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Study · Ex vivo tissue · rat · 2020

9 results

Modulatory effects of BPC 157 on vasomotor tone and the activation of Src-Caveolin-1-endothelial nitric oxide synthase pathway.

Hsieh MJ, Lee CH, Chueh HY, Chang GJ, Huang HY, Lin Y, Pang JS

Scientific reports13 Oct 2020Cited by 54 (Europe PMC)

PMID33051481 (opens in a new tab)PMCIDPMC7555539 (opens in a new tab)DOI10.1038/s41598-020-74022-y (opens in a new tab)PepBankPUB-33051481
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Summary

BPC 157-activated endothelial nitric oxide synthase (eNOS) is associated with tissue repair and angiogenesis as reported in previous studies. However, how BPC 157 regulates the vasomotor tone and intracellular Src-Caveolin-1 (Cav-1)-eNOS signaling is not yet clear. The present study demonstrated a concentration-dependent vasodilation effect of BPC 157 in isolated rat aorta. Attenuation of this vasodilation effect in the absence of endothelium suggested an endothelium-dependent vasodilation effect of BPC 157. Although slightly increased vasorelaxation in aorta without endothelium was noticed at high concentration of BPC 157, there was no direct relaxation effect on three-dimensional model made of vascular smooth muscle cells. The vasodilation effect of BPC 157 was nitric oxide mediated because the addition of L-NAME or hemoglobin inhibited the vasodilation of aorta. Nitric oxide generation was induced by BPC 157 as detected by intracellular DFA-FM DA labeling which was capable of promoting the migration of vascular endothelial cells. BPC 157 enhanced the phosphorylation of Src, Cav-1 and eNOS which was abolished by pretreatment with Src inhibitor, confirming the upstream role of Src in this signal pathway. Activation of eNOS required the released binding with Cav-1 in advance. Co-immunoprecipitation analysis revealed that BPC 157 could reduce the binding between Cav-1 and eNOS. Together, the present study demonstrates that BPC 157 can modulate the vasomotor tone of an isolated aorta in a concentration- and nitric oxide-dependent manner. BPC 157 can induce nitric oxide generation likely through the activation of Src-Cav-1-eNOS pathway.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study9

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

  1. 01LabEx vivo tissueActivity measurement

    In isolated rat aorta, BPC‑157 produced a concentration-dependent vasodilation effect.

    In plain wordsIn lab tests on rat aorta, BPC‑157 widened the blood vessel in a way that depended on its concentration.

    Peptide
    BPC-157
    Outcome
    IncreaseVasodilation of isolated aorta
    Study

    Ratn: not reported in source

    Isolated aorta
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The present study demonstrated a concentration-dependent vasodilation effect of BPC 157 in isolated rat aorta.
  2. 02LabEx vivo tissueMechanism

    In isolated rat aorta, the vasodilation effect of BPC‑157 was attenuated without endothelium (endothelium-dependent), with only slightly increased vasorelaxation at a high BPC‑157 concentration.

    In plain wordsIn lab tests on rat aorta, BPC‑157 widened the vessel less when the inner lining (endothelium) was missing.

    Peptide
    BPC-157
    Outcome
    DecreaseVasodilation in aorta without endothelium
    Study

    Ratn: not reported in source

    Isolated aorta
    Comparator
    Aorta with endothelium
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Attenuation of this vasodilation effect in the absence of endothelium suggested an endothelium-dependent vasodilation effect of BPC 157.
    1 context sentence
    Summary · context
    Although slightly increased vasorelaxation in aorta without endothelium was noticed at high concentration of BPC 157,
  3. 03LabEx vivo tissueMechanism

    In isolated rat aorta, adding L-NAME or hemoglobin inhibited the vasodilation caused by BPC‑157, which indicates nitric oxide mediation.

    In plain wordsIn lab tests on rat aorta, blocking nitric oxide inhibited the vessel widening caused by BPC‑157.

