcome group
Oxidative stress · Cardiovascular
Studied dose
10, 20 or 50 μM · 24 h pretreatmentAs given in this study (rat).
Source sentences
Summary
However, pretreatment with MOTS-c significantly reversed H₂O₂-induced damage in H9c2 cells.
3 context sentences(design, population, supporting numbers)
Summary · context
increased the levels of ROS and MDA
Summary · context
Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H₂O_2.
Summary · context
Then, the cell was treated with 100 μM H₂O₂ for 1 h to induce oxidative stress.
Report a problemFND-3485937704
05LabIn vitro (cells)Efficacy outcome
In rat H9c2 cardiomyocytes, MOTS‑c pretreatment reversed the rise in TNF-α caused by hydrogen peroxide.
In plain wordsIn cells, MOTS‑c pretreatment reversed the rise in the inflammation signal TNF-α caused by hydrogen peroxide.
Peptide
MOTS-c
Outcome
DecreaseTNF-α expression after hydrogen peroxide
Study
ratn: not reported in source
H9c2 cardiomyocytes
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
10, 20 or 50 μM · 24 h pretreatmentAs given in this study (rat).
Source sentences
Summary
However, pretreatment with MOTS-c significantly reversed H₂O₂-induced damage in H9c2 cells.
3 context sentences(design, population, supporting numbers)
Summary · context
upregulated the expression of inflammatory cytokines, including TNF-α, IL-6 and IL-1β
Summary · context
Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H₂O_2.
Summary · context
Then, the cell was treated with 100 μM H₂O₂ for 1 h to induce oxidative stress.
Report a problemFND-3485937705
06LabIn vitro (cells)Efficacy outcome
In rat H9c2 cardiomyocytes, MOTS‑c pretreatment reversed the rise in IL-6 caused by hydrogen peroxide.
In plain wordsIn cells, MOTS‑c pretreatment reversed the rise in the inflammation signal IL-6 caused by hydrogen peroxide.
Peptide
MOTS-c
Outcome
DecreaseIL-6 expression after hydrogen peroxide
Study
ratn: not reported in source
H9c2 cardiomyocytes
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
10, 20 or 50 μM · 24 h pretreatmentAs given in this study (rat).
Source sentences
Summary
However, pretreatment with MOTS-c significantly reversed H₂O₂-induced damage in H9c2 cells.
3 context sentences(design, population, supporting numbers)
Summary · context
upregulated the expression of inflammatory cytokines, including TNF-α, IL-6 and IL-1β
Summary · context
Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H₂O_2.
Summary · context
Then, the cell was treated with 100 μM H₂O₂ for 1 h to induce oxidative stress.
Report a problemFND-3485937706
07LabIn vitro (cells)Efficacy outcome
In rat H9c2 cardiomyocytes, MOTS‑c pretreatment reversed the rise in IL-1β caused by hydrogen peroxide.
In plain wordsIn cells, MOTS‑c pretreatment reversed the rise in the inflammation signal IL-1β caused by hydrogen peroxide.
Peptide
MOTS-c
Outcome
DecreaseIL-1β expression after hydrogen peroxide
Study
ratn: not reported in source
H9c2 cardiomyocytes
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
10, 20 or 50 μM · 24 h pretreatmentAs given in this study (rat).
Source sentences
Summary
However, pretreatment with MOTS-c significantly reversed H₂O₂-induced damage in H9c2 cells.
3 context sentences(design, population, supporting numbers)
Summary · context
upregulated the expression of inflammatory cytokines, including TNF-α, IL-6 and IL-1β
Summary · context
Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H₂O_2.
Summary · context
Then, the cell was treated with 100 μM H₂O₂ for 1 h to induce oxidative stress.
Report a problemFND-3485937707
08LabIn vitro (cells)Mechanism
In rat H9c2 cardiomyocytes, MOTS‑c protected against hydrogen peroxide-induced damage by activating the Nrf2/ARE pathway.
In plain wordsIn cells, MOTS‑c protected against hydrogen peroxide damage by switching on the Nrf2/ARE protective pathway.
Peptide
MOTS-c
Outcome
IncreaseNrf2/ARE pathway activation
Study
ratn: not reported in source
H9c2 cardiomyocytes
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
10, 20 or 50 μM · 24 h pretreatmentAs given in this study (rat).
Source sentences
Summary
