Gut microbiota-derived short-chain fatty acids (SCFAs), key mediators in gut–lung axis interactions, profoundly influence pulmonary immune homeostasis. Toll-like receptor 2 (TLR2) is crucial for initiating innate immunity against bacterial pneumonia by recognizing bacterial molecular patterns, but its signaling requires precise regulation to balance pathogen clearance and prevent excessive inflammation-induced tissue damage. The major SCFAs—acetate, propionate, and butyrate—modulate immune responses via distinct mechanisms, including G protein-coupled receptor (GPR) activation and histone deacetylase (HDAC) inhibition. However, direct evidence on how these SCFAs differentially regulate the pulmonary TLR2 signaling pathway in pulmonary cells is critically lacking. This review reviews current knowledge, examining TLR2’s role in pulmonary immune defense and bacterial pneumonia, along with its regulatory network, and the molecular details of SCFA immunomodulation through GPR activation and HDAC inhibition. Crucially, we propose and thoroughly discuss a central hypothesis based on indirect evidence and molecular understanding: acetate and propionate likely inhibit early TLR2 signaling activation via GPR-mediated rapid pathways, while butyrate predominantly promotes late-stage inflammation resolution and tissue homeostasis by remodeling gene expression through its HDAC inhibitory activity. We further analyze the potential biological significance of this postulated differential regulatory pattern in maintaining inflammatory balance during bacterial pneumonia. This review integrates literature and mechanistic analysis, highlights critical knowledge gaps in SCFA–pulmonary TLR2 axis research (such as lack of direct evidence, unclear in vivo differential effects, and local concentration influence), and outlines future research directions to deepen understanding of gut–lung axis-mediated pulmonary immune regulation, providing a theoretical foundation for innovative bacterial pneumonia prevention and treatment strategies.

Wnt signaling coordinates lung specification, alveolar maturation, adult epithelial maintenance, and injury repair, but its biological output varies with developmental or disease stage, anatomical compartment, responding cell type, receptor context, and signal duration. This review organizes current evidence using a temporal-spatial framework that links Wnt ligands and receptors to source and responding cells, downstream canonical or noncanonical pathways, interacting signaling networks, and cellular outcomes. During development, mesenchymal Wnt2/2 b–β-catenin signaling specifies pulmonary endoderm, whereas canonical and noncanonical Wnt programs subsequently regulate distal progenitor expansion, branching geometry, epithelial differentiation, secondary septation, pulmonary microvascular maturation, and postnatal lung growth; maintenance of an AXIN2+ alveolar type 2 (AT2) progenitor niche becomes a distinct function in the adult lung. After adult alveolar injury, Wnt activity is dynamically remodeled as AT2 cells proliferate and traverse damage-associated transient progenitor and keratin 8-positive (KRT8+) transitional states before restoring the alveolar type 1 cell layer. This framework helps reconcile apparently discordant observations in chronic lung diseases. Bronchopulmonary dysplasia disrupts Wnt timing during alveologenesis; chronic obstructive pulmonary disease can combine deficient canonical Wnt responsiveness in the alveolar compartment with Wnt5a-associated inhibition of repair and distinct airway Wnt activation; and idiopathic pulmonary fibrosis features persistent Wnt-transforming growth factor-β signaling in abnormal epithelial and fibroblast niches. Therapeutic translation should therefore avoid indiscriminate pathway activation or inhibition and instead pursue reversible, local, biomarker-guided modulation matched to disease stage, cellular compartment, receptor profile, dose, and duration.

Necrotizing enterocolitis (NEC) is one of the most severe intestinal diseases affecting preterm infants, characterized by high mortality rates and significant long-term complications, which present substantial challenges to clinical management. The primary pathological mechanism underlying NEC is the immature development of the intestinal barrier in preterm infants, which fails to adequately resist luminal pathogen invasion, triggering uncontrolled inflammatory responses and tissue damage. Additionally, intestinal dysbiosis further compromises the integrity of the intestinal barrier. In recent years, growing attention has been given to the role of tryptophan metabolites in maintaining intestinal barrier integrity. As an essential amino acid, tryptophan metabolites—particularly those derived from gut microbiota, such as indole compounds—have been shown to exert significant barrier-protective effects through multiple mechanisms, including the activation of the aryl hydrocarbon receptor (AhR), upregulation of tight junction protein expression, inhibition of inflammatory responses, and promotion of epithelial cell repair. This review aims to summarize the major biological pathways of tryptophan metabolism, with particular emphasis on the molecular mechanisms by which microbial indole derivatives enhance the physical, chemical, and immune barriers. By synthesizing both preclinical studies and clinical evidence, this article explores the translational potential of tryptophan metabolite-targeted strategies for NEC prevention, providing a theoretical foundation for the development of precise preventive interventions.

