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Study · Animal study (in vivo) · rat · 2017

7 results

Anti-inflammatory Effect of Glucagon Like Peptide-1 Receptor Agonist, Exendin-4, through Modulation of IB1/JIP1 Expression and JNK Signaling in Stroke.

Kim S, Jeong J, Jung HS, Kim B, Kim YE, Lim DS, Kim SD, Song YS

Experimental neurobiology31 Aug 2017Cited by 49 (Europe PMC)

PMID28912645 (opens in a new tab)PMCIDPMC5597553 (opens in a new tab)DOI10.5607/en.2017.26.4.227 (opens in a new tab)PepBankPUB-28912645
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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: CC BY-NC. Results still quote short attributed sentences.

Results from this study7

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

  1. 01AnimalAnimal study (in vivo)Mechanism

    In rats with ischemic injury, exendin‑4 restored GLP-1R expression by 70%.

    In plain wordsIn rats with ischemic injury, exendin‑4 restored GLP-1R expression.

    Peptide
    Exenatide (exendin-4)
    Outcome
    IncreaseGLP-1R expression restoration
    Study

    ratn: not reported in source

    cerebral ischemia-reperfusion injury
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (rat).

    Source sentences

    Summary
    Downregulation of GLP-1R by ischemic injury was 70% restored by GLP-1R agonist, ex-4, which resulted in significant reduction of infarct volume.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In rats with ischemic injury, exendin‑4 significantly reduced infarct volume.

    In plain wordsIn rats with ischemic injury, exendin‑4 reduced infarct volume.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseInfarct volume
    Study

    ratn: not reported in source

    cerebral ischemia-reperfusion injury
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (rat).

    Source sentences

    Summary
    Downregulation of GLP-1R by ischemic injury was 70% restored by GLP-1R agonist, ex-4, which resulted in significant reduction of infarct volume.
  3. 03AnimalAnimal study (in vivo)Mechanism

    In rats after MCAO, exendin‑4 reduced pro-inflammatory COX-2.

    In plain wordsIn rats after MCAO, exendin‑4 reduced COX-2.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseCOX-2
    Study

    ratn: not reported in source

    cerebral ischemia-reperfusion injury
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (rat).

    Source sentences

    Summary
    Moreover, our results showed that ex-4 attenuated pro-inflammatory cyclooxygenase-2 (COX-2) and prostaglandin E2 after MCAO.
  4. 04AnimalAnimal study (in vivo)Mechanism

    In rats after MCAO, exendin‑4 reduced prostaglandin E2.

    In plain wordsIn rats after MCAO, exendin‑4 reduced prostaglandin E2.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseProstaglandin E2
    Study

    ratn: not reported in source

    cerebral ischemia-reperfusion injury
    Outcome group
    Inflammation markers · Nervous system and cognition
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (rat).

    Source sentences

    Summary
    Moreover, our results showed that ex-4 attenuated pro-inflammatory cyclooxygenase-2 (COX-2) and prostaglandin E2 after MCAO.
  5. 05AnimalAnimal study (in vivo)Mechanism

    In rats after MCAO, exendin‑4 inhibited JNK signaling by 36% at 24 h.

    In plain wordsIn rats after MCAO, exendin‑4 reduced JNK signaling.

    Peptide
    Exenatide (exendin-4)
    Outcome
    DecreaseJNK signaling
    Study

    ratn: not reported in source

    cerebral ischemia-reperfusion injury
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (rat).

    Source sentences

    Summary
    C-Jun NH2 terminal kinase (JNK) signaling, which stimulates activation of COX-2, was 36% inhibited by i.c.v. injection of ex-4 at 24 h.
  6. 06AnimalAnimal study (in vivo)Mechanism

    In rats after MCAO, exendin‑4 increased IB1 by 1.7-fold.

    In plain wordsIn rats after MCAO, exendin‑4 increased IB1.

    Peptide
    Exenatide (exendin-4)
    Outcome
    IncreaseIB1 expression
    Study

    ratn: not reported in source

    cerebral ischemia-reperfusion injury
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated · intracerebroventricularAs given in this study (rat).

    Source sentences

    Summary
    Islet-brain 1 (IB1), a scaffold regulator of JNK, was 1.7-fold increased by ex-4.
    1 context sentence
    Summary · context
    Transient middle cerebral artery occlusion (tMCAO) was induced in rats by intracerebroventricular (i.c.v.) administration of ex-4 or ex9-39.

Studies that did not test the peptide alone1

In this study, Exenatide (exendin-4) 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 Exenatide (exendin-4).

  1. 07LabNot a test of Exenatide (exendin-4) aloneOther designMechanism

    In experimental ischemic injury models, high GLP-1R expression was associated with a 2.7-fold increase in intracellular cyclic AMP.

    In plain wordsIn lab tests, high GLP-1R expression was associated with increased intracellular cyclic AMP.

    Peptide
    Exenatide (exendin-4)
    Outcome
    IncreaseIntracellular cyclic AMP
    Study

    n: not reported in source

    Outcome group
    Receptor activity and mechanism · Pharmacology

    Source sentences

    Summary
    Levels of intracellular cyclic AMP, a second messenger of GLP-1R, were also increased by 2.7-fold as a result of high GLP-1R expression.

    In this study, Exenatide (exendin-4) 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 Exenatide (exendin-4).

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Registered trials1

Trials this study reports on, or that list this study as a reference. Registry data from ClinicalTrials.gov.

1 trial · 1 stopped early · source ClinicalTrials.gov (opens in a new tab)

WithdrawnEarly phase 1NCT04133922

Effect of GLP-1 on Microvascular Insulin Responses in Type 1 Diabetes

University of Virginian = 014 Oct 2019 to est. Oct 2024

Type 1 Diabetes · Insulin Sensitivity/Resistance

Trial pageClinicalTrials.govUpdated 22 Mar 2022

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

    22 Oct 2026, 02:26 UTC

    Study results updated

  2. Version 1

    21 Oct 2026, 18:59 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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