Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Anti-inflammatory lipocortin-derived peptides

M Perretti1, R J Flower

  • 1Department of Biochemical Pharmacology, William Harvey Research Institute, London, United Kingdom.

Agents and Actions. Supplements
|January 1, 1995
PubMed
Summary

Peptide Ac2-26, derived from lipocortin 1, effectively inhibits neutrophil elastase release and adhesion. This peptide demonstrates broad efficacy against various neutrophil activators in vitro.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Corrigendum to "Activation of Melanocortin Receptors MC<sub>1</sub> and MC<sub>5</sub> Attenuates Retinal Damage in Experimental Diabetic Retinopathy".

Mediators of inflammation·2021
Same author

Sergio Henrique Ferreira (1934-2016).

British journal of pharmacology·2017
Same author

Activation of Melanocortin Receptors MC 1 and MC 5 Attenuates Retinal Damage in Experimental Diabetic Retinopathy.

Mediators of inflammation·2016
Same author

The role of the Annexin-A1/FPR2 system in the regulation of mast cell degranulation provoked by compound 48/80 and in the inhibitory action of nedocromil.

International immunopharmacology·2016
Same author

On the Eicosanoid Trail with John Vane and Jack McGiff: 1974-1976. A personal reminiscence.

Prostaglandins & other lipid mediators·2015
Same author

'Annexins' themed section.

British journal of pharmacology·2015

Area of Science:

  • Immunology
  • Pharmacology
  • Cell Biology

Background:

  • Neutrophils play a critical role in inflammatory responses.
  • Lipocortin 1 is involved in regulating inflammatory processes.
  • Neutrophil activation leads to the release of enzymes like elastase and increased cell adhesion.

Purpose of the Study:

  • To investigate the in vitro effects of peptide Ac2-26, derived from human lipocortin 1.
  • To determine the inhibitory potential of peptide Ac2-26 on neutrophil elastase release and adhesion.
  • To explore the mechanism of action and scope of peptide Ac2-26's effects.

Main Methods:

  • In vitro assays using human neutrophils and endothelial cells.
  • Concentration-dependent inhibition studies.
  • Evaluation of peptide Ac2-26's efficacy against different neutrophil activators (formyl-Met-Leu-Phe, leukotriene B4, platelet-activating factor).
  • Assessment of peptide Ac2-26's effect on formyl-Met-Leu-Phe receptor binding.

Main Results:

  • Peptide Ac2-26 inhibited elastase release and neutrophil adhesion in a concentration-dependent manner (IC50 ≈ 100 µg/ml, 33 µM).
  • The inhibitory effects were observed regardless of the neutrophil activator used.
  • Peptide Ac2-26 did not interfere with formyl-Met-Leu-Phe binding to its receptor, suggesting a post-receptor mechanism.

Conclusions:

  • Peptide Ac2-26 exhibits significant anti-inflammatory properties by modulating neutrophil activation pathways.
  • The findings support the potential therapeutic applications of peptide Ac2-26 and provide insights into lipocortin 1's function.
  • Further research into peptide Ac2-26's pharmacology is warranted based on these in vitro and complementary in vivo observations.

Related Experiment Videos