Neutrophilic asthma represents a distinct inflammatory phenotype characterized by sputum neutrophilia (≥61% neutrophils), glucocorticoid resistance, and more severe disease course compared to eosinophilic asthma. This review comprehensively examines the molecular mechanisms underlying neutrophilic asthma pathogenesis, focusing on the Th17/IL-17 axis, neutrophil extracellular traps (NETs), and NLRP3 inflammasome activation. We present a precision identification framework integrating molecular endotypes with clinical phenotypes and biomarker profiles to guide therapeutic decisions. Unlike eosinophilic asthma, neutrophilic asthma demonstrates intrinsic resistance to glucocorticoids due to impaired neutrophil apoptosis and persistent activation of pro-inflammatory pathways. Emerging therapeutic approaches targeting IL-17, NET formation, and inflammasome components show promise, with several agents in clinical development. The microbiome-neutrophil axis represents a novel therapeutic target, with evidence suggesting that airway dysbiosis perpetuates neutrophilic inflammation through pattern recognition receptor activation. This review provides a comprehensive framework for understanding neutrophilic asthma pathogenesis and outlines precision medicine approaches for this difficult-to-treat asthma phenotype.

The core pathology of asthma involves not only inflammation amplification but also a systemic failure of inflammation resolution programs. This review first summarizes the Specialized Pro-resolving Mediators (SPM) family, efferocytosis, and their molecular basis in maintaining respiratory system homeostasis, emphasizing the positive feedback loop between lipid mediator class switching and macrophage reprogramming. Subsequently, it delineates the structural and functional characteristics of asthmatic airway remodeling and compiles evidence from human samples, animal models, and in vitro experiments regarding impaired SPM generation, attenuated receptor signaling, and reduced efferocytosis efficiency. This reveals a cascade mechanism of "SPM deficiency--efferocytosis impairment--secondary necrosis--structural damage." Furthermore, the review discusses the links between severe/refractory phenotypes, early-onset airway remodeling, and high eosinophilic/mixed granulocytic inflammation with resolution defects from the perspective of clinical phenotypes and biomarkers. It proposes the potential of composite indicators such as SPM profiles, Damage-Associated Molecular Patterns (DAMPs) levels, and phagocytic indices in stratified management and efficacy prediction. In the therapeutic and translational section, the review systematically compares the effects of exogenous SPMs, SPM generation/receptor modulators, efferocytosis-enhancing strategies, and traditional Inhaled Corticosteroids (ICS) and biologics on resolution pathways. It proposes an approach where "pro-resolving pharmacology" synergizes with existing anti-inflammatory therapies. Finally, the review addresses the limitations of current evidence regarding sample size, detection methods, and model constraints, calling for the inclusion of standardized resolution indicators and imaging/histological endpoints in prospective cohorts and clinical trials to promote a shift from symptom control towards structure-oriented, disease-modifying comprehensive interventions.

目的:观察小儿呼吸操辅助治疗学龄前儿童支气管哮喘缓解期的临床疗效.方法:将60例学龄前期哮喘患儿随机分为对照组和治疗组,对照组予常规糖皮质激素吸入治疗;治疗组在对照组的基础上,辅以小儿呼吸操训练,每次20 min,每日1次,3个月为1个疗程,治疗后评价患儿哮喘急性发作率、肺功能改善情况及哮喘控制情况.结果:两组治疗后肺功能指标FEV1、FEV1/FVC、PEF均得到明显改善,但治疗组较对照组肺功能改善较为显著,差异均具有统计学意义(P＜0.05);治疗组哮喘控制率(96.4％)明显高于对照组(86.2％);治疗期间治疗组患儿哮喘急性发作率明显低于对照组(P＜0.05).结论:小儿呼吸操应用于学龄前哮喘缓解期患儿的辅助治疗可改善患儿肺功能,提高患儿哮喘控制水平,降低哮喘急性发作率.

