Key result
PPARγ agonists such as 15d-PGJ2 and rosiglitazone prevented thrombin-induced CD40L surface expression and release of CD40L and thromboxane B2 in human platelets.
Why the study?
Do PPARgamma agonists reduce the release of proinflammatory and proatherogenic mediators in human platelets?
Population
Human platelets, Meg-01 megakaryocyte cells, and human bone marrow megakaryocytes
Design
Preclinical
Authors
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May inhibit platelet mediators; hypothesis-generating for anti-inflammatory effects, with no clinical implications yet.
Do PPARgamma agonists reduce the release of proinflammatory and proatherogenic mediators in human platelets?
Human platelets express PPARgamma, and its agonists inhibit platelet activation and release of proinflammatory mediators, suggesting a novel mechanism for treating inflammation and thrombosis.
Akbıyık et al. (2004) studied this question. PPARγ agonists (15d-PGJ2, rosiglitazone) was evaluated on Platelet release of CD40L and thromboxane B2, and surface expression of CD40L. PPARγ agonists such as 15d-PGJ2 and rosiglitazone prevented thrombin-induced CD40L surface expression and release of CD40L and thromboxane B2 in human platelets.
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