Background and PurposeWhile Type 2 diabetes mellitus (T2DM) is a recognized risk factor for ischemic stroke (IS), metformin's effect on mortality across distinct IS subtypes remains unclear. This study aimed to investigate the association between metformin and all-cause mortality in patients with concurrent T2DM and IS, exploring TOAST subtype-specific efficacy.MethodsThis retrospective MIMIC-IV cohort study included T2DM and IS patients receiving glucose-lowering agents. Primary and secondary endpoints were 90- and 365-day all-cause mortality. Propensity score matching (PSM) and multivariate logistic regression evaluated associations.ResultsAmong 1946 patients, 375 received metformin. Post-PSM (nonmetformin n = 750; metformin n = 375), 90-day mortality was significantly lower in the metformin cohort (9.6% vs. 15.1%, p = 0.014). Multivariate regression confirmed metformin's independent association with decreased 90-day (odds ratio [OR] = 0.63, 95% confidence interval [CI]: 0.42-0.94, p = 0.025) and 365-day (OR = 0.59, 95% CI: 0.42-0.83, p = 0.002) mortality. Subgroup analyses exploring TOAST classification heterogeneity revealed that in the unmatched cohort, metformin was associated with reduced 90-day mortality in cardioembolism (CE) and stroke of other determined etiology (SOE), as well as reduced 365-day mortality in large-artery atherosclerosis (LAA), CE, SOE, and stroke of undetermined etiology (SUE). However, following PSM adjustment, significant 365-day mortality reduction persisted solely in the SUE subtype (OR = 0.38, 95% CI: 0.16-0.90, p = 0.027).ConclusionMetformin is significantly associated with reduced short- and long-term mortality in patients with T2DM and IS. Prognostic benefits exhibit heterogeneity across stroke etiologies, highlighting the necessity for tailored glucose-lowering strategies based on TOAST classifications.

Cerebral ischemia-reperfusion injury (CIRI) is a common and serious complication of reperfusion therapy in patients with ischemic stroke (IS). The regulation of microglia-mediated neuroinflammation to control CIRI has garnered considerable attention. The balance of iron metabolism is key to maintaining the physiological functions of microglia. Nuclear Receptor Coactivator 4 (NCOA4)-mediated ferritinophagy, an important pathway in regulating iron metabolism, is a promising intervention target. However, studies on the impacts of ferritinophagy on microglia-mediated neuroinflammation are lacking. This study aimed to identify potential treatments for CIRI-induced neuroinflammation by focusing on ferritinophagy and the specific mechanisms whereby iron metabolism regulates microglia-mediated neuroinflammation. CIRI induced the activation of ferritinophagy in microglia, characterized by the upregulation of NCOA4, downregulation of Ferritin Heavy Chain 1 (FTH1), and increased intracellular iron levels. This activation contributes to increased ferroptosis, oxidative stress, and the release of inflammatory factors. Silencing NCOA4 or application of the ferroptosis-specific inhibitor Ferrostatin-1 (Fer-1) effectively suppressed the CIRI-induced damage in vivo and in vitro. While Fer-1 addition did not inhibit the CIRI-activated ferritinophagy, it did partially reverse the alleviation of NCOA4 depletion-induced neuroinflammation, suggesting that ferroptosis is an essential intermediate step in ferritinophagy-induced neuroinflammatory damage. Furthermore, using IS-related transcriptomic data, the cGAS-STING pathway was identified as a crucial mechanism connecting ferritinophagy and ferroptosis. Specific inhibition of the cGAS-STING pathway reduced ferritinophagy-induced ferroptosis and neuroinflammation. In summary, our results indicated that ferritinophagy activates the cGAS-STING signaling pathway, which promotes the inflammatory response and oxidative stress in microglia in a ferroptosis-dependent manner, thereby exacerbating CIRI-induced neuroinflammation. These findings provide theoretical support for the clinical treatment of CIRI.