Background This study summarized the available randomized controlled trials (RCTs) to assess the efficacy and safety of macrolides on pathogens, lung function, laboratory parameters, and safety in children with bronchiectasis. Methods PubMed, EMBASE, and the Cochrane Library were searched for available papers published up to June 2021. The outcomes were the pathogens, adverse events (AEs), and the forced expiratory volume in one second (FEV1%) predicted. Results Seven RCTs (633 participants) were included. The long-term use of macrolides reduced the risk of the presence of Moraxella catarrhalis (RR = 0.67, 95% CI: 0.30–1.50, P = 0.001; I 2 = 0.0%, P heterogeneity = 0.433), but not Haemophilus influenza (RR = 0.19, 95% CI: 0.08–0.49, P = 0.333; I 2 = 57.0%, P heterogeneity = 0.040), Streptococcus pneumonia (RR = 0.91, 95% CI: 0.61–1.35, P = 0.635; I 2 = 0.0%, P heterogeneity = 0.515), Staphylococcus aureus (RR = 1.01, 95% CI: 0.36–2.84, P = 0.986; I 2 = 61.9%, P heterogeneity = 0.033), and any pathogens present (RR = 0.61, 95% CI: 0.29–1.29, P = 0.195; I 2 = 80.3%, P heterogeneity = 0.006). Long-term macrolides had no effect on FEV1% predicted (WMD = 2.61, 95% CI: –1.31, 6.53, P = 0.192; I 2 = 0.0%, P heterogeneity = 0.896). Long-term macrolides did not increase the risk of AEs or serious AEs. Conclusion Macrolides do not significantly reduce the risk of pathogens present (except for Moraxella catarrhalis ) or increase FEV1% predicted among children with bronchiectasis. Moreover, macrolides were not associated with AEs. Considering the limitations of the meta-analysis, further larger-scale RCTs are needed to confirm the findings. Impact Macrolides do not significantly reduce the risk of pathogens present (except for Moraxella catarrhalis ) among children with bronchiectasis. Macrolides do not significantly increase FEV1% predicted among children with bronchiectasis. This meta-analysis reports on the efficacy and safety of macrolides in the treatment of children with bronchiectasis, providing evidence for the management of children with bronchiectasis. This meta-analysis does not support the use of macrolides in the management of children with bronchiectasis unless the presence of Moraxella catarrhalis is provenor suspected.

赵坤依据带状疱疹病因、病机、发病部位及临床表现,应用三焦理论进行辨治.邪犯上焦,多见于疾病早期,为风热毒邪上犯上焦所致,治以疏风散邪解毒,方选普济消毒饮加减.邪犯中焦,多由肝经湿热火毒瘀滞所致,治以清肝利湿、凉血解毒,方用龙胆泻肝汤合五味消毒饮汤,此阶段,由于局部症状明显,疼痛剧烈,赵老师另给予雄黄、冰片、黄柏、利多卡因乳膏调成糊状,涂于患处.邪壅下焦,多见于疾病后期,由中焦湿热火毒证余毒未清,瘀血等邪气阻滞于经络而致,治以活血化瘀、行气止痛,方选桃红四物汤加减.急性期强调清热解毒、利湿止痛之法,后期注重益气散血、搜风通络之功,活血化瘀贯穿整个病程.

