| Autor: |
Chu LX; The Fourth Affiliated Hospital of Guangxi Medical University Department of Cardiology Liuzhou China chullxiang@sina.com., Zhou SX; Affiliated Hospital of Guilin Medical College Department of Endocrine Guilin China., Yang F; The Fourth Affiliated Hospital of Guangxi Medical University Department of Cardiology Liuzhou China., Qin YQ; The Fourth Affiliated Hospital of Guangxi Medical University Department of Cardiology Liuzhou China., Liang ZS; The Fourth Affiliated Hospital of Guangxi Medical University Department of Cardiology Liuzhou China., Mo CG; The Eighth Affiliated Hospital of Guangxi Medical University Department of Cardiology Guigang China., Wang XD; The Fourth Affiliated Hospital of Guangxi Medical University Department of Cardiology Liuzhou China., Xie J; The Fourth Affiliated Hospital of Guangxi Medical University Department of Cardiology Liuzhou China., He LP; The Fourth Affiliated Hospital of Guangxi Medical University Department of Cardiology Liuzhou China. |
| Jazyk: |
angličtina |
| Zdroj: |
Cellular and molecular biology (Noisy-le-Grand, France) [Cell Mol Biol (Noisy-le-grand)] 2016 Feb 29; Vol. 62 (2), pp. 75-80. Date of Electronic Publication: 2016 Feb 29. |
| Abstrakt: |
Protease-activated receptor-1 (PAR-1) plays an important role in mediating activation of human platelets by thrombin. However, mechanism of statin in ADP-induced platelet PAR-1 expression is also unknown. Aggregometry, flow cytometry, immunoblotting and ELISA were used to determine role of pravastatin participating in ADP-induced platelet activation and PAR-1 expression. ADP stimulation significantly increased PAR-1 expression on platelets. PAR-1 antagonist SCH-79797 inhibited platelet aggregation as well as decreased platelet P-selectin expression induced by ADP. CRP inhibited PAR-1 expression induced by ADP in a concentration-dependent manner. Pravastatin treatment reduced PAR-1 expression in a concentration-dependent manner. Combination treatment of CRP and Pravastatin significantly reduced platelet PAR-1 expression induced by ADP. By western-blot analysis, pravastatin treatment did not influence total PAR-1 after ADP treatment. CRP decreased platelet total PAR-1 expression induced by ADP. Pravastatin and CRP reduced TXB2 formation by ADP significantly. CRP decreased thrombin fragment F1+2 level with ADP treatment. Pravastatin, in contrast, did not influence F1+2 level. Upon treatment with Pravastatin reduced platelet LOX-1 expression induced by ADP. In conclusion, PAR-1 served as a critical mechanism to relay platelet activation process induced by ADP. CRP and pravastatin reduce PAR-1 expression in platelet by ADP pathway. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
|
