冠心病是临床高发的心血管疾病，其病理核心为动脉粥样硬化，而炎症反应异常激活是推动病变进展的关键驱动力。PI3K/Akt通路通过调控炎症反应等，在CHD进程中发挥双向调节作用。现代研究表明，该通路保护性激活不足可加剧血管内皮损伤与斑块不稳定性，而炎症反应的持续又可进一步抑制PI3K/Akt通路活性，形成恶性循环。当动脉粥样斑块破裂，AMI发生后炎症级联反应放大，该通路异常激活，诱发MIRI。“荣泣卫除”出自《黄帝内经》，指营气耗损（荣泣）、卫气失守（卫除），荣卫失和则气血运行不畅、脉络瘀阻。本团队结合该理论与现代研究，认为CHD中PI3K/Akt通路介导的异常炎症反应的病理机制，与“荣泣卫除”理论内涵存在对应关系。研究发现，通过调控PI3K/Akt通路活性，抑制炎症因子激活与炎症蛋白表达，可抑制CHD发生发展进程。故本文基于“荣泣卫除”理论，系统梳理了PI3K/Akt通路介导的炎症反应在CHD中的作用及与中医病机的内在关联，总结中医药防治的研究进展，为中西医结合防治CHD提供参考依据。

Coronary heart disease is a clinically prevalent cardiovascular disease, with atherosclerosis as its core pathology. Abnormal activation of the inflammatory response is a key driving force for disease progression. The PI3K/Akt pathway exerts bidirectional regulatory effects on the progression of CHD by modulating inflammatory responses, among other functions. Modern studies indicate that insufficient protective activation of this pathway can exacerbate vascular endothelial injury and plaque instability, while persistent inflammation further suppresses PI3K/Akt pathway activity, forming a vicious cycle. Following atherosclerotic plaque rupture and the onset of AMI, the inflammatory cascade is amplified, leading to aberrant activation of this pathway and triggering MIRI. The theory of "depletion of nutritive level and exhaustion of defensive level" originates from the?Yellow Emperor's Inner Classic, referring to the depletion of nutritive level (Rong Qi) and the exhaustion of defensive level (Wei Qi), resulting in disharmony between nutritive and defensive levels, which impedes the smooth flow of Qi and blood and causes stasis in the collaterals. By integrating this theory with modern research, our team proposes a correspondence between the pathological mechanism of abnormal PI3K/Akt pathway-mediated inflammatory response in CHD and the theoretical connotation of "depletion of nutritive level and exhaustion of defensive level". Studies have found that modulating PI3K/Akt pathway activity to inhibit the activation of inflammatory factors and expression of inflammatory proteins can suppress the occurrence and progression of CHD. Therefore, based on the theory of "depletion of nutritive level and exhaustion of defensive level", this paper systematically reviews the role of the PI3K/Akt pathway-mediated inflammatory response in CHD and its intrinsic relationship with traditional Chinese medicine pathogenesis, summarizes research progress in TCM prevention and treatment, and provides a reference for the integrated traditional Chinese and Western medicine management of CHD.

目的 比较末端可弯曲负压吸引输尿管鞘（FANS-UAS）联合输尿管软镜与传统输尿管通路鞘（T-UAS）联合输尿管软镜治疗单侧上尿路结石的临床效果。方法 选取2023-05至2025-05我院120例单侧上尿路结石患者为研究对象，根据电脑随机法分为研究组、对照组，各60例。研究组采用FANS-UAS联合输尿管软镜治疗，对照组采用T-UAS联合输尿管软镜治疗。比较两组患者手术指标、结石清除效果、疼痛程度[视觉模拟量表（VAS）评分]、炎症反应[血清C反应蛋白（CRP）、白细胞介素-6（IL-6）、降钙素原（PCT）]及并发症情况。结果 研究组手术时间、碎石时间、术后下床活动时间、住院时间较对照组缩短，术中出血量较对照组降低，术后即刻、术后3d结石清除率较对照组显著升高（P＜0.05）；术后1d、3d研究组VAS评分较对照组降低（P＜0.05）；术后1d、3d研究组血清CRP、IL-6、PCT水平较对照组降低（P＜0.05）；两组并发症总发生率比较无显著差异（P＞0.05）。 结论 与T-UAS联合输尿管软镜相比，FANS-UAS联合输尿管软镜治疗单侧上尿路结石患者能优化流程，提升结石清除率，降低疼痛程度，减轻炎症反应，加快围术期恢复，安全性良好。

