Affiliations:
Cardiovascular Department, The Second Hospital of Hebei Medical University, Shijiazhuang, China
Correspondence:
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Corresponding author: Jie Hao, No. 215 Heping West Road, Shijiazhuang City, 050000, Hebei Province, China. Tel.: +86 13833100706; E-mail: haojiemed@hebmu.edu.cn.
Abstract: OBJECTIVE:This study intends to explore the effects of Rosuvastatin on ox-LDL induced platelet activation and its molecular mechanism. METHODS:Platelet aggregation rate was detected by aggregometer. ELISA kit was used to detect the levels of cAMP. Immunofluorescence staining was used to detect the platelet adhesion. The expression levels of platelet surface markers CD62p and PAC-1 were detected by flow cytometry. The protein levels of p-p38, p-IKKa and p-IKKB in platelets were detected by western blot. RESULTS:We found that rosuvastatin significantly inhibited platelet aggregation and increased the level of cAMP in a dose-dependent manner. Immunofluorescence staining results showed that rosuvastatin could inhibit platelet adhesion. Flow cytometry results showed that rosuvastatin could reduce the expression of platelet activation markers. Western blot results showed that rosuvastatin could down-regulate the expression levels of p-p38, p-IKKa and p-IKKb. CONCLUSION:Our study revealed the rosuvastatin could inhibit the aggregation, adhesion and activation of platelet induced by ox-LDL, its mechanism may be related to inhibition of p38/MAPK signal pathway.