目的 通过加味小青龙汤对慢性持续期哮喘大鼠肺肠组织病理学及肺泡灌洗液、肠黏液中IL-6、IL-10、SIgA表达的影响,探讨加味小青龙汤对肺-肠黏膜免疫影响及相关作用机制.方法 将50只SPF级雄性SD大鼠随机分别为空白组、哮喘模型组、加味小青龙汤组、益生菌组、加味小青龙汤+益生菌组,每组各10只,采用苏木-伊红(HE)染色观察肺组织、肠道组织的病理学改变,同时对收集到的支气管肺泡灌洗液、肠黏液采用酶联免疫吸附实验(ELISA),测定其中IL-6、IL-10、SIgA的表达水平.结果 ①肺组织病理学改变与肺泡灌洗液中IL-6、IL-10、SIgA的表达:与空白组相比,哮喘模型组气道上皮出现部分缺损及脱落,管腔狭窄,形状不规则,平滑肌有部分增厚,气道周围有大量炎性细胞浸润.与空白组相比,哮喘模型组大鼠肺泡灌洗液中IL-6的表达明显升高而IL-10、SIgA的表达显著下降,差异均有统计学意义(P＜0.01);与哮喘模型组相比,加味小青龙汤组、益生菌组、加味小青龙汤+益生菌组的IL-6表达显著降低,IL-10、SIgA的表达有所升高,差异均有统计学意义(P＜0.05或P＜0.01);与益生菌组相比,加味小青龙汤、加味小青龙汤+益生菌组的IL-6表达降低,IL-10、SIgA的表达明显升高,差异均有统计学意义(P＜0.05或P＜0.01).②肠组织病理学改变与肠黏液中IL-6、IL-10、SIgA的表达:与空白组相比,哮喘模型组大鼠肠黏膜上皮不完整,部分有脱落,黏膜皱襞增多,周围有炎症细胞的浸润.与空白组相比,哮喘模型组大鼠肠道黏液中IL-6的表达升高,IL-10、SIgA的表达降低,差异有统计学意义(P＜0.05或P＜0.01);与哮喘模型组比较,加味小青龙汤组、加味小青龙汤+益生菌组的IL-6表达降低,IL-10、SIgA的表达明显升高,差异均有统计学意义(P＜0.01),而益生菌组中IL-6表达降低、SIgA的表达明显升高,差异均有统计学意义(P＜0.01);与益生菌组相比,加味小青龙汤组、加味小青龙汤+益生菌组的IL-6表达降低,IL-10、SIgA的表达明显升高,差异有统计学意义(P＜0.05或P＜0.01).结论 加味小青龙汤调节肺与肠道黏膜免疫的作用机制可能是通过调控IL-6、IL-10表达从而影响SIgA的分泌实现的.

目的 探讨苏葶平喘汤对激素抵抗型难治性哮喘小鼠癌蛋白Fos(c-Fos)及血清核转录因子激活蛋白-1(ac-tivator protein 1,AP-1)表达的影响,试分析苏葶平喘汤对难治性哮喘的干预机制.方法 将50只雌性SPF级BALB/c小鼠随机分为5组,分别为空白组(A)、模型组(B)、苏葶平喘汤组(C)、地塞米松组(D)和苏葶平喘汤+地塞米松组(E),每组10只.除空白组外,剩余4组均将小鼠建立为激素抵抗型哮喘模型.药物干预结束后进行取材,利用酶联免疫吸附测定(ELISA)法、实时荧光定量聚合酶链式反应(Real-time PCR)分别检测小鼠血清AP-1、肺组织c-Fos的表达水平.结果 1.ELISA检测结果显示:模型组小鼠较空白组小鼠血清中AP-1的值明显增高(P＜0.05),苏葶平喘汤组、地塞米松组及苏葶平喘汤+地塞米松组较空白组的小鼠血清AP-1值均降低(P＜0.05),其中以苏葶平喘汤+地塞米松组的降低最为显著(P＜0.05).2.PCR检测结果显示:模型组与其余各组相比小鼠肺组织的c-FosmRNA表达明显升高(P＜0.05),苏葶平喘汤组、地塞米松组和苏葶平喘汤+地塞米松组c-FosmRNA表达下降(P＜0.05),地塞米松组、苏葶平喘汤组和苏葶平喘汤+地塞米松组小鼠的肺组织c-FosmRNA表达水平则无明显差异.结论 苏葶平喘汤治疗激素抵抗型哮喘可通过影响AP-1及c-Fos的表达水平来实现抑制哮喘炎症反应控制激素抵抗型哮喘症状的作用.

