Cell Biology International最新文献_第3页

ROS-Dependent GSDMD Activation Drives Intestinal Pyroptosis in Neonatal Necrotizing Enterocolitis (NEC) ros依赖的GSDMD激活驱动新生儿坏死性小肠结肠炎（NEC）的肠道焦亡。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-09-03 DOI: 10.1002/cbin.70206

Cuilian Ye, Jia Luo, Xinli Liu, Yue Ma, Xinyi Yang, Dandan Mo, Qin Deng, Xionghui Ding, Chunbao Guo

{"title":"ROS-Dependent GSDMD Activation Drives Intestinal Pyroptosis in Neonatal Necrotizing Enterocolitis (NEC)","authors":"Cuilian Ye, Jia Luo, Xinli Liu, Yue Ma, Xinyi Yang, Dandan Mo, Qin Deng, Xionghui Ding, Chunbao Guo","doi":"10.1002/cbin.70206","DOIUrl":"10.1002/cbin.70206","url":null,"abstract":"<div>\u0000 \u0000 <p>This study investigates the role of Gasdermin D (GSDMD)-mediated pyroptosis in the pathogenesis of necrotizing enterocolitis (NEC) and reveals the mechanism by which reactive oxygen species (ROS) promote intestinal inflammation and injury through NLRP3/GSDMD pathway activation. Analysis of human NEC tissue samples showed significant oxidative stress (elevated MDA, decreased SOD activity, reduced GSH/GSSG ratio) and activation of the NLRP3/GSDMD/IL-1β pathway in the intestines of NEC patients. In an experimental NEC mouse model, GSDMD knockout (GSDMD-/-) significantly delayed NEC onset, reduced incidence, attenuated intestinal damage, and improved survival. GSDMD deficiency also decreased macrophage pyroptosis, systemic inflammation, and bacterial translocation, while improving intestinal barrier function. Pharmacological inhibition of GSDMD (using disulfiram) similarly mitigated pyroptosis and enhanced the bactericidal capacity of macrophages. Further mechanistic studies indicated that ROS drive pyroptosis by activating GSDMD, and the antioxidant N-acetyl-<span>l</span>-cysteine (NAC) could reverse this effect. The findings suggest that GSDMD is a potential therapeutic target for NEC, and strategies targeting GSDMD inhibition (genetic or pharmacological), combined with antioxidant therapy, may offer novel treatment approaches for NEC.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 9","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148886463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Insights Into Aggregation-Delayed Phenotype of Dictyostelium discoideum 盘状盘基骨柱聚集延迟表型的研究。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-09-01 DOI: 10.1002/cbin.70204

Sarah Abdulaziz Alamer

{"title":"Insights Into Aggregation-Delayed Phenotype of Dictyostelium discoideum","authors":"Sarah Abdulaziz Alamer","doi":"10.1002/cbin.70204","DOIUrl":"10.1002/cbin.70204","url":null,"abstract":"<p><i>Dictyostelium discoideum</i> is a cellular model that has been widely used in cell signal research focusing on different cellular and developmental processes. The unique lifecycle of these cells—which involves switching between vegetative and development phases—makes <i>Dictyostelium</i> a reliable model for investigations in this field. The ability to switch between these phases depends mainly on the availability of nutrients. Specifically, the vegetative phase of <i>Dictyostelium</i> cells is initiated when food is plentiful. This phase is characterized by the unicellular form of this organism, in which it is able to hunt for bacteria and actively divide by mitosis. However, when nutrients are depleted, certain cellular signals are activated that stimulate the development phase, which commences with cell chemotaxis toward cyclic AMP to form aggregates. Based on previously collected data, aggregation-regulating signals in <i>Dictyostelium</i> are thoroughly explained herein. Heterotrimeric G protein signals and downstream effectors are thought to be included in this paradigm, as blocking these signals leads to the aggregation-minus phenotype. Recently, <i>Dictyostelium</i> was used to detect the effect of natural products, some of which caused a noticeable delay of the aggregation stage. However, no clear evidence has been obtained that explains why aggregation is delayed or the science behind this phenomenon. This review provides insights into regulatory factors, beyond the key aggregation regulators, that possibly contribute to the aggregation-delayed phenotype of <i>Dictyostelium</i> cells. The discussion in this review will enhance understanding of the importance of divalent cations/ions in this phenotype.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 9","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sotagliflozin, a Dual SGLT1/2 Inhibitor, Modulates DNMT1 and Class I/II HDAC Expression in Association With Anticancer Effects in Breast and Lung Cancer Cells Sotagliflozin是一种双SGLT1/2抑制剂，可调节DNMT1和I/II类HDAC的表达，与乳腺癌和肺癌细胞的抗癌作用相关。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-09-01 DOI: 10.1002/cbin.70201

