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.

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.

Asthma affects over 260 million people worldwide and remains incompletely explained by the traditional T cell-centric immunological model, which offers incomplete mechanistic explanations for disease chronicity, recurrence during clinical remission, and the poor treatment response observed in T2-low phenotypes. Emerging evidence positions the airway epithelium as a central organizer of asthma pathogenesis rather than a passive barrier. This review proposes a unifying framework in which airway epithelial dysfunction and epigenetic memory drive the persistent and relapse-prone nature of asthmatic airways. We first examine how structural barrier defects—including tight junction dysfunction mediated by claudin-18 and E-cadherin loss—initiate and amplify type 2 inflammation through alarmin release (TSLP, IL-33, IL-25) and ILC2 activation. We then review how environmental exposures and inflammatory signals, particularly IL-13, induce durable epigenetic reprogramming of airway epithelial cells through DNA methylation, histone modifications, and non-coding RNAs, establishing molecular imprints that persist beyond the resolution of acute inflammation. Special attention is given to basal progenitor cells as repositories of allergic epigenetic memory, and to the concept of trained innate immunity as a mechanism underlying chronic airway hyperresponsiveness. We further contrast the epigenetic landscapes of T2-high and T2-low asthma, identifying the latter as a critical unmet need for biomarker and therapeutic development. Finally, we discuss translational opportunities, including HDAC inhibitors, miRNA-based therapies, and the potential of anti-alarmin biologics (tezepelumab, itepekimab) and downstream cytokine receptor antagonists (dupilumab) to partially restore epithelial function and progenitor states. We acknowledge that, given current data availability, this review is weighted toward T2-high (eosinophilic) endotypes; mechanistic characterization of T2-low asthma remains an important area for future investigation. This framework reconceptualizes asthma not only as a disorder of dysregulated immunity, but as a disease of maladaptively reprogrammed barrier tissue, with important implications for disease prevention, endotype-specific treatment, and the goal of achieving true biological remission.

Xiaoqinglong Decoction (XQLD) is a traditional oriental medicine. Modified- Xiaoqinglong Decoction (M-XQLD) was established by adding astragalus membranaceus and codonopsis pilosula on the basis of XQLD. M-XQLD has been shown to be effective in therapying asthma in clinical trials, but the mechanism of M-XQLD in asthma is currently unknown. Mice were sensitized by ovalbumin (OVA) to induce asthma. M-XQLD were administered by oral gavage. Label-free proteomics was conducted to identify the downstream target of M-XQLD. Histopathological assessment, multiple cytokine examination in bronchoalveolar lavage fluid (BALF) were conducted. In vitro, we isolated Naïve CD4 + T cells for analysis. OVA stimulation decreased the expression of StAR Related Lipid Transfer Domain Containing 13 (STARD13), while M-XQLD treatment increased it. STARD13 overexpression reduced the inflammatory cell infiltration and goblet cells. STARD13 overexpression reduced the levels of OVA-specific IgE, IL-4, and IL-5 in serum and BALF. STARD13 overexpression inhibited the expression of IL-1β, IL-17A, and IL-22, and reduced Th17 differentiation. STARD13 overexpression inhibited the RhoA/ROCK2, while knockdown of STARD13 resulted in continuous activation of RhoA. Furthermore, STARD13 overexpression decreased p38 phosphorylation level. SB203580 treatment further inhibited the RORC expression and p38 phosphorylation. More importantly, the therapeutic efficacy of M-XQLD in OVA-induced mice was significantly reduced by STARD13 knockdown. This study revealed that M-XQLD targets to STARD13, and highlighted that STARD13 alleviated asthma by reducing Th17 differentiation via inhibiting the RhoA/ROCK2/p38 signaling.

