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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 death.So far,this effect has been studied in treatment after acute damage.Preconditioning using argon has not yet been investigated.In 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 staining.Surface expressions of Toll-like receptors 2 and 4 were also examined.Cells 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 proteins.Immunohistochemical staining was performed for TLR2 and 4 and interleukin-8.Cells were also pretreated with OxPAPC,an antagonist of TLR2 and 4 to elucidate the molecular mechanism.Results showed that argon preconditioning before rotenone application caused a dose-dependent but not a time-dependent reduction in the number of apoptotic cells.Preconditioning with 74%argon for 2 hours was used for further experiments showing the most promising results.Argon decreased the surface expression of TLR2 and 4,whereas OxPAPC treatment partially abolished the protective effect of argon.Argon increased phosphorylation of ERK1/2 but decreased NF-κB and Akt.Preconditioning inhibited mitochondrial apoptosis and the heat shock response.Argon also suppressed the expression of the pro-inflammatory cytokine interleukin-8.Immunohistochemistry confirmed the alteration of TLRs and interleukin-8.OxPAPC 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 proteins.Taken together,argon preconditioning protects against apoptosis of neuronal cells and mediates its action via Toll-like recep

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

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Supraglottic jet oxygenation and ventilation(SJOV) for resuscitation of injured soldiers and people in war field

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Military Medical Research 2022年第6期9卷 757-758页

作者： Hua-Feng Wei Department of Anesthesiology and Critical Care Perelman School of MedicineUniversity of PennsylvaniaPhiladelphiaPA 19104USA

Dear Editor,Soldiers or people in battlefield settings are frequently injured with acute trauma, resulting in respiratory depression, hypoxia and associated morbidity and mortality. Traumatic brain injury(TBI) is with as much as 80%–90% of mild to moderate in combat casualties and contributed significantly to morbidity and mortality in battlefield settings. Correction of hypoxia at as capable as possible is expected to reduce or minimize the morbidity/mortality due to acute brain injury. An easy, quick and safe setup to promote oxygenation/ventilation of injured military personnel or peoples by non-medical personnel in battlefield settings immediately after acute injury before transfer to hospital is expected to reduce the morbidity/mortality due to injury mediated respiratory depression.

关键词： Battlefield War Trauma Acute injury Respiratory depression Hypoxia Oxygenation Resuscitation Supraglottic jet oxygenation and ventilation(SJOV)

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Potential impact of epidural labor analgesia on the outcomes of neonates and children

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Chinese Medical Journal 2020年第19期133卷 2353-2358页

作者： Zhi-Hua Liu Dong-Xin Wang Department of Anesthesiology and Critical Care Medicine Peking University First HospitalBeijing 100034China.

This review summarizes recent evidences regarding the potential influences of epidural labor analgesia(ELA)on the outcomes of neonates and children.Terms and relevant words including“ELA,”“ELA and neonatal outcomes,”“ELA and children’s development,”and“ELA and children’s neurocognitive development”were used to search articles published in PubMed database up to October 2019.Original articles and reviews regarding potential influences of ELA on neonates and children were identified.Relevant references of the selected articles were also screened.The anesthetics used during ELA can be absorbed,enter the fetus,and produce neonatal depression;however,these effects are less severe than those during systematic opioid analgesia.The impact of anesthetic exposure during ELA on children’s neurodevelopment has not been fully studied,but would be mild if any.ELA increases the risk of intrapartum maternal fever;the latter may be harmful to neonatal outcomes.The use of ELA may increase birth injury by increasing instrumental delivery,although long-term adverse events are rare.On the other hand,ELA may reduce maternal depression and,thus,produce favorable effects on neurocognitive development in childhood;but evidences are still lacking in this aspect.ELA may produce both favorable and unfavorable effects on neonates and children.These effects should be discussed with parturient women before making decisions.The potential harmful effects should be carefully managed.The overall impacts of ELA on neonatal and children’s outcomes need to be studied further.

关键词： Epidural labor analgesia Neonates Children Outcomes

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Molecular Mechanisms of Ventilator-Induced Lung Injury

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Chinese Medical Journal 2018年第10期131卷 1225-1231页

作者： Lin Chen Hai-Fa Xia You Shang Shang-Long Yao department of anesthesiology Institute of Anesthesiology and Critical Care Medicine Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430022 China department of critical care Medicine Institute of Anesthesiology and Critical Care Medicine Union Hospital Tongji Medical College Huazhong University of Science and Technology Wuhan Hubei 430022 China

