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Study · Measured the body's own peptide · 2022

1 result

Targeting Hydrogen Sulfide Modulates Dexamethasone-Induced Muscle Atrophy and Microvascular Rarefaction, through Inhibition of NOX4 and Induction of MGF, M2 Macrophages and Endothelial Progenitors.

Adel M, Elsayed HRH, El-Nablaway M, Hamed S, Eladl A, Fouad S, El Nashar EM, Al-Otaibi ML, Rabei MR

Cells11 Aug 2022Cited by 14 (Europe PMC)

PMID36010575 (opens in a new tab)PMCIDPMC9406793 (opens in a new tab)DOI10.3390/cells11162500 (opens in a new tab)PepBankPUB-36010575
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Summary

Long-term use of Glucocorticoids produces skeletal muscle atrophy and microvascular rarefaction. Hydrogen sulfide (H2S) has a potential role in skeletal muscle regeneration. However, the mechanisms still need to be elucidated. This is the first study to explore the effect of Sodium hydrosulfide (NaHS) H2S donor, against Dexamethasone (Dex)-induced soleus muscle atrophy and microvascular rarefaction and on muscle endothelial progenitors and M2 macrophages. Rats received either; saline, Dex (0.6 mg/Kg/day), Dex + NaHS (5 mg/Kg/day), or Dex + Aminooxyacetic acid (AOAA), a blocker of H2S (10 mg/Kg/day) for two weeks. The soleus muscle was examined for contractile properties. mRNA expression for Myostatin, Mechano-growth factor (MGF) and NADPH oxidase (NOX4), HE staining, and immunohistochemical staining for caspase-3, CD34 (Endothelial progenitor marker), vascular endothelial growth factor (VEGF), CD31 (endothelial marker), and CD163 (M2 macrophage marker) was performed. NaHS could improve the contractile properties and decrease oxidative stress, muscle atrophy, and the expression of NOX4, caspase-3, Myostatin, VEGF, and CD31 and could increase the capillary density and expression of MGF with a significant increase in expression of CD34 and CD163 as compared to Dex group. However, AOAA worsened the studied parameters. Therefore, H2S can be a promising target to attenuate muscle atrophy and microvascular rarefaction.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

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

Natural levels measured1

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. 01AnimalEndogenous levelAnimal study (in vivo)Mechanism

    In rats with dexamethasone-induced muscle atrophy, sodium hydrosulfide increased the body's own MGF expression in soleus muscle compared with dexamethasone alone.

    In plain wordsIn rats with steroid-induced muscle loss, an H2S donor raised the body's own MGF in muscle compared with steroid alone.

    Peptide
    MGF / PEG-MGF
    Outcome
    IncreaseMGF expression in soleus muscle
    Study

    ratn: not reported in source

    Dexamethasone-induced soleus muscle atrophy
    Comparator
    Dexamethasone group
    Outcome group
    Muscle injury and repair · Musculoskeletal

    Source sentences

    Summary
    could increase the capillary density and expression of MGF
    1 context sentence
    Summary · context
    Rats received either; saline, Dex (0.6 mg/Kg/day), Dex + NaHS (5 mg/Kg/day), or Dex + Aminooxyacetic acid (AOAA), a blocker of H2S (10 mg/Kg/day) for two weeks.

    This result measures the body's own MGF / PEG-MGF. Nobody was given the peptide. It is not evidence about taking it.

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, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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