Asthma is a common chronic respiratory disease characterized by Th2-type inflammation in the airways. Leucine zip transcription factor-like 1 (LZTFL1) has been implicated in the regulation of Th2-related factors. The knockdown of LZTFL1 resulted in decreased levels of IL-4, IL-5, and IL-13. We hypothesize that LZTFL1 may have an effect on asthma. We established an acute asthmatic mouse model using the Ovalbumin (OVA) sensitization, and we found that LZTFL1 expression was upregulated in OVA-induced CD4 + T cells. Mice challenged with OVA were administered 5 × 107 TU of lentivirus via tail vein injection. LZTFL1 knockdown reversed the frequency of sneezing and nose rubbing in OVA mice. LZTFL1 knockdown reduced inflammatory cell infiltration, reduced goblet cell numbers, and mitigated collagen deposition in lung tissue. LZTFL1 knockdown decreased the levels of OVA-specific IgE, IL-4, IL-5, and IL-13 in alveolar lavage fluid of asthmatic mice. Furthermore, LZTFL1 knockdown inhibited the aberrant activation of MEK/ERK signaling pathway in asthmatic mice. GATA binding protein 3 (GATA3) is an essential transcription factor in Th2 differentiation. Flow cytometry results revealed that LZTFL1 knockdown reduced the number of GATA3 + CD4 + Th2 cells, while it did not affect the stability of GATA3 mRNA. This may be attributed to ERK signaling which stabilized GATA3 by preventing its ubiquitination and subsequent degradation. In conclusion, LZTFL1 knockdown attenuates inflammation and pathological changes in OVA-induced asthmatic mice through ERK/GATA3 signaling pathway.

哮喘是儿童时期最常见的呼吸系统疾病之一,具有反复发作的特点.防治哮喘反复发作的重要环节就是持续期和缓解期治疗."未发以扶正气为主,既发以攻邪气为先",因此非发作期应以调理肺脾肾三脏功能,消除伏痰夙根为则.其中,肺是哮喘的核心病位,而历代医家多从肺气虚、脾气虚、肾气虚、肾阳虚辨治持续期和缓解期,鲜少提及肺阳.然吾师宋桂华教授经过多年临床经验及理论研究,提出在哮喘发病中肺阳虚一证多见,且创制经验方"参芪青龙汤加减",基于肺阳虚理论从持续期和缓解期论治儿童哮喘,持续期以散寒化饮为主,兼以温补肺阳,理气化痰;缓解期以温阳固本、温肺固表为主,兼以散寒化痰祛瘀,标本兼顾,扶正祛邪,分期据症加减,主次不同,各有侧重,取得了较好的临床疗效.

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.

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.

儿童坏死性肺炎属于中医学"肺痈"范畴,热、毒、痰、瘀既是其病理产物,又是疾病进展至慢性期的重要病因.从"热、毒、痰、瘀、虚"探讨儿童坏死性肺炎慢性期的辨治思路,认为热毒未清、痰瘀互结、气阴虚损是核心病机,提出以清热解毒、化痰祛瘀、益气养阴为主要治法,自拟协定清肺方作为治疗慢性期儿童坏死性肺炎的主方,为临床治疗提供思路.

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.

Asthma is a common respiratory disease associated with airway inflammation. Nerolidol is an acyclic sesquiterpenoid with anti-inflammatory properties. BALB/C mice were sensitized with ovalbumin (OVA) to induce asthma symptoms and given different doses of Nerolidol. We found that Nerolidol reduced OVA-induced inflammatory cell infiltration, the number of goblet cells and collagen deposition in lung tissue. Nerolidol reduced the OVA-specific IgE levels in serum and alveolar lavage fluid in an asthma model. Immunohistochemical staining of α-SMA (the marker of airway smooth muscle) showed that Nerolidol caused bronchial basement membrane thinning in asthmatic mice. The hyperplasia of airway smooth muscle cells (ASMCs) is an important feature of airway remodeling in asthma. ASMCs were treated with 10 ng/mL TGF-β to simulate the pathological environment of asthma in vitro and then treated with different doses of Nerolidol. Nerolidol inhibited the activity of TGF-β/Smad signaling pathway both in the lung tissue of OVA-induced mouse and TGF-β-stimulated ASMCs. 16s rRNA sequencing was performed on feces of normal mice, the changes of intestinal flora in OVA-induced asthmatic mice and Nerolidol-treated asthmatic mice were studied. The results showed that Nerolidol reversed the reduced gut microbial alpha diversity in asthmatic mice. Nerolidol changed the relative abundance of gut bacteria at different taxonomic levels. At the phylum level, the dominant bacteria were Bacteroidota, Firmicutes, and Proteobacteria. At the genus level, the dominant bacteria were Lactobacillus, Muribaculaceae, Bacteroides, and Lachnospiraceae. We conclude that Nerolidol attenuates OVA-induced airway inflammation and alters gut microbes in mice with asthma via TGF-β/Smad signaling.