目的:探讨金匮肾气丸加减方对小儿闭塞性细支气管炎(BO)中医证素的影响.方法:采用随机对照试验的研究方法,将符合纳排标准的BO患儿60例平分为两组,每组各30例.其中治疗组给予金匮肾气丸加减方治疗,对照组给予西医常规治疗,疗程均为14d.根据证素辨证方法,分别提取病位证素及病性证素,观察两组证素分布情况及治疗前后病位及病性证素积分的变化.结果:最终治疗组完成28例、治疗组完成27例,两组病位证素出现频率＞20％的分别为肺、肾、脾、表,病性证素分别为阳虚、气虚、阴虚、血虚、痰、饮.经治疗后,治疗组各病位证素积分均较治疗前下降(P＜0.05),且与对照组相比,肾、脾、表病位证素积分均明显下降(P＜0.05);对照组肺、表2个病位证素积分,在治疗后较治疗前均有下降(P＜0.05).治疗组各病性证素积分均较治疗前下降(P＜0.05),且与对照组相比,阳虚、气虚、阴虚、血虚4个病性证素积分均明显下降(P＜0.05);对照组痰、饮2个病性证素积分,在治疗后较治疗前下降(P＜0.05).结论:金匮肾气丸可有效改善脾肾阳虚型BO患儿病位证素肺、脾、肾、表及病性证素阳虚、气虚、阴虚、血虚、痰、饮的积分情况,研究为金匮肾气方治疗儿童BO的有效性提供了客观依据.

目的:观察青贝苇茎汤口服联合耳穴压豆外用治疗儿童难治性支原体肺炎的临床疗效.方法:选择难治性支原体肺炎患儿95例,按照随机数字表法分为对照组48例,治疗组47例.对照组予西药常规治疗,治疗组在对照组治疗基础上给予青贝苇茎汤口服(每日2次,连服7 d),同时配合耳穴压豆(每日1次,连用7 d),7 d为1个疗程,共两个疗程.观察治疗前后两组患儿的中医证候积分、肺部湿啰音评分、肺功能指标、血清炎性指标、临床疗效及不良反应.结果:两组患儿治疗后主症、次症各单项症状积分及主症、次症总积分均低于治疗前,而治疗组以上评分显著低于同期对照组(P＜0.05);与对照组比较,治疗组治疗后发热、咳嗽、咳痰、喘息、纳差、口渴、便秘单项症状积分及主症、次症总积分均显著低于对照组(P＜0.05),但在改善精神差方面,两组差异无统计学意义(P=0.05).两组患儿治疗后C-反应蛋白(C-re-active protein,CRP)、细胞沉降率(erythrocyte sedimentation rate,ESR)水平及肺部湿啰音评分均明显降低,且治疗组优于对照组(P＜0.05).与治疗前比较,治疗组肺功能用力肺活量(forced vital capcacity,FVC)、第1秒用力呼气容积(forced ex-piratory volume in one second,FEV1)、呼气峰值流量(peak expiratory flow,PEF)、最大呼气中期流速(maximal mid-expirato-ry flow,MMEF)、25％用力肺活量时的用力呼气流量(forced expiratory flow of 25％,FEF25％)、50％用力肺活量时的用力呼气流量(forced expiratory flow of 50％,FEF50％)及75％用力肺活量时的用力呼气流量(forced expiratory flow of 75％,FEF75％)显著升高,且高于同期对照组,差异均有统计学意义(P＜0.05);对照组治疗后FVC、FEV1、MMEF、FEF25％、FEF50％及FEF75％显著高于治疗前,差异均有统计学意义(P＜0.05).治疗组有效率为97.9％,对照组为93.8％,两组比较,差异有统计学意义(P＜0.05).结论:青贝苇茎汤联合耳穴压豆治疗儿童难治性支原体肺炎临床疗效显著,可有效减轻患儿发热、咳嗽、咳痰、精神差、肺部湿啰音等临床症状及肺部体征,改善血清CRP、ESR水平,提高肺功能.

课程思政是当代高校教育的重要环节,是人才培养的关键部分,是做好其他学校工作的前提.高校需要把立德树人贯穿教育工作的全过程,以立德树人为核心的"三全育人"理念是对课程思政教学思想的完善,使得课程思政贯穿教学始终,实现全员、全程、全方位育人,这与中医整体观良好契合,符合中医天人合一、大医精诚、以人为本的思想道德传统.学生标准化病人(SSP)教学以真实模拟典型案例,使学生通过扮演患者、家属、医师等不同角色,切实体验临床患者接诊、病史采集、四诊合参、病历书写、医患沟通、人文关怀等各个环节,可有效提升学生积极性及主动性,符合现代高校中医儿科学临床学科的教学需要.基于"三全育人"理念指导下的SSP教学可在有效提升中医儿科学医学生专业技能的同时,潜移默化地将大医精诚、人文关怀等课程思政内容融入教学过程,以培养出德才兼备的全能型优秀中医儿科人才.