Macrophages play a critical role in the development of acute ischemic stroke (AIS). Cerebral ischemia–reperfusion injury (CIRI) is a pivotal pathological process that exacerbates AIS, with exosomes act as crucial mediators. However, the effects and mechanisms of action of macrophage-derived exosomes on CIRI remain unclear. This study demonstrated that macrophage-derived exosomes induce endothelial ferroptosis and barrier disruption during CIRI. Through proteomic sequencing and the reanalysis of transcriptomic and single-cell sequencing data, thrombospondin-1 (THBS1) was identified as a key exosomal molecule. Elevated THBS1 was observed in exosomes and monocytes from the peripheral blood of patients with AIS in oxygen–glucose deprivation/reoxygenation (OGD/R)-stimulated THP-1 and RAW264.7, in their secreted exosomes, and in macrophages within the brains of transient middle cerebral artery occlusion (tMCAO) mice. Additionally, THBS1 expression in exosomes was positively correlated with vascular barrier injury biomarkers, including MMP-9 and S100B. Modulation of THBS1 in macrophage-derived exosomes affected exosome-induced ferroptosis in endothelial cells. The mechanism by which THBS1 binds directly to OTUD5 and promotes GPX4 ubiquitination was elucidated using RNA interference, adeno-associated virus transfection, and endothelial-specific Gpx4 knockout mice. High-throughput screening of small-molecule compounds targeting THBS1 was performed. Molecular docking, molecular dynamics simulations, and cellular thermal shift assays further confirmed that salvianolic acid B (SAB) has a potent binding affinity for THBS1. SAB treatment inhibited the interaction between THBS1 and OTUD5, leading to reduced GPX4 ubiquitination. Further research revealed that SAB treatment enhanced the cerebral protective effects of THBS1 inhibition. In conclusion, this study explored the role of exosome-mediated signaling between macrophages and cerebral vascular endothelial cells in CIRI, highlighting the THBS1-OTUD5-GPX4 axis as a driver of endothelial ferroptosis and brain injury. Targeting this signaling axis represents a potential therapeutic strategy for treating CIRI.

BACKGROUND:The proinflammatory response triggered by macrophages/microglia plays a crucial role in the prognosis of acute ischemic stroke (AIS). Identifying novel targets to regulate the homeostasis of these cells is essential. Developing therapeutic strategies based on these targets could significantly improve AIS treatment outcomes. PURPOSE:This study aims to identify new regulatory targets for macrophages/microglia homeostasis and to develop effective therapeutic strategies for AIS. STUDY DESIGN AND METHODS:Macrophage infiltration in AIS patients from GSE58294 and transient middle cerebral artery occlusion (tMCAO) mouse brain was observed using ssGSEA and immunofluorescence (IF). Integrating the MSigDB database, differentially expressed macrophage/microglia-associated genes (DEMAGs) were identified and further screened using machine learning. The protein level of the critical DEMAG in PBMCs, BV2 cells, and mouse brain tissues was detected with ELISA, western blot, IHC, and IF. siRNA was applied to investigate the effect of the critical DEMAG. A natural product library was screened to find a compound that targets the protein. The binding of compounds and proteins was analyzed through molecular docking, molecular dynamics simulations, CETSA, and MST analysis. RESULTS:This experiment observed increased macrophage infiltration in AIS patients. The upregulated critical DEMAG, ACP5, was more frequently detected in AIS patients' PBMCs, oxygen-glucose deprivation and reoxygenation (OGD/R)-treated BV2 cells and tMCAO mouse brain. Targeting the ACP5 protein, quercetagetin (QG) was identified as an inhibitor. QG could ameliorate systemic imbalance, brain injury, and cognitive impairment in tMCAO mice, partly by maintaining macrophage/microglia homeostasis and inhibiting ACP5. CONCLUSION:This study shows that ACP5 is a new promoter of macrophages/microglia proinflammatory responses, playing a critical role in regulating the excessive inflammation and oxidative stress associated with AIS. Furthermore, QG mitigates AIS-induced brain damage by inhibiting ACP5.

The polarization of microglia plays a crucial role in cerebral ischemia-reperfusion injury (CI/RI) and has garnered significant attention from researchers. M1-polarized microglia activation drives harmful inflammatory responses in neuronal cells. Although metformin can inhibit inflammatory reactions and improve CI/RI, it has significant toxic side effects. In this study, we designed a novel nanodrug delivery system, apoferritin nanocages encapsulating metformin (APO@Metformin), to address these issues. On the one hand, apoferritin nanocages are naturally available nanoparticles and widely present in biological systems, which possesses good biocompatibility and safety and reduces the toxic side effects of metformin. On the other hand, the small particle size of apoferritin nanocages enable them to have specific blood-brain barrier penetration to achieve brain targeting delivery. Animal experiments demonstrated that APO@Metformin improved CI/RI and reduced neuronal damage caused by inflammatory reactions. Furthermore, in vitro cell experiments showed that APO@Metformin not only could closely interact with transferrin receptors 1 (TfR1) expression in microglia to achieve superior brain targeting, but also inhibit the activity of M1 polarization and NLRP3 in microglia, thereby suppressing inflammatory responses in CI/RI and protecting neuronal cells.

