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Thymoquinone-induced platelet apoptosis.

Syeda Tasneem Towhid¹, Eva-Maria Schmidt, Evi Schmid

¹Department of Physiology, University of Tübingen, Tübingen, Germany.

Journal of Cellular Biochemistry

|June 21, 2011

Summary

Thymoquinone (TQ) induces programmed cell death in blood platelets. This process involves calcium signaling, ceramide formation, and caspase activation, mediated by PI3K signaling.

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Area of Science:

Biochemistry
Cell Biology
Pharmacology

Background:

Thymoquinone (TQ) exhibits anticarcinogenic properties and induces cell death in tumor cells and erythrocytes (eryptosis).
The mechanisms underlying TQ's effects on platelets, crucial for hemostasis, were not fully understood.

Purpose of the Study:

To investigate the impact of Thymoquinone (TQ) on blood platelet apoptosis.
To elucidate the molecular pathways involved in TQ-induced platelet cell death.

Main Methods:

Platelet apoptosis markers assessed via Annexin V binding, cytosolic Ca(2+) activity (Fluo 3-AM), caspase activity (immunofluorescence, Western blot), mitochondrial potential (DiOC(6)), and ceramide levels (FACS).
Experiments included varying extracellular Ca(2+) concentrations and utilizing PI3K inhibitor (wortmannin) and GPCR inhibitor (pertussis toxin).

Main Results:

TQ exposure (≥5 µM) induced platelet membrane scrambling (Annexin V binding), caspase activation, increased cytosolic Ca(2+), mitochondrial depolarization, and ceramide formation.
TQ did not increase P-selectin exposure or integrin α(IIb) β(3) activation.
The TQ-induced effects were partially dependent on extracellular Ca(2+) and significantly inhibited by PI3K and GPCR inhibitors.

Conclusions:

Thymoquinone (TQ) triggers suicidal death (apoptosis) in blood platelets.
This platelet apoptosis is a PI3K-dependent process, potentially involving a GPCR, and is characterized by increased cytosolic Ca(2+), ceramide formation, mitochondrial depolarization, and caspase-3 activation.