目的:基于中医传承辅助系统,对临床治疗儿童闭塞性细支气管炎的方药进行数据分析整理,总结其遣方法则,为本病临床辨证组方及新方开发应用提供客观理论根据.方法:收集中国知网、万方及维普数据库中关于中医中药治疗儿童闭塞性细支气管炎的处方,利用中医传承辅助系统进行数据挖掘,分析总结高频药物的属性、核心组合及新方方析.结果:筛选文献获取71个组方,涵盖157味中药,使用较多的药物有甘草、杏仁、芦根、葶苈子、五味子、鱼腥草、紫苑、红花、炙麻黄,药味前三位为苦、甘、辛,药性为寒、温、平,15个核心组合和4个新处方.结论:儿童闭塞性细支气管炎的中医治疗原则以宣肺利气,化痰平喘,活血化瘀,温补肺肾为主,用药不宜过于寒凉及温热.

目的:观察耳穴压豆联合自拟牛蒡翘荷汤治疗儿童疱疹性咽峡炎的临床疗效.方法:随机将100例疱疹性咽峡炎患儿分为治疗组与对照组各50例.对照组(脱落3例)给予牛蒡翘荷汤,治疗组(脱落2例)在对照组治疗基础上给予耳穴压豆疗法,3 d为1个疗程,共治疗两个疗程.治疗两个疗程后比较两组患者中医症状积分、临床疗效.结果:治疗后,两组患儿纳呆、咳嗽、口渴、大便、精神差、面色积分及次症总积分均显著低于治疗前(P＜0.05);治疗组纳呆、咳嗽、口渴等次症单项积分及总积分均低于同期对照组(P＜0.05).两组发热、咽痛、咽部疱疹积分及主症总积分均低于治疗前(P＜0.05);治疗组发热、咽痛、吞咽困难、咽部疱疹积分及主症总积分均显著低于同期对照组(P＜0.05).治疗组有效率为95.7％,对照组有效率为85.1％,两组比较,差异有统计学意义(P＜0.05).结论:耳穴压豆联合牛蒡翘荷汤治疗儿童疱疹性咽峡炎疗效显著,且能显著降低患儿中医证候积分.

目的:探讨原发性纤毛运动障碍(PCD)的临床特征、基因突变情况和诊治要点.方法:回顾分析1 例PCD患儿的临床表现,实验室检查、影像学检查、基因检测结果和家系相关情况等,总结PCD的临床诊断与治疗.结果:患儿,女,12岁6个月,2 a前出现反复咳嗽、咳痰,经抗感染及中药口服治疗效果不佳.近半个月来症状加重.肺部CT示:双肺多发支气管扩张合并感染;双侧胸膜增厚粘连.电子支气管镜示:支气管扩张;支气管内膜炎.全外显子测序基因检测发现患儿及其弟弟、妹妹 DNAH5 基因杂合突变:63 号外显子 c.10616G>A(p.R3539H)和61号外显子c.10363G>T(p.Q3455*),分别来源于母亲和父亲,c.10616G>A为已知致病突变,c.10363G>T为新发突变,未见文献报道.结论:PCD临床表现多样,治疗主要为抗感染和对症支持.本研究报道了一种新的致PCD的DNAH5基因杂合突变.

