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1、SICENCE 新闻发布 作者：Jang-Yen Wu 稿号：NRR-D-14-00343低剂量舒林酸治疗脑卒中：神经保护效应与疗法舒林酸，一种广泛使用的非类固醇抗炎药物，是一种前体药物，受甲硫氨酸亚砜还原酶还原成其活性，可作为环氧合酶1和2 的抑制剂药物。已被证明通过某些过程会起到组织保护作用，其可以包括至少3个功能：抗氧化作用、预处理和消炎。舒林酸通过抑制线粒体钙超载或减少蛋白质氧化水平，产生神经保护作用。来自美国佛罗里达大西洋大学Jang-Yen Wu教授的研究已经证明了舒林酸治疗可以促进表达中枢神经系统梗死中心和缺血半暗带中的Hsp27、Akt和Bcl-2蛋白的表达。他们指出舒林酸作用
2、于内质网以减少ATF-6，作用于线粒体以增加 Bcl-2蛋白表达，并降低促凋亡元素Bak和PUMA的表达，由此产生的内质网应激减轻和细胞凋亡降低量。舒林酸减少段怎行局灶性脑缺血时后梗死面积，产生神经保护作用机制。低剂量舒林酸给药可获得其对脑卒中模型潜在的强效神经保护作用，也说明舒林酸可对抗脑缺血后氧化应激，是一种有价值的神经保护剂。相关研究内容发表在2014年12月第23期中国神经再生研究（英文版） 杂志上。舒林酸作用机制Article: Sulindac for stroke treatment: neuroprotective mechanism and therapy by Jigar
3、Pravinchandra Modi, Howard Prentice, Jang-Yen Wu (College of Medicine, Florida Atlantic University (Modi JP, Prentice H, Wu JY); Program in Integrative Biology, Florida Atlantic University (Prentice H, Wu JY); Centre of Complex Systems and Brain Sciences, Florida Atlantic University (Modi JP, Prenti
4、ce H, Wu JY)Modi JP, Prentice H, Wu JY. Sulindac for stroke treatment: neuroprotective mechanism and therapy. Neural Regen Res. 2014;9(23):2023-2025.欲获更多资讯： Neural Regen ResSICENCE 新闻发布 作者：Jang-Yen Wu 稿号：NRR-D-14-00343Sulindac for stroke treatment: neuroprotective mechanism and therapySulindac, a wi
5、dely used nonsteroidal anti-inflammatory drug (NSAID) is a prodrug that is reduced by methionine sulfoxide reductase to its active from as an inhibitor of cyclooxygenase 1 and 2. The drug has been shown to elicit tissue protection by processes that may include at least three functions: antioxidant,
6、preconditioning and anti-inflammatory. Sulindac demonstrates neuroprotection that involves inhibition of mitochondrial calcium overload or a decrease in protein oxidation. The group of Prof. Jang-Yen Wu, who come from Florida Atlantic University, USA have demonstrated the induction by sulindac treat
7、ment of pro-survival proteins Hsp27, Akt and Bcl-2 in the ischemic penumbra and core of the central nervous system (CNS) infarct in a rat model of ischemic stroke. Their findings point to sulindac acting on the endoplasmic reticulum (ER) to decrease ATF-6 and on the mitochondrion to increase Bcl-2 a
8、s well as decrease pro-apoptotic components Bak and PUMA. The resulting decrease in ER stress and reduction in apoptosis underlies the protective effect of sulindac in reducing infarct size following transient focal brain ischemia. The potent neuroprotective effect of sulindac in the stroke model is
9、 obtained with low-dose administration of the drug pointing to the potential of sulindac as a valuable neuroprotective agent against oxidative stress in cerebral ischemia. The relevant study has been published in the Neural Regeneration Research (Vol. 9, No. 23, 2014).Proposed Mechanism of action of
10、 sulindac.Article: Sulindac for stroke treatment: neuroprotective mechanism and therapy by Jigar Pravinchandra Modi, Howard Prentice, Jang-Yen Wu (College of Medicine, Florida Atlantic University (Modi JP, Prentice H, Wu JY); Program in Integrative Biology, Florida Atlantic University (Prentice H, Wu JY); Centre of Complex Systems and Brain Sciences, Florida Atlantic University (Modi JP, Prentice H, Wu JY)Modi JP, Prentice H, Wu JY. Sulindac for stroke treatment: neuroprotective mechanism and therapy. Neural Regen Res. 2014;9(23):2023-2025.
