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Tanshinone IIA prevents platelet activation and down-regulates CD36 and MKK4/JNK2 signaling pathway

BACKGROUND: Tanshinone IIA (TS IIA), a multi-pharmaceutical compound from traditional Chinese herb, is effective for treatment of atherothrombosis. However, the underlying mechanisms of TS IIA-mediated anti-platelet activation effect are still poorly understood. As shown in our previous study, plate...

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Detalles Bibliográficos
Autores principales: Wang, Hua, Zhong, Lin, Mi, Shaohua, Song, Nianpeng, Zhang, Wei, Zhong, Ming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7023810/
https://www.ncbi.nlm.nih.gov/pubmed/32059638
http://dx.doi.org/10.1186/s12872-019-01289-z
Descripción
Sumario:BACKGROUND: Tanshinone IIA (TS IIA), a multi-pharmaceutical compound from traditional Chinese herb, is effective for treatment of atherothrombosis. However, the underlying mechanisms of TS IIA-mediated anti-platelet activation effect are still poorly understood. As shown in our previous study, platelet-derived microvesicles (PMVs) generated in response to oxidant insult could activate CD36/mitogen-activated protein kinase kinase 4/Jun N-terminal kinase 2 (CD36/MKK4/JNK2) signals and lead to platelet activation. The present study aims to investigate the effect of TS IIA on platelet activation and the possible mechanisms. METHODS: The production of PMVs induced by Interleukin 6 (IL-6) was detected by flow cytometry. We performed activating studies of platelets with PMVs derived from IL-6–treated platelets (IL-6–PMVs) in vitro. Sometimes, platelet suspensions were incubated with serial concentrations of TS IIA for 15 min before being stimulated with IL-6–PMVs. Expression of platelet integrin α(IIb)β(3) and CD36 was detected by flow cytometry. Phosphorylation of MKK4 and JNK were detected by immunoblotting. RESULTS: Here we demonstrated firstly that TS IIA could prevent platelet activation induced by PMVs and down-regulates CD36 and MKK4/JNK2 signaling pathway. CD36 may be the target of atherosclerosis (AS)-related thrombosis. CONCLUSIONS: This study showed the possible mechanisms of TS IIA-mediated anti-platelet activation and may provide a new strategy for the treatment of AS-related thrombosis by targeting platelet CD36.