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

Surfactin C inhibits platelet aggregation.

Sung Dae Kim1, Sun Kyu Park, Jae Youl Cho

  • 1Laboratory of Veterinary Physiology & Signaling, College of Veterinary Medicine, Kyungpook National University, Daegu 702-701, Republic of Korea.

The Journal of Pharmacy and Pharmacology
|June 1, 2006
PubMed
Summary

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

The ethanolic extract of Rhaphidophora peepla prevents inflammation by inhibiting the activation of Syk/AKT/NF-κB and TAK1/MAPK/AP-1.

Phytomedicine : international journal of phytotherapy and phytopharmacology·2025
Same author

Genetic Variants Associated with Sensitive Skin: A Genome-Wide Association Study in Korean Women.

Life (Basel, Switzerland)·2024
Same author

Syk/Src/NF-κB axis is essentially targeted in anti-inflammatory and anti-gastritis effects of Bletilla striata ethanol extract.

Journal of ethnopharmacology·2024
Same author

Functional Involvement of TANK-Binding Kinase 1 in the MyD88-Dependent NF-<i>κ</i>B Pathway Through Syk.

Mediators of inflammation·2024
Same author

PP2 suppresses proliferation and migration of C6 Glioma and MDA-MB-231 cells by targeting both fibroblast growth factor receptor 1 and Src.

Chemico-biological interactions·2024
Same author

METTL18 functions as a Phenotypic Regulator in Src-Dependent Oncogenic Responses of HER2-Negative Breast Cancer.

International journal of biological sciences·2024

Surfactin C from Bacillus subtilis effectively inhibits platelet aggregation by targeting downstream signaling pathways, not cell membranes. This suggests potential therapeutic benefits for cardiovascular diseases.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Microbiology

Background:

  • Platelet aggregation plays a critical role in cardiovascular diseases.
  • Bacillus subtilis produces surfactin C, a lipopeptide with various biological activities.
  • Understanding the precise mechanisms of surfactin C's action is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the effects of surfactin C on platelet aggregation and homotypic leukocyte aggregation.
  • To elucidate the mechanism by which surfactin C exerts its anti-platelet activity.
  • To assess the potential therapeutic implications of surfactin C for cardiovascular conditions.

Main Methods:

  • Investigated surfactin C's impact on platelet aggregation induced by thrombin and collagen.

Related Experiment Videos

  • Measured intracellular calcium (Ca2+) mobilization in activated platelets.
  • Assessed surfactin C's effect on integrin-mediated U937 cell aggregation.
  • Main Results:

    • Surfactin C demonstrated strong, dose-dependent inhibition of both thrombin- and collagen-induced platelet aggregation.
    • Surfactin C significantly suppressed intracellular Ca2+ mobilization in thrombin-activated platelets.
    • Surfactin C did not inhibit integrin-mediated U937 cell aggregation, indicating a specific mechanism beyond detergent effects.

    Conclusions:

    • Surfactin C's anti-platelet activity is mediated through downstream signaling pathways, not a general detergent effect.
    • The findings suggest surfactin C has therapeutic potential for managing cardiovascular diseases associated with aberrant platelet aggregation.
    • Further research into surfactin C's signaling pathway interactions is warranted.