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．

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．

目的 本研究从细胞生物学角度检测二甲双胍对小鼠胰岛瘤MIN6的影响,并探讨此过程中包含的分子生物学机制。方法 MTT法检测不同浓度二甲双胍(1、2、5、10、20 mmol/L)对MIN6细胞活力的影响,细胞划痕实验检测二甲双胍对MIN6细胞迁移的影响,免疫印记实验检测此过程中细胞凋亡相关蛋白Bcl-2、Bax、caspase3表达的变化,及AMPK和JNK信号通路蛋白磷酸化水平的变化。结果 二甲双胍浓度大于10 mmol/L时可以抑制MIN6细胞的活力(P<0.01),降低其迁移能力(P<0.01),高浓度二甲双胍可以上调细胞内凋亡蛋白Bax(P<0.05)和p-AMPK的表达(P<0.05),降低抗凋亡蛋白Bcl-2的表达,增加caspase3剪切体(P<0.05)。同时,二甲双胍可以降低MIN6细胞内JNK信号通路的磷酸化水平(P<0.05)。结论 高浓度二甲双胍可以抑制MIN6细胞的增殖和迁移,其作用可能与降低了JNK信号的通路活化有关。

Objective This study aims to investigate the effect of metformin on proliferation and migration of MIN6 cells, and to explore the underlying mechanism. Methods The viability of MIN6 cells that were treated with various metformin (1,2,5,10 and 20 mmol/L) was detected by MTT assay. The migration of MIN6 cells was determined by wound-healing assay. Meanwhile, the proteins expression of Bcl-2, Bax, caspase3 and the phosphorylation of AMPK, JNK was detected by western bolt assay. Results The cell viability and the migration of MIN6 cells were decreased when the concentration of metformin above 10 mmol/L(P<0.01). The expression of apoptosis-related protein Bax(P<0.05) and p-AMPK(P<0.05)was up-regulated, anti-apoptosis-related protein Bcl-2 was down-regulated and cleaved caspase3 (P<0.05)was increased after high metformin treatment. At the same time, the phosphorylation of JNK was down-regulated by metformin(P<0.05). Conclusion High concertration of metformin may inhibit the proliferation and migration of MIN6 cells through suppressing the activation of JNK signaling pathway.

目的 在原来研究的基础上进一步研究Wnt-1信号通路蛋白-3（WISP-3）在高氧诱导肺上皮细胞凋亡中的作用。方法 通过Western blot检测和免疫组化检测不同肺上皮细胞中WISP-3的蛋白表达量。利用质粒转染和siRNA的方法在Beas-2B细胞中高表达和基因沉默WISP-3,通过细胞活性检测和流式细胞学技术检测高氧刺激后细胞的凋亡情况。结果 与空气对照相比,高氧刺激使肺上皮细胞的WISP-3蛋白表达量下降;WISP-3基因沉默或高表达使高氧诱导的肺上皮细胞凋亡增加或减少。结论 高氧刺激下,肺上皮细胞中WISP-3表达下降,WISP-3对高氧诱导的肺上皮细胞凋亡具有保护作用。

Objective To explore how Wnt-1 inducible signaling pathway protein-3 （WISP-3） participate in and play a regulatory role in the process of hyperoxia induced apoptosis in lung epithelial cells. Methods The expression of WISP-3 was detected via Western blot and immunohistochemistry. High expression and low expression of WISP-3 were performed by plasmid transfection and siRNA. Cell viability and flow cytometry were executed to detect the hyperoxia-induced apoptosis in Beas-2B. Results Compared to the group of air control,the expression of WISP-3 protein in lung epithelial cells decreased obviously after hyperoxia. Cell survival decrease and apoptosis increased after hyperoxia in Beas-2B cells with low expression of WISP-3. Vice versa. Conclusion The expression of WISP-3 decreased after hyperoxia in lung epithelial cells. The role of WISP-3 in this process may be protective.