Isoquercetin Ameliorates Cerebral Impairment in Focal Ischemia Through Anti-Oxidative, Anti-Inflammatory, and Anti-Apoptotic Effects in Primary Culture of Rat Hippocampal Neurons and Hippocampal CA1 Region of Rats
文献类型：期刊论文
| 作者 | Liang, Xin-Miao1,2,3; Ding, Fei1,2; Wang, Cai-Ping1,2; Shi, Yun-Wei1,2; Tang, Miao1,2; Zhang, Xiao-Chuan1,2; Gu, Yun1,2; Wang, Zhi-Wei1,2,4 |
| 刊名 | MOLECULAR NEUROBIOLOGY
 |
| 出版日期 | 2017-04-01 |
| 卷号 | 54期号:3页码:2126-2142 |
| 关键词 | Ischemic Stroke Apoptosis Oxidative Stress Inflammation Isoquercetin |
| ISSN号 | 0893-7648 |
| DOI | 10.1007/s12035-016-9806-5 |
| 文献子类 | Article |
| 英文摘要 | Ischemic stroke is a major disability and cause of death worldwide due to its narrow therapeutic time window. Neuroprotective agent is a promising strategy to salvage acutely ischemic brain tissue and extend the therapeutic time window for stroke treatment. In this study, we aimed to evaluate the neuroprotective effects of isoquercetin in (1) primary culture of rat hippocampal neurons exposure on oxygen and glucose deprivation and reperfusion (OGD/R) injury and (2) rats subjected to transient middle cerebral artery occlusion and reperfusion (MCAO/R) injury. The results showed that isoquercetin post-treatment reduced the infarct size, number of apoptotic cells, oxidative stress, and inflammatory response after ischemia and reperfusion injury. The underlying mechanism study indicated that the neuroprotective effects of isoquercetin were elicited via suppressing the activation of toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-kappa B) and caspase-1; the phosphorylation of ERK1/2, JNK1/2, and p38 mitogen-activated protein kinase (MAPK); and the secretion of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IL-6. In addition, isoquercetin also effectively alleviated hippocampus neuron apoptosis by regulation of cyclic AMP responsive element-binding protein (CREB), Bax, Bcl-2, and caspase-3. Our report provided new considerations into the therapeutic action and the underlying mechanisms of isoquercetin to improve brain injury in individuals who have suffered from ischemic stroke. As a potent anti-inflammatory and anti-oxidative compound with neuroprotective capacities, the beneficial effects of isoquercetin when used to treat ischemic stroke and related diseases in humans warrant further studies. |
| WOS关键词 | ACTIVATED PROTEIN-KINASES ; BRAIN-INJURY ; IN-VIVO ; REPERFUSION INJURY ; PROSPECTIVE COHORT ; SIGNALING PATHWAY ; EXTRA DOMAIN ; CELL-DEATH ; STROKE ; QUERCETIN |
| WOS研究方向 | Neurosciences & Neurology |
| 语种 | 英语 |
| WOS记录号 | WOS:000398506900044 |
| 出版者 | HUMANA PRESS INC |
| 源URL | [http://cas-ir.dicp.ac.cn/handle/321008/169306]  |
| 专题 | 大连化学物理研究所_中国科学院大连化学物理研究所 |
| 通讯作者 | Liang, Xin-Miao; Ding, Fei; Wang, Zhi-Wei |
| 作者单位 | 1.Nantong Univ, Jiangsu Key Lab Neuroregenerat, 19 Qixiu Rd, Nantong 226001, Jiangsu, Peoples R China 2.Nantong Univ, Coinnovat Ctr Neuroregenerat, Nantong 226001, Jiangsu, Peoples R China 3.Chinese Acad Sci, Dalian Inst Chem Phys, Dalian 116023, Liaoning, Peoples R China 4.Univ Calif Irvine, Dept Pharmacol, Irvine, CA 92697 USA |
| 推荐引用方式 GB/T 7714 | Liang, Xin-Miao,Ding, Fei,Wang, Cai-Ping,et al. Isoquercetin Ameliorates Cerebral Impairment in Focal Ischemia Through Anti-Oxidative, Anti-Inflammatory, and Anti-Apoptotic Effects in Primary Culture of Rat Hippocampal Neurons and Hippocampal CA1 Region of Rats[J]. MOLECULAR NEUROBIOLOGY,2017,54(3):2126-2142. |
| APA | Liang, Xin-Miao.,Ding, Fei.,Wang, Cai-Ping.,Shi, Yun-Wei.,Tang, Miao.,...&Wang, Zhi-Wei.(2017).Isoquercetin Ameliorates Cerebral Impairment in Focal Ischemia Through Anti-Oxidative, Anti-Inflammatory, and Anti-Apoptotic Effects in Primary Culture of Rat Hippocampal Neurons and Hippocampal CA1 Region of Rats.MOLECULAR NEUROBIOLOGY,54(3),2126-2142. |
| MLA | Liang, Xin-Miao,et al."Isoquercetin Ameliorates Cerebral Impairment in Focal Ischemia Through Anti-Oxidative, Anti-Inflammatory, and Anti-Apoptotic Effects in Primary Culture of Rat Hippocampal Neurons and Hippocampal CA1 Region of Rats".MOLECULAR NEUROBIOLOGY 54.3(2017):2126-2142. |
入库方式： OAI收割
来源：大连化学物理研究所
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