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姜黄素对H2O2诱导血小板凋亡的抑制作用及分子机制
引用本文:牙甫礼,XIN Yu,张春梅,陈彬林,李玮琪,马永洁. 姜黄素对H2O2诱导血小板凋亡的抑制作用及分子机制[J]. 食品科学, 2021, 42(13): 151-157. DOI: 10.7506/spkx1002-6630-20200714-187
作者姓名:牙甫礼  XIN Yu  张春梅  陈彬林  李玮琪  马永洁
作者单位:(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)
基金项目:大理大学高层次人才启动基金项目(KY2096107240)
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、100μmo...

关 键 词:姜黄素  血小板  凋亡  过氧化氢  氧化应激  心血管疾病

Inhibition Effects and Mechanisms of Curcumin on Hydrogen Peroxide-Induced Platelet Apoptosis
YA Fuli,XIN Yu,ZHANG Chunmei,CHEN Binlin,LI Weiqi,MA Yongjie. Inhibition Effects and Mechanisms of Curcumin on Hydrogen Peroxide-Induced Platelet Apoptosis[J]. Food Science, 2021, 42(13): 151-157. DOI: 10.7506/spkx1002-6630-20200714-187
Authors:YA Fuli  XIN Yu  ZHANG Chunmei  CHEN Binlin  LI Weiqi  MA Yongjie
Affiliation:(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)
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.
Keywords:curcumin   platelet   apoptosis   hydrogen peroxide   oxidative stress   cardiovascular diseases,
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