Liu Jinming, Jiao Wei, Li Fang, Xie Yanan, Meng Mingjie, Hao Jie
Cardiovascular Department, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Clin Hemorheol Microcirc. 2024;88(4):551-560. doi: 10.3233/CH-242359.
This study intends to explore the effects of Rosuvastatin on ox-LDL induced platelet activation and its molecular mechanism.
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.
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.
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.
本研究旨在探讨瑞舒伐他汀对氧化型低密度脂蛋白（ox-LDL）诱导的血小板活化的影响及其分子机制。
采用血小板聚集仪检测血小板聚集率。使用酶联免疫吸附测定（ELISA）试剂盒检测环磷酸腺苷（cAMP）水平。采用免疫荧光染色检测血小板黏附情况。通过流式细胞术检测血小板表面标志物CD62p和血小板激活依赖的颗粒外膜蛋白-1（PAC-1）的表达水平。采用蛋白质免疫印迹法检测血小板中磷酸化p38、磷酸化IKKα和磷酸化IKKβ的蛋白水平。
我们发现瑞舒伐他汀能显著抑制血小板聚集，并以剂量依赖的方式提高cAMP水平。免疫荧光染色结果显示瑞舒伐他汀可抑制血小板黏附。流式细胞术结果显示瑞舒伐他汀可降低血小板活化标志物的表达。蛋白质免疫印迹法结果显示瑞舒伐他汀可下调磷酸化p38、磷酸化IKKα和磷酸化IKKβ的表达水平。
我们的研究表明瑞舒伐他汀可抑制ox-LDL诱导的血小板聚集、黏附和活化，其机制可能与抑制p38/丝裂原活化蛋白激酶（MAPK）信号通路有关。
