Ferulic acid exerts neuroprotective effects against cerebral ischemia/reperfusion-induced injury via antioxidant and anti-apoptotic mechanisms in vitro and in vivo.
Ferulic acid exerts neuroprotective effects against cerebral ischemia/reperfusion-induced injury via antioxidant and anti-apoptotic mechanisms in vitro and in vivo.
复制标题
DOI：
10.3892/ijmm.2017.3127
复制
发表时间：
2017-11
影响因子：
5.4
通讯作者：
Yang H
中科院分区：
文献类型：
--
作者：
Ren Z;Zhang R;Li Y;Li Y;Yang Z;Yang H
阿魏酸（FA）是肉桂酸的衍生物。它用于治疗心脑血管疾病，对缺氧/缺血诱导的脑细胞损伤具有保护作用。本研究通过苏木精-伊红（H&E）和尼氏染色、流式细胞术、Hoechst 33258染色、定量PCR、western blot分析和荧光显微镜分析等方法，研究了FA对缺血/再灌注（I/R）诱导的脑损伤的保护作用。本研究采用大鼠和嗜铬细胞瘤（PC-12）细胞建立脑I/R损伤模型。结果表明，FA处理显著减轻记忆障碍，并以剂量依赖的方式减少海马神经元凋亡和氧化应激。体外实验结果还表明，FA通过抑制细胞凋亡、Ca 2+内流、超氧阴离子（O2-）、丙二醛（MDA）和谷胱甘肽过氧化物酶（GSH-Px）的产生，以浓度依赖性方式保护PC-12细胞免受I/R诱导的活性氧（ROS）产生和凋亡。此外，FA灭活Toll样受体（TLR）/髓样分化因子88（MyD 88）通路。MyD 88过表达可消除FA的神经保护作用。总的来说，我们发现，FA减轻记忆功能障碍，并通过抑制TLR 4/MyD 88信号通路对I/R损伤诱导的氧化应激和细胞凋亡产生保护作用。本研究支持FA可能是用于治疗脑缺血的有前途的神经保护剂的观点。
Ferulic acid (FA) is a derivative of cinnamic acid. It is used in the treatment of heart head blood-vessel disease and exerts protective effects against hypoxia/ischemia-induced cell injury in the brain. This study investigated the potential neuroprotective effects of FA against ischemia/reperfusion (I/R)-induced brain injury in vivo and in vitro through hematoxylin and eosin (H&E) and Nissl staining assays, flow cytometry, Hoechst 33258 staining, quantitative PCR, western blot analysis and fluorescence microscopic analysis. In this study, models of cerebral I/R injury were established using rats and pheochromocytoma (PC-12) cells. The results revealed that treatment with FA significantly attenuated memory impairment, and reduced hippocampal neuronal apoptosis and oxidative stress in a dose-dependent manner. The results from in vitro experiments also indicated that FA protected the PC-12 cells against I/R-induced reactive oxygen species (ROS) generation and apoptosis by inhibiting apoptosis, Ca2+ influx, superoxide anion (O2−), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) production in a concentration-dependent manner. Moreover, FA inactivated the Toll-like receptor (TLR)/myeloid differentiation factor 88 (MyD88) pathway. MyD88 overexpression abolished the neuroprotective effects of FA. On the whole, we found that FA attenuated memory dysfunction and exerted protective effects against oxidative stress and apoptosis induced by I/R injury by inhibiting the TLR4/MyD88 signaling pathway. This study supports the view that FA may be a promising neuroprotective agent for use in the treatment of cerebral ischemia.
登录
查看更多内容
DOI：
10.1016/b978-0-12-394309-5.00006-7
发表时间：
2012
影响因子：
--
作者：
Kalogeris, Theodore;Baines, Christopher P.;Krenz, Maike;Korthuis, Ronald J.
通讯作者：
Korthuis, Ronald J.
影响因子：
5.7
作者：
Cheng, Chin-Yi;Ho, Tin-Yun;Hsieh, Ching-Liang
通讯作者：
Hsieh, Ching-Liang
影响因子：
3.4
作者：
Feng, Xiaodong;Yang, Shanli;Chen, Lidian
通讯作者：
Chen, Lidian
影响因子：
2.9
作者：
Cheng, Chin-Yi;Su, Shan-Yu;Hsieh, Ching-Liang
通讯作者：
Hsieh, Ching-Liang
影响因子：
2.9
作者：
Erfani, Sohaila;Khaksari, Mehdi;Gorjipour, Fazel
通讯作者：
Gorjipour, Fazel