Objective：Mechanical ventilation （MV） has long been used as a life-sustaining approach for several decades.However,researchers realized that MV not only brings benefits to patients but also cause lung injury if used improperly,which is termed as ventilator-induced lung injury （VILI）.This review aimed to discuss the pathogenesis of VILI and the underlying molecular mechanisms.Data Sources：This review was based on articles in the PubMed database up to December 2017 using the following keywords：＂ventilator-induced lung injury＂,＂pathogenesis＂,＂mechanism＂,and ＂biotrauma＂.Study Selection：Original articles and reviews pertaining to mechanisms of VILI were included and reviewed.Results：The pathogenesis of VILI was defined gradually,from traditional pathological mechanisms （barotrauma,volutrauma,and atelectrauma） to biotrauma.High airway pressure and transpulmonary pressure or cyclic opening and collapse of alveoli were thought to be the mechanisms of barotraumas,volutrauma,and atelectrauma.In the past two decades,accumulating evidence have addressed the importance of biotrauma during VILI,the molecular mechanism underlying biotrauma included but not limited to proinflammatory cytokines release,reactive oxygen species production,complement activation as well as mechanotransduction.Conclusions：Barotrauma,volutrauma,atelectrauma,and biotrauma contribute to VILI,and the molecular mechanisms are being clarified gradually.More studies are warranted to figure out how to minimize lung injury induced by MV.

关键词： Biotrauma Mechanism Pathogenesis Ventilator-Induced Lung Injury

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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 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 na

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

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Effects of plant-derived analgesic compounds sinomenine and salvinorin A in infant rats

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Journal of Integrative Medicine 2020年第2期18卷 174-180页

作者： Conrad J.Mascarenhas Renyu Liu Gordon A.Barr Department of Anesthesiology and Critical Care Children’s Hospital of PhiladelphiaPhiladelphiaPA 19104USA Department of Anesthesiology and Critical Care Perelman School of Medicine at the University of PennsylvaniaPhiladelphiaPA 19104USA department of Psychology University of PennsylvaniaPhiladelphiaPA 19104USA

Objective: Premature and ill neonates undergo painful but medically necessary procedures while hospitalized. Although opiate drugs are administered as analgesics, problems associated with their side effects,tolerance, and potential dependence necessitate research into alternative pain-relieving medications.Here we test two plant-derived compounds in infant rats: sinomenine, which targets the Mas-related G-protein-coupled receptor member X2 opioid receptor;and salvinorin A, which is a j opioid receptor agonist. In adult animals both sinomenine and salvinorin A are analgesic, but neither has been tested in infants.Methods: We used the formalin and thermal plantar tests in rats 7 and 21 days of age(PN7 and PN21) for behavioral signs of pain. In addition, brain sections were stained using Fos immunohistochemistry to examine patterns of brain activation in the midbrain periaqueductal gray and the paraventricular nucleus of the hypothalamus.Results: Sinomenine was analgesic in both the formalin and thermal tests on animals 21 days of age. At PN7 only the highest dose elevated response latencies in the thermal test and there were no effects of sinomenine in the formalin test. Analysis of Fos expression in the sinomenine-treated animals showed no drug effect, in contrast to the behavioral results. Salvinorin A was analgesic in the formalin test only at the highest dose at 21 days of age but not in the thermal test at either age.Conclusion: The increased modest effectiveness of sinomenine in older animals and the minimum salvinorin A drug effect suggest that the compounds act on sites that develop during the preweaning period(sinomenine) or after weaning(salvinorin A).

关键词： Thermal pain Formalin test Fos Ontogeny Sinomenine Salvinorin A

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Iron toxicity, lipid peroxidation and ferroptosis after intracerebral haemorrhage

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Stroke & Vascular Neurology 2019年第2期4卷 93-95页

作者： Jieru Wan Honglei Ren Jian Wang Department of Anesthesiology and Critical Care Medicine Johns Hopkins School of MedicineBaltimoreMarylandUSA

Intracerebral haemorrhage (ICH) is a devastating type of stroke with high mortality and morbidity. However, we have few options for ICH therapy and limited knowledge about post-ICH neuronal death and related mechanisms. In the aftermath of ICH, iron overload within the perihaematomal region can induce lethal reactive oxygen species (ROS) production and lipid peroxidation, which contribute to secondary brain injury. Indeed, iron chelation therapy has shown efficacy in preclinical ICH studies. Recently, an iron-dependent form of non-apoptotic cell death known as ferroptosis was identified. It is characterised by an accumulation of iron-induced lipid ROS, which leads to intracellular oxidative stress. The ROS cause damage to nucleic acids, proteins and lipid membranes, and eventually cell death. Recently, we and others discovered that ferroptosis does occur after haemorrhagic stroke in vitro and in vivo and contributes to neuronal death. Inhibition of ferroptosis is beneficial in several in vivo and in vitro ICH conditions. This minireview summarises current research on iron toxicity, lipid peroxidation and ferroptosis in the pathomechanisms of ICH, the underlying molecular mechanisms of ferroptosis and the potential for combined therapeutic strategies. Understanding the role of ferroptosis after ICH will provide a vital foundation for cell death-based ICH treatment and prevention.