Mounting evidence indicates the involvement of N6-methyladenosine (m6A) alterations in diverse neurological disorders and the activation of microglia. However, the role of m6A methyltransferase Wilms' tumor 1-associated protein (WTAP) in regulating microglial polarization during ischemic stroke (IS) remains unknown. We performed bioinformatics analysis to identify m6A-related differentially expressed genes in IS and validated these genes in a mouse middle cerebral artery occlusion model and a BV2 cell oxygen-glucose deprivation/reperfusion model. We found that microglial m6A modification was increased, and that WTAP was the most significantly differentially expressed m6A regulator during IS. High expression of WTAP is closely correlated with microglia-mediated neuroinflammation in IS. Mechanistically, WTAP promoted m6A modification, which promoted prostaglandin endoperoxide synthase-2 (PTGS2) by enhancing its mRNA stability. WTAP promoted M1 microglial polarization by elevating PTGS2 expression via m6A modification of PTGS2 mRNA in the oxygen-glucose deprivation/reperfusion model. In conclusion, WTAP is a crucial posttranscriptional regulator that contributes to post-IS neuroinflammation. WTAP knockdown confers cerebral protection by shifting the microglial phenotype from M1 to M2, primarily by reducing PTGS2 mRNA stability in an m6A-dependent manner.

目的 基于细胞外调节蛋白激酶 1/2(extracellular regulated protein kinases 1/2,ERK1/2)/血红素加氧酶1(heme oxygenase 1,HO-1)信号通路探讨右美托咪定(dexmedetomidine,Dex)对肝脏缺血再灌注损伤(hepatic ischemia-reperfusion injury,HIRI)的保护作用及其机制.方法 将成年雄性Sprague-Daw-ley(SD)大鼠24只随机分为4组:假手术组(Sham组)、模型组(I/R组)、I/R+Dex组和I/R+Dex+U组,每组6只.Sham组为未进行肝门静脉阻断的正常大鼠.其他各组大鼠通过肝门静脉闭塞1 h再灌注6 h建立HIRI模型.模型组和I/R+Dex组分别在缺血前30 min给予生理盐水和Dex(100 μg/kg),I/R+Dex+U组在I/R+Dex基础上再灌注前30 min给予MEK抑制剂U0126(50 μg/kg).检测4组炎症反应、氧化应激损伤、细胞凋亡以及HO-1和p-ERK1/2水平.结果 I/R组炎性细胞因子肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)和白介素-6(interleukin-6,IL-6)含量升高;I/R+Dex 组炎性细胞因子TNF-α和IL-6含量降低,与I/R组比较差异有统计学意义(P＜0.05).I/R+Dex+U组TNF-α和IL-6含量升高,与I/R+Dex组比较差异有统计学意义(P＜0.05).I/R组超氧化物歧化物(superoxide dis-mutase,SOD)活力降低、丙二醛(malondialdehyde,MDA)含量升高;I/R+Dex 组 SOD 活力升高、MDA 含量降低,与I/R组比较差异有统计学意义(P＜0.05).I/R+Dex+U组SOD活力降低,MDA含量升高,与I/R+Dex组比较差异有统计学意义(P＜0.05).I/R组凋亡指数及凋亡蛋白表达均升高;I/R+Dex组凋亡指数及凋亡蛋白表达均降低,与I/R组比较差异有统计学意义(P＜0.05).I/R+Dex+U组凋亡指数及凋亡蛋白表达均升高,与I/R+Dex组比较差异有统计学意义(P＜0.05).免疫组化结果显示,1/R+Dex组HO-1及ERK1/2的表达均升高.结论 右美托咪定可通过调控ERK1/2/HO-1信号通路在大鼠HIRI过程中发挥抗氧化、抗炎、抗凋亡作用.

