Michael Aviram , Cesare R. Sirtori , Susanna Colli , Paola Maderna , Gabriele Morazzoni , Elena Tremoli
{"title":"血浆脂蛋白影响血小板丙二醛和凝血素B2的产生","authors":"Michael Aviram , Cesare R. Sirtori , Susanna Colli , Paola Maderna , Gabriele Morazzoni , Elena Tremoli","doi":"10.1016/0006-2944(85)90059-6","DOIUrl":null,"url":null,"abstract":"<div><p>Platelet interaction with plasma lipoproteins was studied using gel-filtered platelets free of plasma constituents and purified lipoproteins. On incubation of gel-filtered platelets with plasma lipoproteins at 30°C for 30 min, 100 μg of protein/ml of very-low as well as low-density lipoprotein caused 10% increment in platelet aggregation and [<sup>14</sup>C]serotonin release in parallel to elevation of around 15% of malondialdehyde and thromboxane B<sub>2</sub> production. High-density lipoprotein showed the opposite effect and reduced platelet aggregation as well as thromboxane B<sub>2</sub> synthesis by 17 and 32%, respectively. Lipoprotein-deficient plasma enhanced platelet function. Preincubation of the platelet suspension with prostacyclin did not prevent the effect of the lipoproteins on the <em>in vitro</em> platelet response as well as on the platelet prostaglandin pathway. Our results suggest that the formation of thromboxane B<sub>2</sub> and malondialdlehyde is influenced by plasma lipoproteins and that these, in turn, affect platelet aggregation and the release reaction. The possible significance of these results to platelet function in hyperlipidemic patients is discussed.</p></div>","PeriodicalId":8781,"journal":{"name":"Biochemical medicine","volume":"34 1","pages":"Pages 29-36"},"PeriodicalIF":0.0000,"publicationDate":"1985-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0006-2944(85)90059-6","citationCount":"43","resultStr":"{\"title\":\"Plasma lipoproteins affect platelet malondialdehyde and thromboxane B2 production\",\"authors\":\"Michael Aviram , Cesare R. Sirtori , Susanna Colli , Paola Maderna , Gabriele Morazzoni , Elena Tremoli\",\"doi\":\"10.1016/0006-2944(85)90059-6\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Platelet interaction with plasma lipoproteins was studied using gel-filtered platelets free of plasma constituents and purified lipoproteins. On incubation of gel-filtered platelets with plasma lipoproteins at 30°C for 30 min, 100 μg of protein/ml of very-low as well as low-density lipoprotein caused 10% increment in platelet aggregation and [<sup>14</sup>C]serotonin release in parallel to elevation of around 15% of malondialdehyde and thromboxane B<sub>2</sub> production. High-density lipoprotein showed the opposite effect and reduced platelet aggregation as well as thromboxane B<sub>2</sub> synthesis by 17 and 32%, respectively. Lipoprotein-deficient plasma enhanced platelet function. Preincubation of the platelet suspension with prostacyclin did not prevent the effect of the lipoproteins on the <em>in vitro</em> platelet response as well as on the platelet prostaglandin pathway. Our results suggest that the formation of thromboxane B<sub>2</sub> and malondialdlehyde is influenced by plasma lipoproteins and that these, in turn, affect platelet aggregation and the release reaction. The possible significance of these results to platelet function in hyperlipidemic patients is discussed.</p></div>\",\"PeriodicalId\":8781,\"journal\":{\"name\":\"Biochemical medicine\",\"volume\":\"34 1\",\"pages\":\"Pages 29-36\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1985-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/0006-2944(85)90059-6\",\"citationCount\":\"43\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Biochemical medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/0006294485900596\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biochemical medicine","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/0006294485900596","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Plasma lipoproteins affect platelet malondialdehyde and thromboxane B2 production
Platelet interaction with plasma lipoproteins was studied using gel-filtered platelets free of plasma constituents and purified lipoproteins. On incubation of gel-filtered platelets with plasma lipoproteins at 30°C for 30 min, 100 μg of protein/ml of very-low as well as low-density lipoprotein caused 10% increment in platelet aggregation and [14C]serotonin release in parallel to elevation of around 15% of malondialdehyde and thromboxane B2 production. High-density lipoprotein showed the opposite effect and reduced platelet aggregation as well as thromboxane B2 synthesis by 17 and 32%, respectively. Lipoprotein-deficient plasma enhanced platelet function. Preincubation of the platelet suspension with prostacyclin did not prevent the effect of the lipoproteins on the in vitro platelet response as well as on the platelet prostaglandin pathway. Our results suggest that the formation of thromboxane B2 and malondialdlehyde is influenced by plasma lipoproteins and that these, in turn, affect platelet aggregation and the release reaction. The possible significance of these results to platelet function in hyperlipidemic patients is discussed.