Related Experiment Video
Updated: Oct 6, 2025

Author Spotlight: Developing Parmodulins to Target Protease-Activated Receptors for Inflammation Control
Published on: May 24, 2024
Antiplatelet and Antithrombotic Effects of Isaridin E Isolated from the Marine-Derived Fungus via Downregulating the
Ni Pan1,2, Zi-Cheng Li1, Zhi-Hong Li1
1Department of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Abstract:
Isaridin E, a cyclodepsipeptide isolated from the marine-derived fungus Amphichorda felina (syn. Beauveria felina) SYSU-MS7908, has been demonstrated to possess anti-inflammatory and insecticidal activities. Here, we first found that isaridin E concentration-dependently inhibited ADP-induced platelet aggregation, activation, and secretion in vitro, but did not affect collagen- or thrombin-induced platelet aggregation. Furthermore, isaridin E dose-dependently reduced thrombosis formation in an FeCl3-induced mouse carotid model without increasing the bleeding time. Mechanistically, isaridin E significantly decreased the ADP-mediated phosphorylation of PI3K and Akt. In conclusion, these results suggest that isaridin E exerts potent antithrombotic effects in vivo without increasing the risk of bleeding, which may be due to its important role in inhibiting ADP-induced platelet activation, secretion and aggregation via the PI3K/Akt pathways.
Insights
Isaridin E, a marine compound, effectively prevents blood clots in mice by inhibiting adenosine diphosphate (ADP)-induced platelet aggregation. This antithrombotic effect occurs without increasing bleeding risk, suggesting a potential new therapeutic avenue.
Area of Science:
- Marine natural products
- Pharmacology
- Biochemistry
Background:
- Isaridin E, a cyclodepsipeptide from marine fungus Amphichorda felina, exhibits anti-inflammatory and insecticidal properties.
- Platelet aggregation plays a critical role in thrombosis and hemostasis.
Purpose of the Study:
- To investigate the antithrombotic effects of Isaridin E.
- To elucidate the underlying molecular mechanisms of Isaridin E's action on platelets.
Main Methods:
- In vitro studies on ADP-, collagen-, and thrombin-induced platelet aggregation, activation, and secretion.
- In vivo thrombosis model using FeCl3-induced carotid artery injury in mice.
- Western blot analysis to assess PI3K and Akt phosphorylation.
Main Results:
- Isaridin E inhibited ADP-induced platelet aggregation, activation, and secretion in a concentration-dependent manner.
- Isaridin E dose-dependently reduced thrombosis in a mouse model without affecting bleeding time.
- Isaridin E decreased ADP-mediated phosphorylation of PI3K and Akt.
Conclusions:
- Isaridin E demonstrates significant antithrombotic activity in vivo.
- The mechanism involves the inhibition of ADP-induced platelet activation and aggregation via the PI3K/Akt signaling pathway.
- Isaridin E represents a promising antithrombotic agent with a favorable safety profile regarding bleeding risk.
More Related Videos
13:18Network Pharmacology Prediction and Experimental Validation of Trichosanthes-Fritillaria thunbergii Action Mechanism Against Lung Adenocarcinoma
Published on: March 3, 2023
11:13Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
Published on: June 9, 2023
Related Concept Videos
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
The JAK-STAT Signaling Pathway
Anticoagulant Drugs: Low-Molecular-Weight Heparins
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
PI3K/mTOR/AKT Signaling Pathway
IP3/DAG Signaling Pathway