关键词： peroxidation mortality cerebral

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Role of the Voltage-Gated Proton Channel Hv1 in Nervous Systems

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Neuroscience Bulletin 2023年第7期39卷 1157-1172页

作者： Yu Shen Yuncheng Luo Ping Liao Yunxia Zuo Ruotian Jiang department of anesthesiology West China HospitalSichuan UniversityChengdu 610000China Laboratory of Anesthesia and critical care Medicine National-Local Joint Engineering Research Center of Translational Medicine of AnesthesiologyDepartment of AnesthesiologyWest China HospitalSichuan UniversityChengdu 610000China

Hv1 is the only voltage-gated proton-selective channel in mammalian cells.It contains a conserved voltage-sensor domain,shared by a large class of voltage-gated ion channels,but lacks a pore domain.Its primary role is to extrude protons from the cytoplasm upon pH reduction and membrane depolarization.The best-known function of Hv1 is the regulation of cytosolic pH and the nicotinamide adenine dinucleotide phosphate oxidase-dependent production of reactive oxygen species.Accumulating evidence indicates that Hv1 is expressed in nervous systems,in addition to immune cells and others.Here,we summarize the molecular properties,distribution,and physiological functions of Hv1 in the peripheral and central nervous systems.We describe the recently discovered functions of Hv1 in various neurological diseases,including brain or spinal cord injury,ischemic stroke,demyelinating diseases,and pain.We also summarize the current advances in the discovery and application of Hv1-targeted small molecules in neurological diseases.Finally,we discuss the current limitations of our understanding of Hv1 and suggest future research directions.

关键词： Voltage-gated ion channel Hv1 Proton ROS Neuroinflammation Neurological diseases Pain

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A 20-Year Follow-up after the Fontan Operation in a Population with Hypoplastic Left Heart Syndrome

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Congenital Heart Disease 2022年第5期17卷 579-590页

作者： Eleni P.Asimacopoulos Steven J.Staffa Peter C.Laussen Kirsten C.Odegard department of Boston Children’s Hospital Department of Anesthesiology Critical Care and Pain Medicine Division of Cardiac AnesthesiaBoston02115USA

Background:Thromboembolic events are a cause of significant morbidity and mortality in the Fontan population.We previously reported on coagulation profile changes in a cohort of patients with hypoplastic left heart syndrome(HLHS)from Stage I through Fontan completion.In this report,we examine their clinical status,anticoagulation and incidence of thromboembolic events up to 20 years post Fontan.Methods:A retrospective chart review was conducted for twenty(20)surviving patients,from 1998 through December 2020.Patients who underwent orthotopic heart transplantation(OTx)were followed until their transplant.Patients who were found in the original study to have a factor VIII activity level>160%,were examined separately.Results:Most patients had follow-up within the last two years(2018–2020).Two patients underwent OTx and two patients died.Anticoagulation strategy was variable.Most patients were on aspirin monotherapy.There was a total of twelve thrombotic events(63.2%).These included six cerebrovascular accidents(two of which were fatal).Three out of the seven patients with elevated factor VIII activity from the original study had thromboembolic events(42.9%).Fontan complications were variable.Some degree of Fontan Associated Liver Disease was universal.Conclusions:This retrospective review of a group of single-ventricle patients post Fontan,illustrates the variability in anticoagulation therapy that exists in this population.A large proportion of patients suffered a significant thromboembolic event,including the patients with elevated factor VIII.Further investigation into the patients with elevated factor VIII may help determine whether a different antithrombotic strategy post Fontan would be beneficial.

关键词： Fontan procedure hypoplastic left heart syndrome antiplatelet drugs anticoagulation strategy thrombosis

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The changes of oligodendrocytes induced by anesthesia during brain development

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Neural Regeneration Research 2015年第9期10卷 1386-1387页

作者： Danye Jiang Sanghee Lim Minhye Kwak Yun Kyoung Ryu C.David Mintz Department of Anesthesiology and Critical Care Medicine Johns Hopkins Medical Institutes

With the advent of modern techniques, drugs, and monitoring, general anesthesia has come to be considered an unlikely cause of harm, particularly for healthy patients. While this is largely true, newly emerging clinical and laboratory studies have sug- gested that exposure to anesthetic agents during early childhood may have long-lasting adverse effects on cognitive function. This concern has been the focus of intense study in the field of anesthesia research. A recent high-profile review by Rappaport et al. （2015） concluded that while many questions remain un- answered, there is strong evidence from laboratory studies that commonly used anesthetics interfere with brain development and that clinical studies suggest a correlation between early childhood exposure to these agents and subsequent effects on learning and cognition. The issue is of sufficient public health importance that a public-private partnership known as Smar- Tots （Strategies for Mitigating Anesthesia-Related Neurotoxicity in Tots） was developed by the FDA to study pediatric anesthetic neurotoxicity. The mechanism of injury underlying this phe- nomenon has yet to be fully elucidated, and there is evidence to suggest that anesthetics may have direct cytotoxic effects on neurons leading to cell death or suppressed neurogenesis （Strat- mann et al., 2010） and that they may interfere with key pro- cesses in neuronal growth and development that underlie brain circuit development （Wagner et al., 2014）.

关键词： The changes of oligodendrocytes induced by anesthesia during brain development

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