目的 比较末端可弯曲负压吸引输尿管鞘（FANS-UAS）联合输尿管软镜与传统输尿管通路鞘（T-UAS）联合输尿管软镜治疗单侧上尿路结石的临床效果。方法 选取2023-05至2025-05我院120例单侧上尿路结石患者为研究对象，根据电脑随机法分为研究组、对照组，各60例。研究组采用FANS-UAS联合输尿管软镜治疗，对照组采用T-UAS联合输尿管软镜治疗。比较两组患者手术指标、结石清除效果、疼痛程度[视觉模拟量表（VAS）评分]、炎症反应[血清C反应蛋白（CRP）、白细胞介素-6（IL-6）、降钙素原（PCT）]及并发症情况。结果 研究组手术时间、碎石时间、术后下床活动时间、住院时间较对照组缩短，术中出血量较对照组降低，术后即刻、术后3d结石清除率较对照组显著升高（P＜0.05）；术后1d、3d研究组VAS评分较对照组降低（P＜0.05）；术后1d、3d研究组血清CRP、IL-6、PCT水平较对照组降低（P＜0.05）；两组并发症总发生率比较无显著差异（P＞0.05）。 结论 与T-UAS联合输尿管软镜相比，FANS-UAS联合输尿管软镜治疗单侧上尿路结石患者能优化流程，提升结石清除率，降低疼痛程度，减轻炎症反应，加快围术期恢复，安全性良好。

目的 比较末端可弯曲负压吸引输尿管鞘（FANS-UAS）联合输尿管软镜与传统输尿管通路鞘（T-UAS）联合输尿管软镜治疗单侧上尿路结石的临床效果。方法 选取2023-05至2025-05我院120例单侧上尿路结石患者为研究对象，根据电脑随机法分为研究组、对照组，各60例。研究组采用FANS-UAS联合输尿管软镜治疗，对照组采用T-UAS联合输尿管软镜治疗。比较两组患者手术指标、结石清除效果、疼痛程度[视觉模拟量表（VAS）评分]、炎症反应[血清C反应蛋白（CRP）、白细胞介素-6（IL-6）、降钙素原（PCT）]及并发症情况。结果 研究组手术时间、碎石时间、术后下床活动时间、住院时间较对照组缩短，术中出血量较对照组降低，术后即刻、术后3d结石清除率较对照组显著升高（P＜0.05）；术后1d、3d研究组VAS评分较对照组降低（P＜0.05）；术后1d、3d研究组血清CRP、IL-6、PCT水平较对照组降低（P＜0.05）；两组并发症总发生率比较无显著差异（P＞0.05）。 结论 与T-UAS联合输尿管软镜相比，FANS-UAS联合输尿管软镜治疗单侧上尿路结石患者能优化流程，提升结石清除率，降低疼痛程度，减轻炎症反应，加快围术期恢复，安全性良好。

      目的   免疫球蛋白A肾病（IgAN）与炎症性肠病（IBD）的相互作用机制尚未阐明。本研究旨在解析IBD与IgAN共病的关键特征基因及核心信号通路，以揭示肠－肾轴的分子调控网络。方法   于GEO数据库获取IBD（GSE75214）和IgAN（GSE93798）基因表达谱，筛选差异表达基因（DEGs）。通过蛋白互作网络（PPI）和拓扑算法（MCC、MNC、Degree、EPC等）识别核心特征基因，并结合公共数据库（CTD、DISEASES和GeneCards）和单细胞转录组测序（GSE171314）进行验证。通过Nephroseq数据库验证基因表达与临床表型的相关性。结果   共筛选出17个IBD-IgAN共病DEGs，PPI网络分析等确定以FOS、EGR1、CXCL2和JUNB为核心特征基因。功能富集分析显示白细胞介素-17（IL-17）信号通路显著激活。单细胞测序验证FOS、EGR1、CXCL2和JUNB基因在IgAN特异性高表达，并通过Nephroseq数据库验证其与尿蛋白和估算的肾小球滤过率下降（eGFR）显著相关。结论  本研究揭示IBD与IgAN共享IL-17通路异常激活及FOS、EGR1、CXCL2和JUNB的基因网络，为开发基于肠－肾轴调控的靶向治疗策略提供理论依据。

       Objective  The complex interplay between immunoglobulin A nephropathy（IgAN）and inflammatory bowel disease（IBD）remains poorly understood．This  study  aimed to identify  key  cross-talk  genes  and  pivotal  signaling pathways shared between IBD and IgAN，thereby elucidating the molecular regulatory network underlying the gut-kidney axis．Methods  Transcriptomic datasets for IBD（GSE75214）and IgAN（GSE93798）were retrieved from the GEO database．Differentially expressed genes（DEGs）were screened，and shared DEGs were intersected．Protein-protein interaction（PPI）networks were constructed using STRING and Cytoscape，with topological algorithms applied to identify hub genes．Gene expression profiles were validated through（CTD，DISEASES and GeneCards）and single-cell RNA sequencing（GSE171314）and the Nephroseq database，focusing on clinical correlations with proteinuria and estimated glomerular filtration rate（eGFR）．Results  Seventeen shared DEGs were identified between IBD and IgAN．PPI network analysis revealed FOS，EGR1，CXCL2 and JUNB as core hub genes．Functional enrichment analysis demonstrated significant activation of the interleukin-17（IL-17）signaling pathway．Single-cell sequencing confirmed the specific upregulation of these genes in renal tubular epithelial cells of IgAN patients，which was further validated to correlate with proteinuria and eGFR decline．Conclusions  IBD and  IgAN share aberrant activation of the IL-17 pathway and a co-regulatory gene network involving FOS，EGR1，CXCL2 and JUNB，providing a theoretical foundation for developing therapeutic strategies centered on the gut-kidney axis．

目的 探讨重楼皂苷Ⅰ（PPI）对慢性髓系白血病细胞（K562）细胞的抑制作用及可能的作用机制。方法 采用CCK-8法筛选药物最适浓度,将培养时间为24 h的药物最适浓度作为后续实验的干预浓度。分组如下：（1）空白组;（2）PPI组;（3）抑制剂组;（4）PPI+抑制剂组。采用CCK-8法检测细胞增殖率;AO/EB染色观察细胞形态;流式细胞术检测凋亡率;ROS检测试剂盒检测活性氧（ROS）含量、还原型谷胱甘肽含量检测试剂盒检测谷胱甘肽（GSH）含量、细胞亚铁比色法测试盒检测细胞亚铁（Fe²⁺）含量;qRT-PCR法和蛋白免疫印迹法检测各组肿瘤蛋白53（p53）、钠氯离子依赖性氨基酸转运蛋白11（SLC7A11）、谷胱甘肽过氧化物酶4（GPX4）mRNA及蛋白表达量。结果 PPI抑制K562细胞的生长,且呈一定的剂量及时间依赖性（与同时间段的对照组0μmol/L比较,均P<0.01）。与空白组相比,PPI抑制K562细胞的增殖,提高了凋亡率,而铁死亡抑制剂（Ferrostian-1）的使用逆转了PPI对K562凋亡的促进作用（P<0.01）。与空白组相比,PPI组ROS、Fe²⁺含量升高,GSH含量下降,而铁死亡抑制剂的使用可下调ROS、Fe²⁺,上调GSH的含量（P<0.01）。PPI组较空白组p53 mRNA和蛋白表达水平升高,而SLC7A11、GPX4 mRNA和蛋白表达水平下降（P<0.05）;PPI+抑制剂组细胞较重楼皂苷组p53 mRNA和蛋白表达水平下降,而SLC7A11、GPX4 mRNA和蛋白表达水平升高（P<0.05）。结论 PPI能够有效抑制K562细胞增殖,促进K562细胞铁死亡,其分子机制可能与p53信号通路的调控有关。

Objective To investigate the inhibitory effect of polyphyllin I（PPI）on chronic myeloid leukemia cells（K562）and its possible mechanism．Methods K562 cell line was cultured in suitable environment,and the optimal concentration of the drug was screened by CCK-8 method．The optimal concentration of the drug cultured for 24 hours was used as the intervention concentration of the follow-up experiment．Cells were divided into the following groups：（1）blank group,（2）saponins group,（3）inhibitor group and（4）saponins + inhibitor group．The cell proliferation rate was detected by CCK-8 method．The cell morphology was observed by AO/EB staining．The apoptosis rate was detected by flow cytometry．The contents of reactive oxygen species（ROS）,glutathione（GSH）and ferrous（Fe²⁺）in different groups were detected,and the expression of mRNA and protein in different groups were detected by qRT- PCR and Western blot respectively．Results PPI significantly inhibited the growth of K562 cells in a dose-and time-dependent manner．Compared with the blank group,PPI significantly inhibited the proliferation of K562 cells and increased the apoptosis rate of K562 cells,while the use of ferroptosis inhibitor（Ferrostian-1）reversed the promoting effect of PPI on apoptosis of K562 cells．Compared with the blank group,the contents of reactive oxygen species（ROS）and ferrous iron（Fe²⁺）increased and the content of glutathione（GSH）decreased in the saponins group．The use of Ferrostian-1 could down-regulate the contents of ROS and Fe²⁺ and increase the content of GSH in the cells treated with the drug．Compared with the blank group,the expression of p53 mRNA and protein in the saponins group increased,while the expression of SLC7A11,GPX4 mRNA and protein decreased．The expression of p53 mRNA and protein in the saponins + inhibitor group was lower than that in the saponins group,while the expression levels of SLC7A11,GPX4 mRNA and protein increased．Conclusions PPI can effectively inhibit the proliferation of K562 cells and promote ferroptosis in K562 cells．The molecular mechanism can be related to the regulation of p53 signal pathway．

目的 探讨谷氨酸对HT22细胞线粒体自噬和细胞凋亡的影响,并评估虾青素预处理的保护作用及其分子机制。方法 用谷氨酸及虾青素处理HT22细胞,通过蛋白印迹及聚合酶联反应等评估其对线粒体自噬的影响。结果 谷氨酸处理显著抑制线粒体初级自噬（PINK1、Parkin、pULK1^ser555和LC3Ⅱ）和次级自噬（LAMP1和Rab7）,上调cleaved Caspase-3的表达（P<0.05）。虾青素预处理减少细胞凋亡,恢复了线粒体自噬,PINK1、Parkin、pULK1^ser555和LC3Ⅱ的表达水平上升（分别为2.3倍、2.6倍、83.3%及81.1%）（P<0.05）,该作用被自噬抑制剂BafA1阻断。此外,谷氨酸抑制Nrf2核内转移和NLRX1表达,而预处理显著促进Nrf2的核内转移并上调NLRX1,分别上调25.8%、33.2%。生物信息学分析显示NLRX1启动子区域含有3个Nrf2结合位点,提示Nrf2通过调控NLRX1转录活性发挥作用。结论 文章首次揭示虾青素通过Nrf2/NLRX1通路激活线粒体自噬,展现神经保护作用。

Objective To explore the effects of glutamate on mitophagy and apoptosis in HT22 cells and evaluate the protective effects and molecular mechanisms of astaxanthin pretreatment．Methods HT22 cells were treated with glutamate and astaxanthin．The effects on mitophagy were assessed using Western Blot and PCR．Results Glutamate treatment significantly inhibited primary mitophagy（PINK1,Parkin,pULK1^ser555 and LC3II）and secondary mitophagy（LAMP1 and Rab7）while upregulating cleaved Caspase-3 expression．Astaxanthin pretreatment notably reduced apoptosis and restored mitophagy,the expression levels of PINK1,Parkin,pULK1^Ser555 and LC3II were significantly upregulated（by 2.3-fold,2.6-fold,83.3% and 81.1% respectively,P<0.05）,but this effect was blocked by the autophagy inhibitor BafA1．Additionally,glutamate suppressed Nrf2 nuclear translocation and NLRX1 expression,whereas astaxanthin promoted Nrf2 nuclear translocation and increased NLRX1 expression by 25.8% and 33.2%,respectively．Bioinformatics analysis revealed three Nrf2 binding sites in the NLRX1 promoter region,suggesting that Nrf2 may regulate NLRX1 transcriptional activity．Conclusions The study demonstrates that astaxanthin exhibited potential neuroprotective effect by activating mitophagy through the Nrf2/NLRX1 pathway．

目的 研究SOCS6/STAT6通路在前列腺细胞炎性增殖作用中的调控作用。方法 使用人前列腺细胞株RWPE-1建立炎症模型,将细胞分为对照（CON）组和炎症刺激（INF）组,后者通过添加脂多糖（LPS）模拟炎症环境。采用ELISA检测白细胞介素-1β（IL-1β）-1β、白细胞介素-6（IL-6）和白细胞介素-8（IL-8）表达水平,蛋白免疫印迹法检测细胞因子信号抑制物-6（SOCS6）、信号转导和转录激活因子-6（STAT6）及磷酸化STAT6蛋白的表达水平。结果 经过LPS处理后,RWPE-1细胞中的SOCS6蛋白表达水平显著下降（P<0.01）,而磷酸化STAT6表达水平上升（P<0.01）。结论 SOCS6/STAT6通路可能通过调节炎症环境下STAT6的磷酸化水平,参与调节前列腺细胞的炎性增殖作用。

