食品科学 ›› 2021, Vol. 42 ›› Issue (9): 130-136.doi: 10.7506/spkx1002-6630-20200608-108

• 营养卫生 • 上一篇    下一篇

辅酶Q10经蛋白激酶A/胞浆型磷脂酶A2信号通路抑制血小板血栓素A2的生成

牙甫礼,张春梅,陈彬林,谷仕艳,贾小娥   

  1. (1.大理大学公共卫生学院,预防医学研究所,云南 大理 671000;2.河口海关,云南 河口 661300;3.广西壮族自治区妇幼保健院营养科,广西 南宁 530000)
  • 出版日期:2021-05-15 发布日期:2021-06-02
  • 基金资助:
    大理大学2020年度高层次人才科研启动基金项目(KY2096107240);

Coenzyme Q10 Attenuates Platelet Thromboxane A2 Generation through Regulating the Protein Kinase A/Cytosolic Phospholipase A2 Signaling Pathway

YA Fuli, ZHANG Chunmei, CHEN Binlin, GU Shiyan, JIA Xiao’e   

  1. (1. Institute of Preventive Medicine, School of Public Health, Dali University, Dali 671000, China; 2. Hekou Customs of the People’s Republic of China, Hekou 661300, China;3. Department of Nutrition, Maternity and Child Health Care of Guangxi Zhuang Autonomous Region, Nanning 530000, China)
  • Online:2021-05-15 Published:2021-06-02

摘要: 目的:血小板来源血栓素A2(thromboxane A2,TxA2)可诱发动脉粥样硬化和血栓形成,辅酶Q10(coenzyme Q10,CoQ10)可以抑制血小板活化、聚集和血栓形成。本实验旨在通过体外实验探讨CoQ10对血小板TxA2生成的影响及其调控机制。方法:用不同浓度(0、1、10、100 μmol/L)CoQ10与健康人纯化血小板在体外共同孵育50 min,在激动剂激活条件下,采用酶联免疫吸附测定法测定血小板分泌TxB2水平;用Western blot蛋白免疫印迹法检测胞浆型磷脂酶A2(cytosolic phospholipase A2,cPLA2)蛋白的磷酸化水平。结果:CoQ10显著抑制多种激动剂(如凝血酶、胶原和Convulxin)诱导的血小板TxA2生成;Western blot结果显示CoQ10下调凝血酶和胶原诱导的血小板cPLA2磷酸化水平;cPLA2特异性抑制剂苯乙酮与CoQ10联合使用时,对血小板TxA2的生成没有协同效果;此外,蛋白激酶A(protein kinase A,PKA)特异性抑制剂H89可完全逆转CoQ10对激动剂诱导的血小板cPLA2 磷酸化和TxA2生成的抑制作用。结论:CoQ10具有显著抑制激动剂诱导的血小板TxA2生成的作用,其机制主要是调控PKA/cPLA2介导的信号通路。

关键词: 辅酶Q10;血小板;血栓素A2;胞浆型磷脂酶A2;心血管疾病

Abstract: Objective: Thromboxane A2 (TxA2) derived from platelets can facilitate atherosclerosis and thrombosis. Previous studies have demonstrated that coenzyme Q10 (CoQ10) attenuates platelet activation, aggregation and thrombus formation. Our present study aimed to investigate the effect of CoQ10 on TxA2 generation and to clarify the underlying mechanisms. Methods: Gel-filtered platelets prepared from heathy adults were incubated with different concentrations of CoQ10 (0, 1, 10 and 100 μmol/L) for 50 min. After agonist activation, the level of TxB2 secreted from platelets was determined by enzyme-linked immunosorbent assay. The phosphorylation of cytosolic phospholipase A2 (cPLA2) was measured by Western blot. Results: CoQ10 significantly inhibited platelet TxA2 generation induced by several agonists, including thrombin, collagen and convulxin. Western blot showed that CoQ10 significantly down-regulated thrombin- and collagen-induced cPLA2 phosphorylation. Moreover, pyrrophenone, a cPLA2 specific inhibitor, showed no any additive effects on TxA2 generation when combined with CoQ10. Furthermore, the inhibitory effect of CoQ10 on agonist-induced platelet cPLA2 phosphorylation and TxA2 generation was almost completely reversed by protein kinase A (PKA) inhibitor H89. Conclusion: CoQ10 can attenuate agonist-induced platelet TxA2 generation, and the mechanism is mainly through regulating the PKA/cPLA2 signaling pathway.

Key words: coenzyme Q10; platelet; thromboxane A2; cytosolic phospholipase A2; cardiovascular diseases

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