Ethnopharmacological relevance: Danlou tablet (DLT) is a traditional Chinese medicinal formulation known for replenishing Qi, promoting blood circulation, and resolving stasis. Its pharmacological actions primarily involve anti-inflammatory, antioxidant stress reduction, antiapoptotic, proangiogenic, and improved energy metabolism. DLT has been confirmed to have favorable therapeutic effects on ischemic stroke (IS). However, the underlying mechanism through which DLT affects IS-induced brain injury remains unknown. Aim of the study: This study aims to investigate the effects and underlying mechanisms of danlou tablet on ischemic stroke based on network pharmacology and experimental verification. Materials and methods: Using a transient middle cerebral artery occlusion (tMCAO) mouse model, the impact of DLT on the blood-brain barrier (BBB) and brain injury in mice was assessed. Network pharmacology and bioinformatics analyses were utilized to explore the potential mechanisms of DLT in treating IS. Endothelial cells were cultured to observe the effects of DLT on vascular endothelial cells after oxygen-glucose deprivation/ reperfusion, and these findings were validated in the brains of tMCAO mice. Results: DLT alleviated oxidative stress and brain damage in tMCAO mice, mitigating BBB damage. A total of 185 potential targets through which DLT regulates IS were identified, including COX2, a known critical marker of ferroptosis, which identified as a key target. In vitro and in vivo experiments demonstrated that DLT significantly (p < 0.05) improved cell death and vascular barrier damage in IS, reducing intracellular oxidative stress and COX2 protein levels while increasing SLC7A11 and GPX4 protein levels. Conclusions: This study demonstrated that DLT maintained BBB integrity and alleviated brain injury of tMCAO mice by inhibiting ferroptosis. The study partially unraveled the mechanism through which DLT functioned in treating IS and further clarified the pivotal active components of DLT, thereby providing a theoretical scientific basis for treating IS with DLT.

Ischemic stroke (IS) is a neurological condition associated with high mortality and disability rates. Although the molecular mechanisms underlying IS remain unclear, ferroptosis was shown to play an important role in its pathogenesis. Hence, we applied bioinformatics analysis to identify ferroptosis-related therapeutic targets in IS. IS-related microarray data from the GSE61616 dataset were downloaded from the Gene Expression Omnibus (GEO) database and intersected with the FerrDb database. In total, 33 differentially expressed genes (DEGs) were obtained and subjected to functional enrichment and protein–protein interaction (PPI) network analyses. Four candidate genes enriched in the HIF-1 signaling pathway (HMOX1, STAT3, CYBB, and TLR4) were selected based on the hierarchical clustering of the PPI dataset. We also downloaded the IR-related GSE35338 dataset and GSE58294 dataset from the GEO database to verify the expression levels of these four genes. ROC monofactor analysis demonstrated a good performance of HMOX1, STAT3, CYBB, and TLR4 in the diagnosis of ischemic stroke. Transcriptional levels of the above four genes, and translational level of GPX4, the central regulator of ferroptosis, were verified in a mouse model of middle cerebral artery occlusion (MCAO)-induced IS by qRT-PCR and western blotting. Considering the regulation of the HIF-1 signaling pathway, dexmedetomidine was applied to the MCAO mice. We found that expression of these four genes and GPX4 in MCAO mice were significantly reduced, while dexmedetomidine reversed these changes. In addition, dexmedetomidine significantly reduced MCAO-induced cell death, improved neurobehavioral deficits, and reduced the serum and brain levels of inflammatory factors (TNF-α and IL-6) and oxidative stress mediators (MDA and GSSG). Further, we constructed an mRNA-miRNA-lncRNA network based on the four candidate genes and predicted possible transcription factors. In conclusion, we identified four ferroptosis-related candidate genes in IS and proposed, for the first time, a possible mechanism for dexmedetomidine-mediated inhibition of ferroptosis during IS. These findings may help design novel therapeutic strategies for the treatment of IS.

临床麻醉学课程是麻醉学专业学生临床主干课程之一,其任务是通过理论教学和临床实习使学生掌握临床麻醉学有关的基本理论、基本知识和基本技能.针对传统临床麻醉学课程线下单一灌输式课堂教学方式的弊端,及与课程内容相关医学生思想政治工作疏离与缺失的问题,研究如何将传统课堂教学方式转变为符合新时代教育教学发展的线上线下混合式教学的授课方式,并深入挖掘课程思政元素,将其导入和融合到课程之中,使经历了多次教材更新和近三十年历史沿革的临床麻醉学课程历久弥新,是作为国家一流本科专业建设点的哈尔滨医科大学麻醉学本科专业的历史使命.

