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Xyloketal-derived small molecules show protective effect by decreasing mutant Huntingtin protein aggregates in Caenorhabditis elegans model of Huntington's disease.源自木酮糖缩醛的小分子通过减少秀丽隐杆线虫亨廷顿舞蹈症模型中的突变亨廷顿蛋白聚集体而显示出保护作用。
Drug Des Devel Ther. 2016 Apr 13;10:1443-51. doi: 10.2147/DDDT.S94666. eCollection 2016.
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Therapeutic benefits of combined treatment with tissue plasminogen activator and 2-(4-methoxyphenyl)ethyl-2-acetamido-2-deoxy-β-d-pyranoside in an animal model of ischemic stroke.组织纤溶酶原激活剂与2-(4-甲氧基苯基)乙基-2-乙酰氨基-2-脱氧-β-D-吡喃糖苷联合治疗在缺血性脑卒中动物模型中的治疗益处。
Neuroscience. 2016 Jul 7;327:44-52. doi: 10.1016/j.neuroscience.2016.04.006. Epub 2016 Apr 7.
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Splenectomy following MCAO inhibits the TLR4-NF-κB signaling pathway and protects the brain from neurodegeneration in rats.大脑中动脉闭塞后进行脾切除术可抑制大鼠的TLR4-NF-κB信号通路,并保护大脑免受神经退行性变。
J Neuroimmunol. 2016 Apr 15;293:105-113. doi: 10.1016/j.jneuroim.2016.03.003. Epub 2016 Mar 4.
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NF-kappaB Signaling Pathways in Neurological Inflammation: A Mini Review.神经炎症中的核因子κB信号通路:一篇小型综述
Front Mol Neurosci. 2015 Dec 18;8:77. doi: 10.3389/fnmol.2015.00077. eCollection 2015.
5
Inhibition of TNF-α protects in vitro brain barrier from ischaemic damage.抑制肿瘤坏死因子-α可在体外保护脑屏障免受缺血性损伤。
Mol Cell Neurosci. 2015 Nov;69:65-79. doi: 10.1016/j.mcn.2015.11.003. Epub 2015 Nov 9.
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Biomol Ther (Seoul). 2015 Nov;23(6):531-8. doi: 10.4062/biomolther.2015.124. Epub 2015 Nov 1.
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Stroke. 2015 Dec;46(12):3523-31. doi: 10.1161/STROKEAHA.115.011031. Epub 2015 Nov 3.
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Neuroinflammatory biomarkers: From stroke diagnosis and prognosis to therapy.神经炎症生物标志物:从中风诊断、预后到治疗
Biochim Biophys Acta. 2016 Mar;1862(3):411-24. doi: 10.1016/j.bbadis.2015.10.025. Epub 2015 Oct 30.
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Prophylactic Edaravone Prevents Transient Hypoxic-Ischemic Brain Injury: Implications for Perioperative Neuroprotection.预防性依达拉奉可预防短暂性缺氧缺血性脑损伤:对围手术期神经保护的意义。
Stroke. 2015 Jul;46(7):1947-55. doi: 10.1161/STROKEAHA.115.009162. Epub 2015 Jun 9.
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Xyloketal B suppresses glioblastoma cell proliferation and migration in vitro through inhibiting TRPM7-regulated PI3K/Akt and MEK/ERK signaling pathways.木酮糖酮醇B通过抑制瞬时受体电位通道M7(TRPM7)调节的磷脂酰肌醇-3激酶(PI3K)/蛋白激酶B(Akt)和丝裂原活化蛋白激酶/细胞外信号调节激酶(MEK/ERK)信号通路,在体外抑制胶质母细胞瘤细胞的增殖和迁移。
Mar Drugs. 2015 Apr 22;13(4):2505-25. doi: 10.3390/md13042505.

木榴醇 B 通过抑制 ROS/TLR4/NF-κB 炎症信号通路缓解小鼠卒中模型中的脑梗死和神经功能缺损。

Xyloketal B alleviates cerebral infarction and neurologic deficits in a mouse stroke model by suppressing the ROS/TLR4/NF-κB inflammatory signaling pathway.

