2篇
您的检索式：作者名="Nils Schallner"
|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Argon reduces microglial activation and inflammatory cytokine expression in retinal ischemia/reperfusion injury显示文摘We previously found that argon exerts its neuroprotective effect in part by inhibition of the toll-like receptors(TLR)2 and 4.The downstream transcription factors signal transducer and activator of transcription 3(STAT3)and nuclear factor kappa B(NF-κB)are also affected by argon and may play a role in neuroprotection.It also has been demonstrated that argon treatment could mitigate brain damage,reduce excessive microglial activation,and subsequently attenuate brain inflammation.Despite intensive research,the further exact mechanism remains unclear.In this study,human neuroblastoma cells were damaged in vitro with rotenone over a period of 4 hours(to mimic cerebral ischemia and reperfusion damage),followed by a 2-hour post-conditioning with argon(75%).In a separate in vivo experiment,retinal ischemia/reperfusion injury was induced in rats by increasing intraocular pressure for 1 hour.Upon reperfusion,argon was administered by inhalation for 2 hours.Argon reduced the binding of the transcription factors signal transducer and activator of transcription 3,nuclear factor kappa B,activator protein 1,and nuclear factor erythroid 2-related factor 2,which are involved in regulation of neuronal damage.Flow cytometry analysis showed that argon downregulated the Fas ligand.Some transcription factors were regulated by toll-like receptors;therefore,their effects could be eliminated,at least in part,by the TLR2 and TLR4 inhibitor oxidized phospholipid 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine(OxPAPC).Argon treatment reduced microglial activation after retinal ischemia/reperfusion injury.Subsequent quantitative polymerase chain reaction analysis revealed a reduction in the pro-inflammatory cytokines interleukin(IL-1α),IL-1β,IL-6,tumor necrosis factorα,and inducible nitric oxide synthase.Our results suggest that argon reduced the extent of inflammation in retinal neurons after ischemia/reperfusion injury by suppression of transcription factors crucial for microglial activation.Argon has no known side effects or narcotic properties;therefore,therapeutic use of this noble gas appears ideal for treatment of patients with neuronal damage in retinal ischemia/reperfusion injury.The animal experiments were approved by the Commission for Animal Care of the University of Freiburg(approval No.35-9185.81/G14-122)on October 19,2012. | Ulrich Goebel Stefanie Scheid Sashko Spassov Nils Schallner Jakob Wollborn Hartmut Buerkle Felix Ulbrich | 2021 | Neural Regeneration Research2021，16，1： | 8 |
| 2 | 一氧化碳通过调节CD36表面表达控制小胶质细胞的红细胞吞噬作用减轻出血性损伤显示文摘小胶质细胞的红细胞吞噬作用在出血性卒中后的损伤反应中至关重要。我们假设通过HO-1/CO调节小胶质细胞的红细胞吞噬作用依赖于涉及活性氧(ROS)和CD36表面表达的信号通路。我们在有/无血液和有/无一氧化碳(CO)暴露条件下孵育小胶质细胞BV-2细胞系和原代小胶质细胞(PMG)。我们用从组织特异性HO-1缺陷(LyzM-Cre-Hmoxlfl/fl)和CD36-/-小鼠中分离出的PMG,或针对AMPK(AMP激活的蛋白激酶)的siRNA来检验我们的假设。在鼠蛛网膜下腔出血(SAH)模型中,我们比较了野生型和CD36-/-小鼠的神经元损伤。观察指标包括血管痉挛、小胶质细胞活化、神经元凋亡和空间记忆。我们观察到在血液暴露后,小胶质细胞HO-1表达增加。CO暴露后,ROS产生显著增加,导致磷酸化的AMPK数量增加,随后CD36表面表达增强。来自LyzM-CreHmoxlfl/fl小鼠的PMG表现出ROS产生和CD36表面表达均降低,并且CO不能诱导其CD36表面表达增加。缺乏HO-1和CD36导致的红细胞吞噬作用降低无法用CO逆转。在存在外源性CO的情况下,BV-2细胞的红细胞吞噬作用增强,而在经AMPK的siRNA处理的细胞中没有发现该现象。经历SAH的CD36-/-小鼠神经元细胞死亡增加,空间记忆功能受损。我们证明,小胶质细胞的吞噬功能部分与HO-1相关通路有关,该通路涉及ROS产生、磷酸化的AMPK和CD36的表面表达的变化。CD36为出血后血液清除的关键因子之一,与神经元的预后密切相关。这些结果需要进一步研究以明确CO潜在的神经保护特性。 | Sandra Kaiser Lisa Selzner JanickWeber Nils Schallner 杜一星(编译) | 2020 | 神经损伤与功能重建2020，15，6： | 2 |
您所在的机构暂未开通此部分的功能，请联系管理员