经尿道前列腺切除术（TURP）是前列腺增生最常见的手术方式。膀胱痉挛是导致患者术后疼痛和不适，严重影响患者康复的主要因素，表现为术后突发的膀胱间歇性痉挛性绞痛、急迫的尿失禁和导尿管周漏尿，并伴有心动过速、血压升高，对老年患者极为不利[1-3]。目前膀胱痉挛的预防和治疗方法主要包括膀胱内注药、全身用药等[4-9]，但治疗效果均欠佳，

Increased microglial NADPH oxidase (NOX2) production may make an important contribution to the increased incidence and severity of ischemic stroke associated with diabetes. Imidazoline receptors are closely associated with neuroprotection, but the neuroprotective effects of the selective I2-imidazoline receptor ligand 2-(2-benzofuranyl)-2-imidazoline (2BFI) in diabetes has not been established. The effect of 2BFI on microglial NOX2 production was investigated using a co-culture of neurons and microglia, and the effect on cerebral ischemia-reperfusion (IR) injury was determined in diabetic rats. Garcia neurological scores, brain infarct volumes, brain water content, TUNEL staining, blood-brain barrier, and immunofluorescent labeling for microglia were evaluated. Western blots were used to determine gp91phox and Tyr1472 expression. Anti-inflammatory cytokine (IL-10) and inflammatory cytokine secretion was determined using ELISA kits. The brain infarct volumes, TUNEL-positive neurons, expression of microglia, brain water content, blood-brain barrier structure damage, and gp91phox and Tyr1472 expression were increased, the Garcia neurological scores were significantly decreased in the IR group, and 2BFI relieved these alterations. The IL-10 concentration was increased in the IR group; 2BFI significantly improved this increase. The neuron apoptosis and necrosis rates, and production of reactive oxygen species (ROS) and inflammatory cytokines, including IL-6, IL-8, TNF-α, and 8-iso-PGF2α, were significantly increased by high glucose stimulation combined with oxygen-glucose deprivation treatment, which were inhibited by 2BFI. The 2BFI ameliorated cerebral ischemia-reperfusion injury in diabetes and decreased neuron death in an in vitro model. The mechanism underlying these findings may be related to the decreased production of inflammatory factors and reactive oxygen species from microglia.

目的 探讨经皮穴位电刺激(TAES)对甲状腺切除患者术后恶心呕吐的预防效果.方法 选择2019年6—11月择期行甲状腺切除术女性患者80例,年龄25～60岁,BMI 18～30 kg/m2,ASAⅠ或Ⅱ级.采用随机数字表将患者分为两组:经皮穴位电刺激组(E组)和对照组(C组),每组40例.麻醉诱导前30 min E组行双侧内关穴、合谷穴TAES;手术结束前30 min C组静脉注射格拉司琼3 mg.记录术后30 min和术后6、12、24 h恶心、呕吐例数及严重程度.术后12 h每组随机选择15例患者检测血浆5-羟色胺(5-HT)浓度.结果 与C组比较,术后12、24 h E组恶心发生率和严重程度明显降低(P<0.05),术后6、12、24 h E组呕吐发生率和严重程度明显降低(P<0.05),术后12 h血浆5-HT浓度明显降低(P<0.05).术后30 min两组恶心、呕吐发生率和严重程度差异无统计学意义.结论 双侧内关穴、合谷穴经皮穴位电刺激应用于甲状腺切除术后,可以降低血浆5-HT浓度,有效预防甲状腺手术后恶心、呕吐.

缺血性脑卒中患者脑组织缺血一定时间后,再恢复血液灌注,脑组织细胞损伤反而进一步加重,称为脑缺血再灌注损伤,其通过多种机制对神经元造成损害,使神经元凋亡.目前,脑卒中的治疗主要使用脑保护药物,在缺血再灌注损伤后主要通过抗凝,抗血小板聚集,抑制炎症反应和氧化应激,神经元保护等措施来减轻神经元的损伤.具体药物包括盐酸右美托咪啶[1]、含有川芎嗪和肉碱亚结构的新型双化合物[2]、去纤维蛋白原酶,巴曲霉等[3],但疗效有限.近年来,很多学者研究2-(2-苯并呋喃)-2-咪唑啉(2-(2-benzofuranyl)-2-imidazoline,2-BFI)在缺血再灌注损伤中有脑保护作用,为其治疗提供了一个新的方向.

本综述总结归纳了咪唑啉I2受体生物学功能研究的最新进展.咪唑啉I2受体配体是探讨与I2受体有关的药理作用的一种非常有价值的研究工具,大量证据提示咪唑啉I2受体配体本身具有抗伤害感受性作用,并且与镇痛药的联合使用不仅增强镇痛药的抗伤害性感受性作用,还可以减轻长期使用镇痛药产生的耐受性和依赖性等副作用.咪唑啉I2受体配体的另一作用是具有确切的神经保护作用,但其具体机制需要进一步探索及研究.此外,一些研究表明咪唑啉I2受体具有改善阿尔兹海默病、抗抑郁、调节体温等作用.