机构信息

Department of Pharmacology, Cardiac and Cerebral Vascular Research Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.

VIP Healthcare Center, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China.

出版信息

Acta Pharmacol Sin. 2017 Sep;38(9):1236-1247. doi: 10.1038/aps.2017.22. Epub 2017 May 29.

DOI:10.1038/aps.2017.22
PMID:28552908
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5589963/
Abstract

Xyloketal B (Xyl-B) is a novel marine compound isolated from mangrove fungus Xylaria sp. We previously demonstrated that pretreatment with Xyl-B exerted neuroprotective effects and attenuated hypoxic-ischemic brain injury in neonatal mice. In the present study we investigated the neuroprotective effects of pre- and post-treatment with Xyl-B in adult mice using a transient middle cerebral artery occlusion (tMCAO) model, and explored the underlying mechanisms. Adult male C57 mice were subjected to tMCAO surgery. For the pre-treatment, Xyl-B was given via multiple injections (12.5, 25, and 50 mg·kg·d, ip) 48 h, 24 h and 30 min before ischemia. For the post-treatment, a single dose of Xyl-B (50 mg/kg, ip) was injected at 0, 1 or 2 h after the onset of ischemia. The regional cerebral perfusion was monitored using a laser-Doppler flowmeter. TTC staining was performed to determine the brain infarction volume. We found that both pre-treatment with Xyl-B (50 mg/kg) and post-treatment with Xyl-B (50 mg/kg) significantly reduced the infarct volume, but had no significant hemodynamic effects. Treatment with Xyl-B also significantly alleviated the neurological deficits in tMCAO mice. Furthermore, treatment with Xyl-B significantly attenuated ROS overproduction in brain tissues; increased the MnSOD protein levels, suppressed TLR4, NF-κB and iNOS protein levels; and downregulated the mRNA levels of proinflammatory cytokines, including IL-1β, TNF-α, IL-6 and IFN-γ. Moreover, Xyl-B also protected blood-brain barrier integrity in tMCAO mice. In conclusion, Xyl-B administered within 2 h after the onset of stroke effectively protects against focal cerebral ischemia; the underlying mechanism may be related to suppressing the ROS/TLR4/NF-κB inflammatory signaling pathway.

摘要

木酮糖 B(Xyl-B)是从红树林真菌 Xylaria sp 中分离得到的一种新型海洋化合物。我们之前的研究表明,Xyl-B 预处理可发挥神经保护作用并减轻新生小鼠缺氧缺血性脑损伤。在本研究中,我们使用短暂性大脑中动脉闭塞(tMCAO)模型研究了 Xyl-B 在成年小鼠中的预处理和后处理的神经保护作用,并探讨了其潜在机制。成年雄性 C57 小鼠接受 tMCAO 手术。对于预处理,在缺血前 48 小时、24 小时和 30 分钟通过多次注射(12.5、25 和 50mg·kg·d,ip)给予 Xyl-B。对于后处理,在缺血后 0、1 或 2 小时给予单次剂量的 Xyl-B(50mg/kg,ip)。使用激光多普勒血流计监测局部脑灌注。使用 TTC 染色确定脑梗死体积。我们发现,Xyl-B(50mg/kg)预处理和 Xyl-B(50mg/kg)后处理均显著减少梗死体积,但对血液动力学没有显著影响。Xyl-B 治疗还显著减轻 tMCAO 小鼠的神经功能缺损。此外,Xyl-B 治疗还显著减轻脑组织中 ROS 过度产生;增加 MnSOD 蛋白水平,抑制 TLR4、NF-κB 和 iNOS 蛋白水平;下调促炎细胞因子(包括 IL-1β、TNF-α、IL-6 和 IFN-γ)的 mRNA 水平。此外,Xyl-B 还可保护 tMCAO 小鼠血脑屏障的完整性。总之,在中风发作后 2 小时内给予 Xyl-B 可有效保护局灶性脑缺血;其潜在机制可能与抑制 ROS/TLR4/NF-κB 炎症信号通路有关。