Our investigation indicated that MOTS-c could protect against H₂O₂-induced inflammation and oxidative stress in H9c2 cells by inhibiting NF-κB and activating the Nrf2/ARE pathways.
3 context sentences(design, population, supporting numbers)
Summary · context
The expression levels of Nrf2, HO-1 and NQO-1 were significantly downregulated
Summary · context
Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H₂O_2.
Summary · context
Then, the cell was treated with 100 μM H₂O₂ for 1 h to induce oxidative stress.
Report a problemFND-3485937708
09LabIn vitro (cells)Mechanism
In rat H9c2 cardiomyocytes, MOTS‑c protected against hydrogen peroxide-induced inflammation by inhibiting the NF-κB pathway.
In plain wordsIn cells, MOTS‑c protected against hydrogen peroxide inflammation by switching off the NF-κB pathway.
Peptide
MOTS-c
Outcome
DecreaseNF-κB pathway inhibition
Study
ratn: not reported in source
H9c2 cardiomyocytes
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
10, 20 or 50 μM · 24 h pretreatmentAs given in this study (rat).
Source sentences
Summary
Our investigation indicated that MOTS-c could protect against H₂O₂-induced inflammation and oxidative stress in H9c2 cells by inhibiting NF-κB and activating the Nrf2/ARE pathways.
3 context sentences(design, population, supporting numbers)
Summary · context
the phosphorylation of NF-κBp65 was promoted by H₂O₂.
Summary · context
Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H₂O_2.
Summary · context
Then, the cell was treated with 100 μM H₂O₂ for 1 h to induce oxidative stress.
Report a problemFND-3485937709
10LabIn vitro (cells)Mechanism
In rat H9c2 cardiomyocytes, inhibiting the Nrf2/ARE pathway decreased the protective effects of MOTS‑c.
In plain wordsIn cells, blocking the Nrf2/ARE pathway reduced the protective effects of MOTS‑c.
Peptide
MOTS-c
Outcome
Not applicableEffect of Nrf2 inhibition on MOTS-c action
Study
ratn: not reported in source
H9c2 cardiomyocytes
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
10, 20 or 50 μM · 24 h pretreatmentAs given in this study (rat).
Source sentences
Summary
Moreover, both inhibition of the Nrf2/ARE pathway and activation of the NF-κB pathway significantly decreased the effects of MOTS-c, suggesting that MOTS-c might play a role in alleviating oxidative damage via the Nrf2/ARE and NF-κB pathways.
2 context sentences(design, population, supporting numbers)
Summary · context
Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H₂O_2.
Summary · context
Then, the cell was treated with 100 μM H₂O₂ for 1 h to induce oxidative stress.
Report a problemFND-3485937710
11LabIn vitro (cells)Mechanism
In rat H9c2 cardiomyocytes, activating the NF-κB pathway decreased the protective effects of MOTS‑c.
In plain wordsIn cells, switching on the NF-κB pathway reduced the protective effects of MOTS‑c.
Peptide
MOTS-c
Outcome
Not applicableEffect of NF-κB activation on MOTS-c action
Study
ratn: not reported in source
H9c2 cardiomyocytes
Outcome group
Receptor activity and mechanism · Cardiovascular
Studied dose
10, 20 or 50 μM · 24 h pretreatmentAs given in this study (rat).
Source sentences
Summary
Moreover, both inhibition of the Nrf2/ARE pathway and activation of the NF-κB pathway significantly decreased the effects of MOTS-c, suggesting that MOTS-c might play a role in alleviating oxidative damage via the Nrf2/ARE and NF-κB pathways.
2 context sentences(design, population, supporting numbers)
Summary · context
Rat H9c2 cardiomyocytes were obtained, and 10, 20 or 50 μM MOTS-c was pretreated for 24 h before treatment with H₂O_2.
Summary · context
Then, the cell was treated with 100 μM H₂O₂ for 1 h to induce oxidative stress.
Report a problemFND-3485937711

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
9 Oct 2026, 18:17 UTC
Study results updated
Version 1
9 Oct 2026, 02:47 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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The Mitochondrial-Derived Peptide MOTS-c Attenuates Oxidative Stress Injury and the Inflammatory Response of H9c2 Cells Through the Nrf2/ARE and NF-κB Pathways.

Summary

Results from this study11

Version history

Subjects

Publication types

MeSH terms

Keywords