河北医科大学学报
河北醫科大學學報
하북의과대학학보
JOURNAL OF HEBEI MEDICAL UNIVERSITY
2014年
12期
1365-1368
,共4页
都虹%郝杰%鲁静朝%杨秀春%崔炜%刘凡
都虹%郝傑%魯靜朝%楊秀春%崔煒%劉凡
도홍%학걸%로정조%양수춘%최위%류범
血小板活化%过氧化物酶体增殖物激活受体%辛伐他汀
血小闆活化%過氧化物酶體增殖物激活受體%辛伐他汀
혈소판활화%과양화물매체증식물격활수체%신벌타정
platelet activation%peroxisome proliferator-activated receptors%simvastin
目的:探讨辛伐他汀体外恒温孵育对胶原诱导的血小板活化的影响及相关机制。方法采集河北医科大学第二医院门诊健康成人志愿者外周静脉血,并制备血小板悬液,应用全血阻抗法、流式细胞术、酶联免疫吸附测定及荧光分光光度法测定不同浓度辛伐他汀体外孵育对胶原诱导的血小板聚集及活化的影响,检测辛伐他汀体外孵育对血小板胞浆过氧化物酶体增殖物激活受体(peroxisome proliferator-activated receptors,PPARs)活化的影响,以及 PPARs 活化后对血小板功能的作用。结果辛伐他汀体外孵育可活化 PPARs (P <0.05),并可通过活化 PPARγ进而抑制胶原诱导的血小板聚集、活化标志物表达以及胞浆钙离子浓度升高。结论辛伐他汀可通过PPARγ激活抑制胶原诱导的血小板活化。
目的:探討辛伐他汀體外恆溫孵育對膠原誘導的血小闆活化的影響及相關機製。方法採集河北醫科大學第二醫院門診健康成人誌願者外週靜脈血,併製備血小闆懸液,應用全血阻抗法、流式細胞術、酶聯免疫吸附測定及熒光分光光度法測定不同濃度辛伐他汀體外孵育對膠原誘導的血小闆聚集及活化的影響,檢測辛伐他汀體外孵育對血小闆胞漿過氧化物酶體增殖物激活受體(peroxisome proliferator-activated receptors,PPARs)活化的影響,以及 PPARs 活化後對血小闆功能的作用。結果辛伐他汀體外孵育可活化 PPARs (P <0.05),併可通過活化 PPARγ進而抑製膠原誘導的血小闆聚集、活化標誌物錶達以及胞漿鈣離子濃度升高。結論辛伐他汀可通過PPARγ激活抑製膠原誘導的血小闆活化。
목적:탐토신벌타정체외항온부육대효원유도적혈소판활화적영향급상관궤제。방법채집하북의과대학제이의원문진건강성인지원자외주정맥혈,병제비혈소판현액,응용전혈조항법、류식세포술、매련면역흡부측정급형광분광광도법측정불동농도신벌타정체외부육대효원유도적혈소판취집급활화적영향,검측신벌타정체외부육대혈소판포장과양화물매체증식물격활수체(peroxisome proliferator-activated receptors,PPARs)활화적영향,이급 PPARs 활화후대혈소판공능적작용。결과신벌타정체외부육가활화 PPARs (P <0.05),병가통과활화 PPARγ진이억제효원유도적혈소판취집、활화표지물표체이급포장개리자농도승고。결론신벌타정가통과PPARγ격활억제효원유도적혈소판활화。
ABSTRACT:Objective To examine the mechanisms by which the peroxisome proliferator-activated receptors (PPARs )-mediated pathways contribute to the antiplatelet activity of simvastatin.Methods Blood samples were donated from healthy volunteers in order to prepare human platelet suspensions.The effects of simvastatin on collagen-induced platelet activation and the activity of PPARs were measured by impedance aggregometry,flow cytometric analysis, enzyme-linked immunosorbent assay,and spectrofluorimetry.Results Simvastatin induced PPARα and PPARγ activation in a dose-dependent manner in platelet suspensions (P < 0.05). Additionally,simvastatin inhibited collagen-induced platelet aggregation,expression of CD62 and PAC-1,and Ca2+ mobilization.These effects of simvastatin on platelet responses were strongly reduced by adding selective PPARγ antagonist (P <0.05),but not PPARα antagonist.Conclusion Simvastin inhibition of platelet activation induced by collagen is mediated by PPARγ-dependent processes.