NSAIDs, Mitochondria and Calcium Signaling: Special Focus on Aspirin/Salicylates.
NSAIDs, Mitochondria and Calcium Signaling: Special Focus on Aspirin/Salicylates.
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非甾体抗炎药、线粒体和钙信号： 特别关注阿司匹林/水杨酸盐。
DOI：
10.3390/ph3051594
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发表时间：
2010-05-19
期刊：
影响因子：
--
通讯作者：
Ra C
中科院分区：
文献类型：
--
作者：
Suzuki Y;Inoue T;Ra C
阿司匹林（乙酰水杨酸）是一种众所周知的非甾体抗炎药（NSAID），长期以来一直被用作解热镇痛药。近年来，非甾体类抗炎药对癌细胞的化学预防和诱导凋亡作用受到广泛关注。这些作用被认为主要归因于抑制环氧合酶活性和前列腺素合成。然而，最近的研究已经明确表明，某些NSAID，包括阿司匹林及其代谢物水杨酸，发挥其抗炎和化学预防作用，独立于环氧合酶活性和前列腺素合成抑制。越来越明显的是，NSAID的两个潜在的共同靶点是线粒体和Ca2+信号通路。在这篇综述中，我们提供了一个关于线粒体和Ca2+的作用，以及阿司匹林，水杨酸类药物和其他NSAID的副作用的概述，并介绍了新兴的作用L型钙通道，一个新的Ca2+进入途径在非兴奋细胞，在人类癌细胞上调。
Aspirin (acetylsalicylic acid) is a well-known nonsteroidal anti-inflammatory drug (NSAID) that has long been used as an anti-pyretic and analgesic drug. Recently, much attention has been paid to the chemopreventive and apoptosis-inducing effects of NSAIDs in cancer cells. These effects have been thought to be primarily attributed to the inhibition of cyclooxygenase activity and prostaglandin synthesis. However, recent studies have demonstrated unequivocally that certain NSAIDs, including aspirin and its metabolite salicylic acid, exert their anti-inflammatory and chemopreventive effects independently of cyclooxygenase activity and prostaglandin synthesis inhibition. It is becoming increasingly evident that two potential common targets of NSAIDs are mitochondria and the Ca2+ signaling pathway. In this review, we provide an overview of the current knowledge regarding the roles of mitochondria and Ca2+ in the apoptosis-inducing effects as well as some side effects of aspirin, salicylates and other NSAIDs, and introducing the emerging role of L-type Ca2+ channels, a new Ca2+ entry pathway in non-excitable cells that is up-regulated in human cancer cells.