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Study · In vitro (cells) · 2022

4 results

Mycophenolic Acid Induces the Intestinal Epithelial Barrier Damage through Mitochondrial ROS.

Deng Y, Zhang Z, Yang H, Wang J, Feng L, Su Y, Xu D

Oxidative medicine and cellular longevity5 Jul 2022Cited by 25 (Europe PMC)

PMID35847589 (opens in a new tab)PMCIDPMC9277164 (opens in a new tab)DOI10.1155/2022/4195699 (opens in a new tab)PepBankPUB-35847589
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Summary

Mycophenolic acid (MPA) may cause gastrointestinal adverse effects by damaging the intestinal epithelial barrier, the underlying mechanisms remain elusive. Studies have demonstrated that oxidative stress caused by reactive oxygen species (ROS) is linked to tight junction (TJ) proteins and apoptosis, both of which cause abnormalities in intestinal barrier function. Mitochondria, one of the main sources of ROS and abnormally high levels of ROS are linked to mitochondrial dysfunction. The aim of this study was to investigate whether MPA induces intestinal barrier dysfunction through regulation of the mitochondrial ROS. MPA-induced intestinal injury model in Kunming mice and Caco-2 cells. The effect of MPA on Caco-2 cell viability was measured by MTT; tissue diamine oxidase and endotoxin expression were determined by ELISA; expression of total proteins of ZO-1, occludin, Bax, Bcl-2, and mitochondrial proteins of Cytochrome C and Bax was measured by Western blot; and the localization of Cytochrome C with MitoTraker was observed by immunofluorescence staining. Caco-2 cell apoptosis, ROS levels, and mitochondrial membrane potential were detected by flow cytometry, while intramitochondrial ROS levels were observed by MitoSOX fluorescence staining. The results showed that MPA increased intracellular and mitochondrial ROS production to promote oxidative stress and the antioxidant NAC effectively restored ZO-1 and occludin expressions, reduced apoptosis in intestinal epithelial cells. Furthermore, we found that low concentrations of MPA caused mitochondrial damage, induced hyperpolarization of the mitochondrial membrane potential and the translocation of Cytochrome C and Bax proteins from the cytoplasm to the mitochondria. The mitochondrial protectant SS-31 reduces intracellular and intramitochondrial ROS, upregulates TJ, and reduces apoptosis. Our studies suggest that MPA-induced intestinal barrier dysfunction in vivo and in vitro is mediated, at least in part, by impairing mitochondrial function and promoting oxidative stress.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study4

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

  1. 01LabIn vitro (cells)Efficacy outcome

    In the mycophenolic acid intestinal barrier model, SS‑31 reduced intracellular ROS.

    In plain wordsIn a lab model of gut-lining damage, SS‑31 lowered reactive oxygen species inside cells.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseIntracellular ROS
    Study

    n: not reported in source

    Outcome group
    Mitochondrial function · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The mitochondrial protectant SS-31 reduces intracellular and intramitochondrial ROS, upregulates TJ, and reduces apoptosis.
    1 context sentence
    Summary · context
    MPA-induced intestinal injury model in Kunming mice and Caco-2 cells.
  2. 02LabIn vitro (cells)Efficacy outcome

    In the mycophenolic acid intestinal barrier model, SS‑31 reduced intramitochondrial ROS.

    In plain wordsIn a lab model of gut-lining damage, SS‑31 lowered reactive oxygen species inside mitochondria.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseIntramitochondrial ROS
    Study

    n: not reported in source

    Outcome group
    Mitochondrial function · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The mitochondrial protectant SS-31 reduces intracellular and intramitochondrial ROS, upregulates TJ, and reduces apoptosis.
    1 context sentence
    Summary · context
    MPA-induced intestinal injury model in Kunming mice and Caco-2 cells.
  3. 03LabIn vitro (cells)Efficacy outcome

    In the mycophenolic acid intestinal barrier model, SS‑31 upregulated tight junction proteins.

    In plain wordsIn a lab model of gut-lining damage, SS‑31 raised levels of proteins that seal the gut lining.

    Peptide
    Elamipretide (SS-31)
    Outcome
    IncreaseTight junction protein expression
    Study

    n: not reported in source

    Outcome group
    Gastrointestinal protection · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The mitochondrial protectant SS-31 reduces intracellular and intramitochondrial ROS, upregulates TJ, and reduces apoptosis.
    1 context sentence
    Summary · context
    MPA-induced intestinal injury model in Kunming mice and Caco-2 cells.
  4. 04LabIn vitro (cells)Efficacy outcome

    In the mycophenolic acid intestinal barrier model, SS‑31 reduced apoptosis.

    In plain wordsIn a lab model of gut-lining damage, SS‑31 reduced cell death.

    Peptide
    Elamipretide (SS-31)
    Outcome
    DecreaseApoptosis of intestinal epithelial cells
    Study

    n: not reported in source

    Outcome group
    Cell viability and death · Gastrointestinal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The mitochondrial protectant SS-31 reduces intracellular and intramitochondrial ROS, upregulates TJ, and reduces apoptosis.
    1 context sentence
    Summary · context
    MPA-induced intestinal injury model in Kunming mice and Caco-2 cells.

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

    10 Oct 2026, 08:19 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 02:47 UTC

    First added · source update from Europe PMC

Subjects

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