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Argon preconditioning protects neuronal cells with a Toll-like receptor-mediated effect

Neural Regeneration Research 2023年第6期18卷 1371-1377页

作者： Stefanie Scheid Adrien Lejarre Jakob Wollborn hartmut buerkle Ulrich Goebel Felix Ulbrich Department of Anesthesiology and Critical Care Medical Center-University of FreiburgFaculty of MedicineFreiburgGermany Department of Anesthesiology Perioperative and Pain MedicineBrigham and Women’s HospitalHarvard Medical SchoolBostonMAUSA Department of Anesthesiology and Critical Care Medicine St.Franziskus-HospitalMuensterGermany

The noble gas argon has the potential to protect neuronal cells from cell *** far,this effect has been studied in treatment after acute *** using argon has not yet been *** this study,human neuroblastoma SH-SY5Y cells were treated with different concentrations of argon(25%,50%,and 74%;21%O_(2),5%CO_(2),balance nitrogen)at different time intervals before inflicting damage with rotenone(20μM,4 hours).Apoptosis was determined by flow cytometry after annexin V and propidium iodide *** expressions of Toll-like receptors 2 and 4 were also *** were also processed for analysis by western blot and qPCR to determine the expression of apoptotic and inflammatory proteins,such as extracellular-signal regulated kinase(ERK1/2),nuclear transcription factor-κB(NF-κB),protein kinase B(Akt),caspase-3,Bax,Bcl-2,interleukin-8,and heat shock *** staining was performed for TLR2 and 4 and *** were also pretreated with OxPAPC,an antagonist of TLR2 and 4 to elucidate the molecular *** showed that argon preconditioning before rotenone application caused a dose-dependent but not a time-dependent reduction in the number of apoptotic *** with 74%argon for 2 hours was used for further experiments showing the most promising *** decreased the surface expression of TLR2 and 4,whereas OxPAPC treatment partially abolished the protective effect of *** increased phosphorylation of ERK1/2 but decreased NF-κB and *** inhibited mitochondrial apoptosis and the heat shock *** also suppressed the expression of the pro-inflammatory cytokine *** confirmed the alteration of TLRs and *** reversed the argon effect on ERK1/2,Bax,Bcl-2,caspase-3,and interleukin-8 expression,but not on NF-κB and the heat shock *** together,argon preconditioning protects against apoptosis of neuronal c

关键词： apoptosis inflammation interleukin-8 neuroprotection rotenone SH-SY5Y Toll-like receptor 2 Toll-like receptor 4

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Hepatic steatosis prevents heme oxygenase-1 induction by isoflurane in the rat liver

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World Journal of Gastroenterology 2011年第37期17卷 4184-4190页

作者： Patrick Stoll Christian I Schwer Ulrich Goebel hartmut buerkle Alexander Hoetzel Rene Schmidt Department of Anesthesiology and Critical Care Medicine Freiburg University Medical Center

AIM:To characterize the inductive effects of isoflurane(ISO) on hepatic heme oxygenase-1(HO-1) in an animal model of hepatic ***:Lean(LEAN) and obese(FAT) Zucker rats were randomized into 4 groups:1:LEAN + pentobarbital sodium(PEN);2:LEAN + ISO;3:FAT + PEN;4:FAT + *** animals were mechanically ventilated for 6 *** vitro analyses of liver tissue included determination of HO-1 mRNA and protein expression as well as measurement of HO enzyme activity and immunohistochemical ***:Compared to PEN treatment,ISO administration profoundly induced hepatic HO-1 mRNA and protein expression and significantly increased HO enzyme activity in lean Zucker *** contrast,no difference in HO-1 gene expression was observed after ISO or PEN anesthesia in obese Zucker ***:The present study demonstrates that ISO is an inducer of hepatic HO-1 gene expression in non-steatotic organs but failed to upregulate HO-1 in steatotic livers.

关键词： Isoflurane Heme oxygenase Hepatic steatosis Heme oxygenase-1 Volatile anesthetics

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Argon reduces microglial activation and inflammatory cytokine expression in retinal ischemia/reperfusion injury

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Neural Regeneration Research 2021年第1期16卷 192-198页

作者： Ulrich Goebel Stefanie Scheid Sashko Spassov Nils Schallner Jakob Wollborn hartmut buerkle Felix Ulbrich Department of Anesthesiology and Critical Care Medical Center–University of FreiburgFaculty of MedicineUniversity of FreiburgFreiburgGermany

We previously found that argon exerts its neuroprotective effect in part by inhibition of the toll-like receptors(TLR)2 and *** 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 *** also has been demonstrated that argon treatment could mitigate brain damage,reduce excessive microglial activation,and subsequently attenuate brain *** intensive research,the further exact mechanism remains *** 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 *** reperfusion,argon was administered by inhalation for 2 *** 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 *** cytometry analysis showed that argon downregulated the Fas *** 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 *** 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 *** results suggest that argon reduced the extent of inflammation in retinal neurons after ischemia/reperfusion injury by suppression of transcription factors crucial for microglial

关键词： argon ischemia/reperfusion injury microglia neuroinflammation neuroprotection noble gas SH-SY5Y toll-like receptor transcription factor

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