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绿茶多酚抗心肌缺血损伤的抗氧化保护分子靶点。

Molecular targets for anti-oxidative protection of green tea polyphenols against myocardial ischemic injury.

作者信息

Hsieh Shih-Rong, Cheng Wei-Chen, Su Yi-Min, Chiu Chun-Hwei, Liou Ying-Ming

机构信息

Department of Cardiovascular Surgery, Taichung Veterans General Hospital, 407 Taichung, Taiwan.

Institute of Bioinformatics and Structural Biology, National Tsing Hua University, 300 Hsinchu, Taiwan.

出版信息

Biomedicine (Taipei). 2014;4(4):23. doi: 10.7603/s40681-014-0023-0. Epub 2014 Nov 20.

Abstract

Ischemic heart disease is the leading cause of death worldwide. An improved understanding of the mechanisms involved in myocardial injury would allow intervention downstream in the pathway where certain drugs including natural products could be efficiently applied to target the end effectors of the cell death pathway. Green tea polyphenols (GTPs) have potent anti-oxidative capabilities, which may account for their beneficial effects in preventing oxidative stress associated with ischemia injury. Although studies have provided convincing evidence to support the protective effects of GTPs in cardiovascular system, the potential end effectors that mediate cardiac protection are only beginning to be addressed. Proteomics analyses widely used to identify the protein targets for many cardiovascular diseases have advanced the discovery of the signaling mechanism for GTPs-mediated cardio-protection. This review focuses on putative triggers, mediators, and end effectors for the GTPs-mediated cardio-protection signaling pathways engaged in myocardial ischemia crisis, allowing a promising natural product to be used for ameliorating oxidative stress associated with ischemic heart diseases.

摘要

缺血性心脏病是全球主要的死亡原因。更好地理解心肌损伤所涉及的机制,将有助于在信号通路的下游进行干预,在该通路中,某些药物(包括天然产物)可以有效地应用于靶向细胞死亡通路的终效应器。绿茶多酚(GTPs)具有强大的抗氧化能力,这可能是它们在预防与缺血性损伤相关的氧化应激方面产生有益作用的原因。尽管研究已经提供了令人信服的证据来支持GTPs在心血管系统中的保护作用,但介导心脏保护的潜在终效应器才刚刚开始得到研究。蛋白质组学分析广泛用于确定许多心血管疾病的蛋白质靶点,推动了对GTPs介导心脏保护的信号机制的发现。本综述重点关注参与心肌缺血危机的GTPs介导心脏保护信号通路的假定触发因素、介质和终效应器,从而使一种有前景的天然产物可用于改善与缺血性心脏病相关的氧化应激。

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