Asthma is characterized by airway inflammation and remodeling. 2-Undecanone (methyl nonyl ketone), a volatile organic compound originating from Houttuynia cordata, has the potential to ameliorate inflammatory diseases. This study aimed to explore potential benefits of 2-undecanone in asthma. 2-Undecanone (100, 200, or 400 mg/kg) was administered intragastrically to ovalbumin (OVA)-challenged BALB/c mice. Lung tissues were collected to observe histopathological changes, and bronchoalveolar lavage fluid (BALF) was collected for the detection of inflammatory cells and cytokine production. The results showed that 2-undecanone ameliorated OVA-induced pathologic changes of lungs, including reducing inflammatory cell infiltration, goblet cell hyperplasia, and airway smooth muscle thickness. The number of inflammatory cells and the levels of IL-4, IL-5, IL-13, and IgE in BALF were decreased by 2-undecanone in asthmatic mice. Furthermore, abnormal activation of NF-κB pathway in lung tissues of asthmatic mice was impeded by 2-undecanone. In vitro, 2-undecanone (12.5, 25, or 50 µM) suppressed platelet-derived growth factor-BB-induced proliferation and migration of primary airway smooth muscle cells (ASMCs), and inhibited the switching of ASMCs from contractile phenotype to synthetic phenotype. Consistently, 2-undecanone blocked NF-κB activation in ASMCs. Collectively, 2-undecanone relieves asthma through alleviating airway inflammation and remodeling, and this beneficial effect is achieved by inhibiting NF-κB pathway.

目的 探讨基于五禽戏之鸟戏的康复呼吸操对大叶性肺炎患儿肺功能的影响.方法 将74例大叶性肺炎患儿按病区分为对照组和观察组各37例.对照组实施常规治疗护理方案,观察组在此基础上实施基于五禽戏之鸟戏的大叶性肺炎康复呼吸操方案.结果 干预1周、3周观察组第1秒用力呼气容积占用力肺活量比值(FEV1/FVC)、用力肺活量(FVC)、最高呼气流速(PEF)显著优于对照组(P＜0.05,P＜0.01),咳嗽消失时间、肺部啰音消失时间、住院时间显著短于对照组(P＜0.05,P＜0.01).结论 对大叶性肺炎患儿实施基于五禽戏之鸟戏的康复呼吸操有利于促进患儿肺康复.

文章总结赵坤教授诊治儿童难治性哮喘的经验,认为该病反复发作,症情复杂,缠绵难愈的主要原因是痰瘀互结于肺形成窠囊,久病阳气耗损,肾阳不足.故肺有窠囊,肾阳衰惫是本病的病机实质,两者相互影响,互为因果.临床治疗以虚实为纲,注重标本兼治,攻补兼施,提出"破窠囊,补肾阳"的治疗基本法则,组方善用破痰化瘀之青皮、葶苈子、三棱、莪术,以化痰破瘀,疏通肺中经络,促进阳气的输布,补肾阳之附子、鹿茸、阳起石温补肾阳,治病求本,使痰瘀生化无源.通过该法临床治疗儿童难治性哮喘疗效显著.附典型案例1则,以资验证.

目的:探讨沉默信息调控因子6(silent information regulator 6,Sirt6)在炎症微环境下对骨髓间充质干细胞(bone marrow mesenchymal stem cells,BMSCs)的骨生成作用.方法:利用原代细胞贴壁法培养BMSCs,脂多糖(lipopolysaccharide,LPS)刺激BMSCs产生炎症反应;利用酶联免疫吸附试验(enzyme-linked immunosorbent assay,ELISA)检测促炎细胞因子:肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-1β(interleukin-1β,IL-1β)、IL-6的分泌.实验分为LPS组、LPS+空载体组及LPS+过表达Sirt6组,实时定量聚合酶链反应(real-time quantitative polymerase chain reaction,RT-qPCR)检测炎性状态下各组中Sirt6的mRNA表达;Western印迹法(Western blot)检测炎性状态下各组中Sirt6蛋白的表达水平;茜素红染色法检测炎性状态下各组BMSCs骨向分化中生成的钙结节.结果:培养出的BMSCs在LPS炎性刺激下可以产生炎性反应;炎症因子TNF-α、IL-1β、IL-6的含量均明显升高(P<0.05);成功构建了过表达Sirt6质粒载体并用其转染BMSCs;RT-qPCR和Western blot检测结果显示,LPS+过表达Sirt6组的Sirt6 mRNA和蛋白水平均明显高于LPS组和LPS+空载体组,并且LPS+过表达Sirt6组中成骨相关标志物骨钙素(osteocalcin,OCN)、碱性磷酸酶(alkaline phosphatase,ALP)、骨涎蛋白(bone sialoprotein,BSP)呈现高表达;茜素红染色检测结果显示,LPS+过表达Sirt6组中钙结节量也呈现高表达趋势.结论:过表达Sirt6显著抑制了促炎细胞因子的分泌,促进了炎症条件下BMSCs的成骨分化.