P. K. Hima, K. Aswathy, Govinda Rao Duddukuri

{"title":"Sotagliflozin, a Dual SGLT1/2 Inhibitor, Modulates DNMT1 and Class I/II HDAC Expression in Association With Anticancer Effects in Breast and Lung Cancer Cells","authors":"P. K. Hima, K. Aswathy, Govinda Rao Duddukuri","doi":"10.1002/cbin.70201","DOIUrl":"10.1002/cbin.70201","url":null,"abstract":"<div>\u0000 \u0000 <p>Sodium–glucose cotransporter (SGLT) inhibitors are increasingly recognised for anticancer activity beyond their established glycaemic effects. While selective SGLT2 inhibitors have been reported to suppress tumour cell proliferation and modulate AMPK/mTOR and PI3K/AKT signalling, whether dual SGLT1/2 inhibition is associated with modulation of epigenetic regulators has remained largely unexplored. Here, we investigated the anticancer effects of sotagliflozin, a dual SGLT1/2 inhibitor, in breast (MCF-7) and lung (A549) cancer cells. Sotagliflozin reduced cell viability, clonogenic survival, migration, and invasion, and these effects were accompanied by G2/M cell-cycle arrest, increased AMPK activation, and changes in PTEN–AKT–mTOR signalling. Molecular docking analysis predicted favourable interactions between sotagliflozin and DNA methyltransferases (DNMT1, DNMT3A, and DNMT3B), with the strongest predicted binding to DNMT1 (−8.9 kcal/mol). Consistent with these computational predictions, sotagliflozin treatment was associated with reduced total DNMT enzymatic activity, decreased DNMT1 mRNA and protein abundance, and reduced protein abundance of class I and class II histone deacetylases (HDAC1–4 and HDAC6) in both cell lines. In addition, sotagliflozin treatment was associated with autophagy-related changes, including increased acidic vesicular organelles together with elevated LC3-II and Beclin-1 protein abundance. Collectively, these findings demonstrate that sotagliflozin exerts broad anticancer effects in breast and lung cancer cells and provide preliminary evidence that its treatment is associated with modulation of DNMT1 and HDAC expression. Further studies are required to determine whether these epigenetic changes contribute directly to the observed cellular responses or represent downstream consequences of metabolic perturbation.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 9","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immunometabolic Control of Neutrophil Plasticity in Tuberculosis 结核中性粒细胞可塑性的免疫代谢控制。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-09-01 DOI: 10.1002/cbin.70205

Khaldoun Hamdan, Jasur Rizaev, Dhara N. Patel, Swayamsidha Mangaraj, Ahmed Faisal Mutee, Urazbaeva Yulduz, Erdonov Bekmurod, Shefali

{"title":"Immunometabolic Control of Neutrophil Plasticity in Tuberculosis","authors":"Khaldoun Hamdan, Jasur Rizaev, Dhara N. Patel, Swayamsidha Mangaraj, Ahmed Faisal Mutee, Urazbaeva Yulduz, Erdonov Bekmurod,  Shefali","doi":"10.1002/cbin.70205","DOIUrl":"10.1002/cbin.70205","url":null,"abstract":"<div>\u0000 \u0000 <p>The development of tuberculosis (TB) is dictated by a complicated interplay between antimicrobial defense and host-mediated immunopathology. Neutrophils are known to exhibit striking functional plasticity with phenotypes associated with both bacterial containment and tissue damage. However, the mechanisms that connect the granuloma microenvironment to neutrophil fate remain poorly understood. This review aims to fill this gap by integrating emerging evidence that defines immunometabolic adaptation as a key determinant of neutrophil plasticity in TB. The core of this analysis delineates how the spatially organized granuloma characterized by hypoxia, nutrient limitation, iron dysregulation, and extracellular acidosis imposes metabolic pressures that remodel neutrophil function. Environmental signals converge on regulatory networks, including HIF-1α, mTOR/AMPK signaling, glycolytic pathways, the pentose phosphate pathway, and redox control systems, thereby affecting the switch between antimicrobial activity and pathological inflammation. This paradigm presents metabolic rewiring as a potentially important determinant of neutrophil fate in TB and offers a mechanistic view of how protective antimicrobial programs could evolve into dysfunctional states characterized by excessive NETosis, matrix destruction, ferroptotic stress, and tissue injury. Ultimately, a better understanding of these metabolic checkpoints may provide opportunities for the development of host-directed therapeutic approaches to enhance protective neutrophil functions while limiting immunopathology.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 9","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tumor-Associated Macrophages in the Chemoresistant Microenvironment of Gastric Cancer: Key Mechanisms and Intercellular Crosstalk 胃癌化疗耐药微环境中的肿瘤相关巨噬细胞：关键机制和细胞间串扰

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-08-26 DOI: 10.1002/cbin.70203

Saeb Younis Abdul-Rahman, Abdulkareem Shareef, S. Renuka Jyothi, Priya Priyadarshini Nayak, J. Bethanney Janney, Gurjant Singh, Aashna Sinha, Munisa Ergasheva, Hayder Naji Sameer, Ahmed Yaseen, Rasim M. Salih, Mohaned Adil

{"title":"Tumor-Associated Macrophages in the Chemoresistant Microenvironment of Gastric Cancer: Key Mechanisms and Intercellular Crosstalk","authors":"Saeb Younis Abdul-Rahman, Abdulkareem Shareef, S. Renuka Jyothi, Priya Priyadarshini Nayak, J. Bethanney Janney, Gurjant Singh, Aashna Sinha, Munisa Ergasheva, