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关键词： CD93   interleukin-17D   oxidative stress  

摘要： This review explores interleukin (IL)-17D and its receptor CD93, highlighting their structural, functional, and clinical aspects. Identifying CD93 as the receptor for IL-17D has advanced understanding of the IL-17 family and its signaling pathways. IL-17D, with its unique glycoprotein structure, plays diverse roles in oxidative stress response and potential antitumor therapies. It is involved in autoimmune diseases, infections, and cancers, making it a promising therapeutic target. CD93 is crucial in various biological processes, from angiogenesis to inflammatory diseases. CD93's implications in cancers, neuroinflammation, and metabolism highlight its significance as a potential prognostic marker and therapeutic target. The review emphasizes IL-17D and CD93 as promising areas for future research, offering insights into their signaling pathways and potential applications in personalized medicine. Deciphering the relationship between IL-17D and CD93 is in its infancy and invites exploration for transformative advancements in immunology and beyond.

关键词： 奥美拉唑   阿莫西林   慢性胃炎   炎症因子  

摘要： 研究奥美拉唑搭配阿莫西林治疗对慢性胃炎患者C反应蛋白(CRP)、白细胞介素-6(IL-6)等生化指标的作用效果。方法 在2023年1月至2024年8月期间,筛选100例慢性胃炎患者作为实验对象,通过随机分组法将其分为观察组和对照组,每组50名患者。对照组仅使用奥美拉唑进行治疗,而观察组则联合应用奥美拉唑与阿莫西林。两组的治疗效果通过治疗前后的生化指标、临床症状评分以及治疗有效率进行比较。结果 观察组患者在完成治疗后,CRP、IL-6、TNF-α水平以及临床症状评分均显著低于对照组,PGI水平显著升高,PGII水平显著降低,治疗有效率同样显著高于对照组(P<0.05)。结论 联合使用奥美拉唑与阿莫西林能有效地减缓慢性胃炎患者的炎症反应,调整胃蛋白酶原水平,改善临床表征,从而提升整体治疗效果。

关键词： Osteomyelitis   PTGS2   Staphylococcus aureus   Ferroptosis   IL-17A signaling pathway  

摘要： ObjectiveOsteomyelitis caused by Staphylococcus aureus (S. aureus) infection is an inflammatory bone disease characterized by continuous bone destruction, which is difficult to treat. This research aimed to explore the molecular mechanisms of S. aureus-induced *** the GSE166522 and GSE227521 datasets, hub differentially expressed genes (DEGs) were screened by bioinformatics analysis. Hub gene expression levels were validated in S. aureus-induced mouse models. An inhibitor of PTGS2, etoricoxib, was used to assess the role of PTGS2 in the osteomyelitis mouse model. PTGS2 was silenced in an LPS-induced MC3T3-E1 cell model to study its effect on cell *** hub genes were screened, including ARG1, TIMP1, NOS2, PTGS2, SOCS3, and IL1B, highly expressed in the S. aureus-induced osteomyelitis model. Etoricoxib treatment attenuated the inflammatory infiltration of tibial tissue in mice with osteomyelitis. In vivo and in vitro, etoricoxib treatment and PTGS2 silencing reduced inflammatory factor (TNF-alpha, IL-1 beta, and IL-6) levels. PTGS2 silencing promoted LPS-induced MC3T3-E1 cell viability and inhibited apoptosis and ferroptosis. GPX4 and SLC7A11 protein levels were significantly increased after PTGS2 silencing. Mechanistically, IL-17A intervention significantly counteracted the impact of PTGS2 silencing on cell behaviors and secukinumab combined with PTGS2 silencing more effectively suppressed inflammation and ferroptosis, indicating that PTGS2 impeded the osteomyelitis progression by inhibiting the IL-17A *** PTGS2 reduces ferroptosis in S. aureus-induced osteomyelitis by obstructing the IL-17A pathway, which suggests a new approach for the treatment of osteomyelitis.

关键词： 补阳还五汤   醒脑开窍针法   缺血性脑卒中恢复期   气虚证   血液流变学   IL-6   TNF-α  

摘要： 目的：分析补阳还五汤加减结合醒脑开窍针法对缺血性脑卒中恢复期（气虚证）患者血液流变学、血清白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）水平的影响。方法：选取2022年4月至2024年3月我院康复医学科收治的缺血性脑卒中恢复期患者80例，依据随机数字表法将其分为对照组（予以补阳还五汤加减等常规治疗4周）、观察组（予以补阳还五汤加减联合醒脑开窍针法治疗4周）各40例，比较两组中医临床效果、治疗前后血液流变学[全血高切黏度、全血低切黏度、血浆黏度、纤维蛋白原（FIB）]、神经功能指标[美国国立卫生研究院卒中量表（NIHSS）、神经生长因子（NGF）、脑源性神经生长因子（BDNF）]、血清IL-6、TNF-α水平、生活质量[简明健康状况量表（SF-36）]、不良反应发生率。结果：观察组治疗有效率92.50%高于对照组75.00%（P＜0.05）；治疗后观察组全血高切黏度、全血低切黏度、血浆黏度、FIB低于对照组（P＜0.05）；治疗后观察组NIHSS评分低于对照组，NGF、BDNF水平高于对照组（P＜0.05）；观察组治疗2周、4周血清IL-6、TNF-α水平低于对照组（P＜0.05）；观察组治疗2周、4周SF-36评分高于对照组（P＜0.05）；两组不良反应发生率12.50%、10.00%差异无统计学意义（P＞0.05）。结论：补阳还五汤加减结合醒脑开窍针法用于气虚型缺血性脑卒中恢复期患者中，可明显提高临床疗效，改善患者血液流变学、血清IL-6、TNF-α水平及神经功能、生活质量，且安全性可靠，值得在临床推广实践。

关键词： Tumor microenvironment   IL-35   iTr35   Immune evasion  

摘要： Dendrobium huoshanense has received special attention for its advantages in the treatment of lung cancer, but the underlying molecular mechanisms are not yet well understood. First, we obtained 8 active ingredients and 159 effective action targets of Dendrobium huoshanense using network pharmacology, and searching target interactions through STRING, constructing the PPI network and KEGG, GO and Hallmark enrichment analysis. Then, we combined target's enrichment analysis and GSEA enrichment analysis of IL-35, indicating the mechanism of cDHPs for non-small cell lung cancer (NSCLC) may be related to tight junction and NSCLC pathway. Further, FXR1 and ACTR3 were identified as core therapeutic targets, and high expression of FXR1 or ACTR3 was significantly associated with poor prognosis of patients. The analysis of single-cell data also indicated that the percentage of CD4-CTLA4-Treg cells may be increased by the expression of IL-35, resulting in a suppressive immune microenvironment. Next, In vivo experiment, we detected iTr35 by flow cytometry, detected IL-35 level by RT-PCR, Western blotting and ELISA, and detected NK cell activity to explore the immunomodulatory effects and anti-tumor mechanism of cDHPs. After cDHPs administration, the conversion of CD4+ T cells to iTr35 is inhibited, p35 and EBI3 in both protein and mRNA levels, the levels of IL-35 and IL-4 in serum decreased. The levels of IFN-gamma, while the activity of NK cells in mice increased, enhancing the anti-tumor immune effect of the organism. Finally, analysis of sequencing data from the immunotherapy cohort of tumor-bearing mice obtained from the TISMO database shows that the combination of cDHPs and PD-1/PD-L1 antibodies improves effector and thus PD-1/PD-L1 antibody efficacy. These findings suggest that cDHPs inhibit NSCLC proliferation and immune escape via the FXR1-IL-35 axis signaling pathway.

关键词： 急性细菌性肠炎   头孢克肟   头孢克洛   家属满意度  

摘要： 研究急性细菌性肠炎采取头孢克肟和头孢克洛治疗,对CRP以及IL-8等指标的影响,并作对照实验。方法 2023年12月至2024年11月期间,本院共接收84例急性细菌性肠炎患者进行治疗,随机抽取这些患者并分为:参考组(接受头孢克洛),有42例,实验组(接受头孢克肟),有42例。两组之间进行对比的内容为:治疗效果、腹泻次数以及血清指标。结果 经治疗效果对比,参考组总有效率80.95%,而实验组高达97.62%,显示实验组疗效明显优于参考组(P<0.05);在腹泻次数方面,治疗前两组无显著差异,但治疗1d和3d后,实验组的腹泻频次显著低于参考组(P<0.05);对于血清指标的对比,治疗前两组没有显著差异,而治疗后3d,实验组的TNF-α指标、PCT、CER、IL-8以及CRP指标的水平均低于参考组(P<0.05)。结论 急性细菌性肠炎的患者,采取头孢克肟进行治疗,其效果相较于头孢克洛的疗效更为显著,患者的腹泻次数在一天至三天内明显下降,同时炎症得到有效控制,显著改善消化道的症状,具有较高的有效性,可实行应用并推广。

关键词： 剖宫产瘢痕妊娠   细胞因子   酶联免疫吸附试验  

摘要： 探讨Th1、Th2细胞因子在剖宫瘢痕妊娠(cesarean scar pregnancy,CSP)患者血清中的表达及相互关系。方法 选取2023年1月-2024年1月就诊于我院诊断为CSP的患者30例(CSP组)及同期剖宫产后正常妊娠并行人工流产的患者30例(对照组)作为研究对象,采用流式细胞术检测两组患者血清中 Th1、Th2 细胞比例及比值,酶联免疫吸附法检测血清Th1型细胞因子IFN-γ、IL-2,Th2型细胞因子IL-4、IL-10的水平并进一步分析相关性。结果 CSP组Th1比例高于对照组,Th2比例低于对照组,Th1/Th2比值高于对照组,差异均有统计学意义(P<0.05);CSP组血清IFN-γ、IL-2水平均高于对照组,IL-4、IL-10水平低于对照组,差异均有统计学意义(P<0.05);CSP组INF-γ 与IL-4、INF-γ 与IL-10、IL-2 与IL-10均有相关性,呈负相关(P<0.05)。结论 INF-γ、IL-4细胞因子水平升高,IL-4、IL-10细胞因子水平降低,Th1/Th2细胞比例升高可能是导致CSP发生的机制之一。

关键词： 2型固有淋巴细胞   呼吸道疾病   白细胞介素   PD-1/PD-L1  

摘要： 2型固有淋巴细胞（type 2 innate lymphoid cells,ILC2）作为一种免疫细胞亚群，在呼吸道疾病中的作用备受关注。ILC2通过产生白细胞介素-5(interleukin-5,IL-5)和白细胞介素-13(interleukin-13,IL-13)等细胞因子，参与了呼吸道炎症、过敏反应以及组织修复等过程。近年来的研究表明，在哮喘、慢性阻塞性肺病（chronic obstructive pulmonary disease,COPD）、支气管扩张等呼吸道疾病中，ILC2的活化和异常增生与疾病的发生和发展密切相关。ILC2在呼吸道疾病的发病机制中扮演着重要的角色。此外，PD-1/PD-L1通路在调控ILC2的功能中起着重要作用。PD-1/PD-L1通过抑制ILC2的细胞因子产生和增殖，可能对哮喘等疾病的病程产生调节作用。因此，深入研究ILC2及其与PD-1/PD-L1通路的相互作用不仅有助于更好地理解呼吸道疾病的发病机制，也为疾病的治疗提供了新的靶点和策略。

关键词： Asthma, airway remodeling   Interlukin-4 (IL-4)   Interlukin-13 (IL-13)   Anti-IL-4   Anti-IL-13  

摘要： Asthma is a chronic respiratory disorder affecting individuals across all age groups. It is characterized by airway inflammation and remodeling and leads to progressive airflow restriction. While corticosteroids remain a mainstay therapy, their efficacy is limited in severe asthma due to genetic and epigenetic alterations, as well as elevated pro-inflammatory cytokines interleukin-4 (IL-4), interleukin-13 (IL-13), and interleukin-5 (IL-5), which drive structural airway changes including subepithelial fibrosis, smooth muscle hypertrophy, and goblet cell hyperplasia. This underscores the critical need for biologically targeted therapies. This review systematically examines the roles of IL-4 and IL-13, key drivers of type-2 inflammation, in airway remodeling and their potential as therapeutic targets. IL-4 orchestrates eosinophil recruitment, immunoglobulin class switching, and Th2 differentiation, whereas IL-13 directly modulates structural cells, including fibroblasts and epithelial cells, to promote mucus hypersecretion and extracellular matrix (ECM) deposition. Despite shared signaling pathways, IL-13 emerges as the dominant cytokine in remodeling processes including mucus hypersecretion, fibrosis and smooth muscle hypertrophy. While IL-4 primarily amplifies inflammatory cascades by driving IgE switching, promoting Th2 cell polarization that sustain cytokine release, and inducing chemokines to recruit eosinophils. In steroid-resistant severe asthma, biologics targeting IL-4/IL-13 show promise in reducing exacerbations and eosinophilic inflammation. However, their capacity to reverse established remodeling remains inconsistent, as clinical trials prioritize inflammatory biomarkers over long-term structural outcomes. This synthesis highlights critical gaps in understanding the durability of IL-4/IL-13 inhibition on airway structure and advocates for therapies combining biologics with remodeling-specific strategies. Through the integration of mechanistic insights and