Objective To explore the regulatory role of SOCS6/STAT6 pathway in the inflammatory proliferation of prostate cells．Methods The human prostate cell line RWPE-1 was used to establish an inflammation model．Cells were divided into a control（CON）group and an inflammation-stimulated（INF）group,with the latter subjected to lipopolysaccharide（LPS）treatment to simulate an inflammatory environment．The expression levels of interleukin（IL）-1β、IL-6 and IL-8 were detected by ELISA,and the expression levels of suppressor of cytokine signaling 6（SOCS6）,signal transducer and activator oftranscription-6,（STAT6）,and phosphorylated STAT6 proteins were detected by Western blot．Results The results showed that after LPS treatment,the expression of SOCS6 protein in RWPE-1 cells significantly decreased,while the expression of phosphorylated STAT6 increased．Conclusions The SOCS6/STAT6 pathway may be involved in regulating the inflammatory proliferation of prostate cells by modulating the phosphorylation level of STAT6 under inflammatory conditions．

Wnt/β-catenin信号通路是一种在胚胎发育,细胞增殖分化、迁移,干细胞更新等中起关键作用的蛋白质家族。Wnt/β-catenin信号通路的失调常常会导致各种严重的疾病,例如肿瘤、心脏疾病、肺部疾病、肝脏疾病、骨骼疾病、神经疾病等。大量研究表明,Wnt/β-catenin信号通路在心肌纤维化发病机制中起重要作用,本文结合最新研究成果,从心肌纤维化相关疾病的角度对Wnt/β-catenin通路进行综述,为预防心肌纤维化提供新的思路,进一步达到防治心血管疾病的目的。

The Wnt/β-catenin signaling pathway is a family of proteins that play a key role in embryonic development,cell proliferation and differentiation,migration,stem cell renewal,etc．Dysfunctions of Wnt/β-catenin signaling pathway often lead to various serious diseases,such as tumor,heart,lung,liver,bone and neurological diseases,etc．Numerous studies have shown that the Wnt/β-catenin signaling pathway plays an important role in the pathogenesis of cardiac fibrosis．This article,in combination with the latest research findings,presents a review of the Wnt/β-catenin pathway from the perspective of myocardial fibrosis-related diseases,in order to provide new ideas for preventing myocardial fibrosis and achieving the goal of combating cardiovascular disease．

慢性萎缩性胃炎是常见的胃癌前病变,不仅治疗过程漫长,治疗难度大,而且患者依从性欠佳。不仅会对患者的生理、心理健康和生活质量造成严重不良的影响,还会给患者家属造成负担,成为临床上不可忽视的难题。但是本病发病机制目前尚未完全明确,临床治疗还未达成共识。文章综述了近10年基于Hedgehog信号通路的中医药干预慢性萎缩性胃炎的研究概况。中医药调控Hedgehog信号通路辨证论治是治疗慢性萎缩性胃炎的一种独具特色的疗法,近年来有关基于Hedgehog信号通路的中医药干预治疗慢性萎缩性胃炎的报道越来越多。文章主要通过遵循疾病本虚标实的病性,以脾胃虚弱为本,瘀血、气滞、湿热、痰浊等为标,探讨选方治疗对慢性萎缩性胃炎的影响,认为中医药联合Hedgehog信号通路实行现代化发展能够有效干预治疗慢性萎缩性胃炎,以期为进一步临床研究与应用提供参考。

Chronic atrophic gastritis,a common precancerous lesion of gastric cancer,requires a long-term treatment and is difficult to cure．Therefore,it usually leads to decreased patient compliance．It will not only have a serious adverse impact on the patient’s physical and mental health and quality of life,but also cause a burden to the patient’s family,which has become a difficult problem that can not be ignored clinically．However,the pathogenesis has not yet been totally clarified,not to mention a consensus on the clinical treatment．This paper reviews the research revolving around Chinese medicine intervention in chronic atrophic gastritis based on the Hedgehog signaling pathway in the last decade．It’s creative therapy of chronic atrophic gastritis that utilizing Traditional Chinese Medicine to regulate and control Hedgehog signaling pathway,which has been increasingly reported in recent years．This paper is based on “deficiency in origin” and “excess in superficiality” principle．Concretely,spleen-stomach vacuity is characterized by deficiency in origin,and excess in superficiality manifests blood stasis,qi stagnation,dampness-heat and phlegm turbidity as excess in superficiality．By this way,the paper explores the effect of prescription selection on chronic atrophic gastritis．It is believed that the modern therapy that combines traditional Chinese medicine with Hedgehog signaling pathway can tackle chronic atrophic gastritis,thus providing a reference for further clinical trials and practices．