中文摘要：

Xyloketal B (Xyl-B ) 是从红树属植物真菌 Xylaria sp 孤立的新奇海洋的混合物。我们以前证明有 Xyl-B 的那个预告的处理施加了 neuroprotective 效果并且在新生的老鼠稀释了 hypoxic-ischemic 大脑损害。在现在的学习，我们调查了预告的处理的 neuroprotective 效果并且与在用短暂中间的成年老鼠的 Xyl-B 处理以后服的动脉吸藏(tMCAO ) 模型，并且探索了内在的机制。成年男 C57 老鼠受到 tMCAO 外科。为预告的处理， Xyl-B 经由多重注射被给(12.5， 25，和 50 mg ?@

英文摘要：

Xyloketal B （Xyl-B） is a novel marine compound isolated from mangrove fungus Xylaria sp. We previously demonstrated that pretreatment with XyI-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 XyI-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, XyI-B was given via multiple injections （12.5, 25, and 50 mg.kgl-d1, ip） 48 h, 24 h and 30 min before ischemia. For the post-treatment, a single dose of XyI-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 XyI-B （50 mg/kg） and post-treatment with XyI-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 XyI-B significantly attenuated ROS overproduction in brain tissues; increased the MnSOD protein levels, suppressed TLR4, NF-KB and iNOS protein levels; and downregulated the mRNA levels of proinflammatory cytokines, including IL-1β, TNF-α IL-6 and IFN-y. Moreover, XyI-B also protected blood-brain barrier integrity in tMCAO mice. In conclusion, XyI-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-KB inflammatory signaling pathway.