    Peptide
    BPC-157
    Outcome
    DecreaseInhibition of BPC 157 vasodilation by L-NAME or hemoglobin
    Study

    Ratn: not reported in source

    Isolated aorta
    Comparator
    Aorta without L-NAME or hemoglobin
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The vasodilation effect of BPC 157 was nitric oxide mediated because the addition of L-NAME or hemoglobin inhibited the vasodilation of aorta.
  4. 04LabIn vitro (cells)Mechanism

    In a three-dimensional model made of vascular smooth muscle cells, BPC‑157 had no direct relaxation effect.

    In plain wordsIn lab tests on a model of blood vessel muscle cells, BPC‑157 did not relax the cells directly.

    Peptide
    BPC-157
    Outcome
    No significant changeDirect relaxation of vascular smooth muscle cell model
    Study

    n: not reported in source

    Three-dimensional model made of vascular smooth muscle cells
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    there was no direct relaxation effect on three-dimensional model made of vascular smooth muscle cells.
  5. 05LabIn vitro (cells)Mechanism

    In cells, BPC‑157 induced nitric oxide generation, detected by intracellular DFA-FM DA labeling.

    In plain wordsIn cells, BPC‑157 led to nitric oxide being made inside the cells.

    Peptide
    BPC-157
    Outcome
    IncreaseNitric oxide generation in endothelial cells
    Study

    n: not reported in source

    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Nitric oxide generation was induced by BPC 157 as detected by intracellular DFA-FM DA labeling
  6. 06LabIn vitro (cells)Mechanism

    In vascular endothelial cells, the nitric oxide generation induced by BPC‑157 was capable of promoting cell migration.

    In plain wordsIn cells, nitric oxide made after BPC‑157 could promote the movement of blood vessel lining cells.

    Peptide
    BPC-157
    Outcome
    IncreaseVascular endothelial cell migration
    Study

    n: not reported in source

    Vascular endothelial cells
    Outcome group
    Wound healing · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    which was capable of promoting the migration of vascular endothelial cells.
    1 context sentence
    Summary · context
    Nitric oxide generation was induced by BPC 157 as detected by intracellular DFA-FM DA labeling
  7. 07LabIn vitro (cells)Mechanism

    In cells, BPC‑157 enhanced the phosphorylation of Src, Cav-1 and eNOS.

    In plain wordsIn cells, BPC‑157 increased the activation of three signaling proteins: Src, Cav-1 and eNOS.

    Peptide
    BPC-157
    Outcome
    IncreasePhosphorylation of Src, Cav-1 and eNOS
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    BPC 157 enhanced the phosphorylation of Src, Cav-1 and eNOS
  8. 08LabIn vitro (cells)Mechanism

    In cells, pretreatment with a Src inhibitor abolished the BPC‑157-enhanced phosphorylation of Src, Cav-1 and eNOS, which confirms an upstream role of Src.

    In plain wordsIn cells, blocking Src stopped the signaling activation caused by BPC‑157.

    Peptide
    BPC-157
    Outcome
    DecreaseEffect of Src inhibitor on BPC 157-induced phosphorylation
    Study

    n: not reported in source

    Comparator
    Without Src inhibitor pretreatment
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    which was abolished by pretreatment with Src inhibitor, confirming the upstream role of Src in this signal pathway.
    1 context sentence
    Summary · context
    BPC 157 enhanced the phosphorylation of Src, Cav-1 and eNOS
  9. 09LabIn vitro (cells)Mechanism

    In co-immunoprecipitation analysis, BPC‑157 could reduce the binding between Cav-1 and eNOS.

    In plain wordsIn lab tests, BPC‑157 reduced the binding between two proteins, Cav-1 and eNOS.

    Peptide
    BPC-157
    Outcome
    DecreaseBinding between Cav-1 and eNOS
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Co-immunoprecipitation analysis revealed that BPC 157 could reduce the binding between Cav-1 and eNOS.

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 3Current

    9 Oct 2026, 12:39 UTC

    Study results updated

  2. Version 2

    9 Oct 2026, 03:03 UTC

    Study data updated · source update from Europe PMC

  3. Version 1

    9 Oct 2026, 02:56 UTC

    First added · source update from Europe PMC

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Terms as the source lists them.

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