Atherothrombosis is the leading cause of morbidity and mortality worldwide. Tanshinone IIA (TS IIA), a pharmacological active components extracting from the rhizome of the Chinese herb Salvia miltiorrhiza Bunge, has been used widely for effective treatment of atherothrombosis in traditional Chinese medicine for a long history [
1,
2]. However, its underlying molecular mechanisms of anti-thrombotic effect are still poorly understood. Platelet activation has been implicated as central components of the Virchow’s triad for thrombus formation [
3]. Platelet-derived microvesicles (PMVs) have a critical role in activation of platelets [
4]. It is well established that PMVs, carrying inflammation factors, oxidation factors, various growth factors and coagulation factors, can participate in a wide range of pathophysiological process [
5,
6]. Similarly, TS IIA has been reported to have multi-pharmaceutical activities, such as anti-inflammatory capacity [
7], antioxidant properties [
8] and the ability to prevent platelet activation [
9]. Moreover, Tang et al. [
10] had showed that TS IIA attenuates atherosclerosis in ApoE (-/-) mice through down-regulation of CD36 expression. CD36, a class B scavenger receptor, promotes platelet activation by binding with PMVs. As shown in our previous study, PMV-CD36 complex could activate mitogen-activated protein kinase kinase 4/Jun N-terminal kinase 2 (MKK4/JNK2) signals and lead to platelet activation [
11]. We hypothesized that TS IIA could inhibit platelet activation by suppressing the effects of MKK4/JNK2 signaling pathway mediated by PMV-CD36 complex, which has never been reported.
The present study intends to investigate whether TS IIA could prevent platelet activation induced by PMV-complex and down-regulates MKK4/JNK2 signaling pathway. PMV-CD36 complex could be the target of atherosclerosis (AS)-related thrombosis.