阿尔茨海默症(Alzheimer's disease,AD)、多发性硬化(multiple sclerosis,MS)、脑梗死(cerebral infarction,CI)、抑郁症等疾病是临床多发且严重的颅脑疾病,几种疾病的发病机制涉及部分相似的过程,疾病的发作给患者带来生理和心理上的打击,严重时可危及患者的生命.疼痛虽然不是一种疾病,但疼痛的感知也涉及神经的传递和中枢系统的整合,疼痛更是对包括颅脑在内的全身脏器具有损伤.

Objective To investigate the role of extracellular signal-regulated kinase 1/2 (ERK1/2) in attenuation of hepatic ischemia/reperfusion injury by dexmedetomidine (Dex) preconditioning in rats. Methods Adult male SD rats were randomly allocated into four groups (n=6): Sham group (group S), hepatic ischemia/reperfusion injury (HI/RI) group (group HI/RI), Dex pretreatment in HI/RI group (group D), U0126 (MEK inhibitor) pretreatment followed by same treatments as D group (group U). The results were observed at 6 h of reperfusion. The effects of Dex on phosphorylate (p)-ERK1/2 expression in the ischemic liver were measured by immunohistochemistry. Hepatic injuries were evaluated with the activity of ALT and AST, levels of Cleaved caspase-3, TUNEL assay, and H-E staining. Results Compared with group HI/RI, group D exhibited reduce activity of ALT and AST, lower levels of Cleaved casepase-3, and attenuated apoptosis index(P<0.05), but elevated levels of p-ERK1/2 (P<0.05). Compared with group D, group U showed enhanced activity in ALT and AST, raised expression of Cleaved casepase-3, increased apoptosis index (P<0.05), but reduced, expression of p-ERK1/2 (P<0.05). Conclusions Dex treatment reduced expression of casepase-3 and inflammation in HI/RI rats, probably through activationg the ERK1/2 pathway.

BACKGROUND/AIMS:Peri-operative cerebral ischemia reperfusion injury is one of the most serious peri-operative complications that can be aggravated in patients with diabetes. A previous study showed that microglia NOX2 (a NADPH oxidase enzyme) may play an important role in this process. Here, we investigated whether increased microglial derived gp91phox, also known as NOX2, reduced oxygen glucose deprivation (OGD) after induction of hyperglycemia (HG).METHODS:A rat neuronal-microglial in vitro co-culture model was used to determine the effects of gp91phox knockdown on OGD after HG using six treatment groups: A rat microglia and neuron co-culture model was established and divided into the following six groups: high glucose + scrambled siRNA transfection (HG, n = 5); HG + gp91phoxsiRNA transfection (HG-gp91siRNA, n = 5); oxygen glucose deprivation + scrambled siRNA transfection (OGD, n = 5); OGD + gp91phoxsiRNA transfection (OGD-gp91siRNA, n = 5); HG + OGD + scrambled siRNA transfection (HG-OGD, n = 5); and HG + OGD + gp91phoxsiRNA transfection (HG-OGD-gp91siRNA, n = 5). The neuronal survival rate was measured by the MTT assay, while western blotting was used to determine gp91phox expression. Microglial derived ROS and neuronal apoptosis rates were analyzed by flow cytometry. Finally, the secretion of cytokines, including IL-6, IL-8, TNF-α, and 8-iso-PGF2α was determined using an ELISA kit.RESULTS:Neuronal survival rates were significantly decreased by HG and OGD, while knockdown of gp91phox reversed these rates. ROS production and cytokine secretion were also significantly increased by HG and OGD but were significantly inhibited by knockdown of gp91phoxsiRNA.CONCLUSION:Knockdown of gp91phoxsiRNA significantly reduced oxidative stress and the inflammatory response, and alleviated neuronal damage after HG and OGD treatment in a rat neuronal-microglial co-culture model.

近年来单肺通气( One-lung ventilation ,OLV)技术广泛应用于胸外科手术. 以往我们认为OLV存在绝对适应症与相对适应症,但在现在看来界线并不那么分明了. 因为相对适应症不仅仅要满足方便手术的要求,还要能够减轻术中以及术后并发症的发生[1]. 现将OLV的适应症归类为适合肺隔离和肺分离[2].