Cardioprotective Effects of Quercetin in Cardiomyocyte under Ischemia/Reperfusion Injury.
Cardioprotective Effects of Quercetin in Cardiomyocyte under Ischemia/Reperfusion Injury.
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DOI：
10.1155/2013/364519
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发表时间：
2013
期刊：
影响因子：
--
通讯作者：
Chan HL
中科院分区：
文献类型：
--
作者：
Chen YW;Chou HC;Lin ST;Chen YH;Chang YJ;Chen L;Chan HL
槲皮素是一种存在于多种蔬菜、水果中的多酚类化合物，对哺乳动物细胞具有促凋亡、抗增殖和抗氧化作用。槲皮素对心肌细胞缺血/再灌注损伤有保护作用，但其保护机制尚不清楚。槲皮素的心脏保护作用是通过降低Src激酶、信号转导和转录激活因子3（STAT 3）、caspase 9、Bax、细胞内活性氧产生以及炎症因子和诱导型MnSOD表达的活性来实现的。荧光双向差异凝胶电泳（2D-DIGE）和基质辅助激光解吸电离飞行时间质谱（MALDI-TOF MS）技术可以揭示H2 O2和槲皮素处理后H9 C2细胞差异表达的蛋白质。虽然H2 O2诱导的细胞中有17个鉴定的蛋白质发生了改变，但这些蛋白质如α-可溶性NSF附着蛋白（α-SNAP），Ena/VASP样蛋白（Evl）和异戊烯基-二磷酸δ-异构酶1（Idi-1）通过槲皮素预处理而恢复，这与激酶激活，DNA修复，脂质和蛋白质代谢相关。槲皮素在H2 O2诱导的H9 C2细胞中使Src激酶去磷酸化，并可能通过STAT 3激酶调节来阻断H2 O2诱导的炎症反应。这可能有助于防止心肌细胞的缺血/再灌注损伤。
Quercetin, a polyphenolic compound existing in many vegetables, fruits, has antiinflammatory, antiproliferation, and antioxidant effect on mammalian cells. Quercetin was evaluated for protecting cardiomyocytes from ischemia/reperfusion injury, but its protective mechanism remains unclear in the current study. The cardioprotective effects of quercetin are achieved by reducing the activity of Src kinase, signal transducer and activator of transcription 3 (STAT3), caspase 9, Bax, intracellular reactive oxygen species production, and inflammatory factor and inducible MnSOD expression. Fluorescence two-dimensional differential gel electrophoresis (2D-DIGE) and matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF MS) can reveal the differentially expressed proteins of H9C2 cells treated with H2O2 or quercetin. Although 17 identified proteins were altered in H2O2-induced cells, these proteins such as alpha-soluble NSF attachment protein (α-SNAP), Ena/VASP-like protein (Evl), and isopentenyl-diphosphate delta-isomerase 1 (Idi-1) were reverted by pretreatment with quercetin, which correlates with kinase activation, DNA repair, lipid, and protein metabolism. Quercetin dephosphorylates Src kinase in H2O2-induced H9C2 cells and likely blocks the H2O2-induced inflammatory response through STAT3 kinase modulation. This probably contributes to prevent ischemia/reperfusion injury in cardiomyocytes.
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