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.

闭塞性细支气管炎(BO)是以小气道上皮细胞炎症反应及纤维化收缩,致使气道管腔狭窄或闭塞为主要病理学表现的严重的呼吸系统慢性疾病.建立理想的BO动物模型,在研究者了解疾病的复杂病理生理学并制定新的预防和治疗策略的过程中起着至关重要的作用.不同造模方法所建立的BO动物模型均拥有各自的优势和局限性.本文就BO动物模型的相关研究进展进行综述.

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.

伏邪是伏藏于体内不立即发病的病邪,儿童感染后闭塞性细支气管炎(PIBO)的发病与伏邪关系密切.本文认为痰、饮、瘀为PIBO主要伏邪,痰饮内阻、血瘀互结,肺脾气虚、肾阳亏虚、肺肾阴虚为主要病机.倡导分期论治,结合本病及伏邪发病特点,以透达伏邪贯穿各期,因势利导,给邪出路.治疗上强调窗口期提前干预,扶正祛邪;发作期注重祛除内外合邪;迁延期临床症状相对稳定,则以扶正固本为基本治则,根据各病期不同病机,组方用药辨治儿童PIBO,临床疗效满意.

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:研究苏葶平喘汤对难治性哮喘激素抵抗型小鼠肺组织c-jun表达的影响,探讨苏葶平喘汤干预难治性哮喘相关作用机制.方法:将无特定病质体(SPF)级BALB/C雌性小鼠50只随机分为空白对照组、模型对照组、苏葶平喘汤组、地塞米松组、苏葶平喘汤和地塞米松组5组,每组10只.除空白对照组外,其余各组均建立难治性哮喘激素抵抗型小鼠模型.苏葶平喘汤组灌胃苏葶平喘汤水煎剂16.68 g/(kg·d),并腹腔注射0.5 mL生理盐水;地塞米松组灌胃生理盐水0.5 mL,并给予地塞米松1μg/(g·d),腹腔注射0.5 mL盐水;苏葶平喘汤和地塞米松组灌胃苏葶平喘汤水煎剂16.68 g/kg,并给予地塞米松针1μg/(g·d),腹腔注射0.5 mL盐水.空白对照组和模型对照组给予等量生理盐水灌胃及腹腔注射.各组均1d1次,连续3周.采用苏木精-伊红染色法检测实验前后各组小鼠肺组织病理改变;采用以实时聚合酶链反应检测c-jun表达水平.结果:①模型对照组小鼠肺组织出现明显病理改变,苏葶平喘汤组、地塞米松组和苏葶平喘汤+地塞米松组各组均有缓解作用;②模型对照组c-Jun mRNA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-Jun mRNA表达下降(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-Jun mRNA表达无明显差异.结论:苏葶平喘汤治疗难治性哮喘激素抵抗型哮喘有效,可能是通过降低c-Jun表达来实现的.

目的:基于网络药理学技术探讨小青龙汤治疗变应性鼻炎(Allergic Rhinitis,AR)的作用机制.方法:通过中药系统药理学数据库与分析平台获取小青龙汤中8味药物的化学成分并筛选主要活性成分,通过Swiss Target Prediction数据库、SEA数据库预测主要活性成分作用靶点,并将其导入Cytoscape 3.2.1软件构建"成分-靶点"网络;检索TTD、Drugbank及DisGeNET数据库收集与AR有关的疾病靶点,取交集获取小青龙汤治疗AR的靶点,导入STRING数据库构建蛋白质-蛋白质相互作用(Protein-Protein Interoution,PPI)网络并通过Cytoscape 3.2.1软件进行网络可视化及拓扑结构分析,通过Clue GO插件和DAVID数据库对核心靶点进行基因本体(The Gene Ontology,GO)分析和京都基因和基因组数据库(Kyoto Encyclopediaof Genes and Genomes,KEGG)通路富集分析.结果:本研究得到小青龙汤主要活性成分150个,作用于364个靶点,疾病靶点209个,小青龙汤与AR共有靶点38个,通过GO分析获得11个生物过程,KEGG富集显示与77个信号通路相关.结论:小青龙汤可通过多靶点、多途径发挥治疗AR的作用,可为进一步临床和实验研究提供一定的理论基础.