食品科学 ›› 2021, Vol. 42 ›› Issue (13): 151-157.doi: 10.7506/spkx1002-6630-20200714-187

• 营养卫生 • 上一篇    下一篇

姜黄素对H2O2诱导血小板凋亡的抑制作用及分子机制

牙甫礼,XIN Yu,张春梅,陈彬林,李玮琪,马永洁   

  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.大理大学代谢性疾病转化医学研究院,云南 大理 671000;3.大理大学基础医学院,云南 大理 671000;4.河口海关,云南 河口 661300;5.广西壮族自治区妇幼保健院营养科,广西 南宁 530000)
  • 出版日期:2021-07-15 发布日期:2021-07-27
  • 基金资助:
    大理大学高层次人才启动基金项目(KY2096107240)

Inhibition Effects and Mechanisms of Curcumin on Hydrogen Peroxide-Induced Platelet Apoptosis

YA Fuli, XIN Yu, ZHANG Chunmei, CHEN Binlin, LI Weiqi, MA Yongjie   

  1. (1. Institute of Preventive Medicine, School of Public Health, Dali University, Dali 671000, China; 2. Institute of Translational Medicine for Metabolic Diseases, Dali University, Dali 671000, China; 3. School of Basic Medicine Sciences, Dali University, Dali 671000, China; 4. Hekou Customs, Hekou 661300, China; 5. Nutritional Department, Maternity and Child Health Care of Guangxi Zhuang Autonomous Region, Nanning 530000, China)
  • Online:2021-07-15 Published:2021-07-27

摘要: 目的:血小板凋亡在心血管疾病发生发展过程中发挥重要作用,姜黄素(curcumin,Cur)是存在于姜科植物根茎中的一种多酚类化合物,具有多种生物学活性,但是Cur对血小板凋亡是否具有调控作用尚鲜见报道,本研究通过体外实验探讨Cur对H2O2诱导血小板凋亡的影响及其潜在的机制。方法:用不同浓度(0、1、10、100 μmol/L)的Cur与健康人纯化血小板在体外共同孵育30 min,然后加入H2O2(100 μmol/L)干预血小板60 min,用流式细胞术检测血小板磷脂酰丝氨酸的暴露水平和线粒体膜电位(ΔΨm)去极化水平;用酶联免疫吸附法测定血小板凋亡蛋白Caspase-3和Caspase-9活化水平、胞内总活性氧以及超氧化物生成水平;用Western blot蛋白免疫印迹法检测血小板促凋亡蛋白Bax、Bak和细胞色素c的表达水平。结果:与对照组相比,10、100 μmol/L Cur显著抑制H2O2诱导的血小板磷脂酰丝氨酸暴露和ΔΨm去极化(P<0.05);同时,Western blot结果显示,Cur能显著降低H2O2诱导的血小板促凋亡蛋白Bax、Bak和细胞色素c的表达水平的升高(P<0.05);酶联免疫吸附测定结果表明,H2O2诱导的血小板Caspase-3和Caspase-9的活化可被10、100 μmol/L Cur显著抑制(P<0.05);此外,H2O2处理时,血小板内总活性氧水平和超氧化物水平显著上调,Cur干预可显著抑制胞内总活性氧和超氧化物生成(P<0.05)。结论:Cur具有显著抑制H2O2诱导的血小板凋亡的作用。

关键词: 姜黄素;血小板;凋亡;过氧化氢;氧化应激;心血管疾病

Abstract: Objective: Platelet apoptosis plays an important role in the development and progression of cardiovascular diseases. Curcumin (Cur), a polyphenol compound enriched in the rhizomes of turmeric (Curcuma longa), exerts a wide range of biological activities. Whether Cur acts on platelet apoptosis has not been reported. We therefore sought to investigate the effects of Cur on platelet apoptosis induced by H2O2 as well as to clarify the underlying mechanisms in vitro. Methods: Gel-filtered human platelets were pre-incubated with different concentrations of Cur (0, 1, 10 and 100 μmol/L) for 30 min, followed by intervention with H2O2 (100 μmol/L) for 60 min. The levels of platelet phosphatidylserine (PS) exposure and mitochondrial membrane potential (ΔΨm) depolarization were determined by flow cytometry. Enzyme linked immunosorbent assay was used to measure caspase-3 and caspase-9 activation, and reactive oxygen species (ROS) and superoxide generation. The expression of Bax, Bak and cytochrome c were evaluated by Western blot. Results: H2O2-induced platelet PS exposure and ΔΨm depolarization were significantly attenuated by 10、100 μmol/L Cur treatment when compared with the control group (P < 0.05). Moreover, Cur significantly down-regulated Bax, Bak and cytochrome c expression in platelets treated with H2O2 (P < 0.05). H2O2-induced platelet caspase-3 and caspase-9 activation were significantly inhibited by 10、100 μmol/L Cur (P < 0.05). Additionally, the levels of intracellular total ROS and superoxide were significantly increased in H2O2-treated platelets, which were attenuated by Cur intervention (P < 0.05). Conclusion: Cur can inhibit H2O2-induced platelet apoptosis in vitro.

Key words: curcumin; platelet; apoptosis; hydrogen peroxide; oxidative stress; cardiovascular diseases

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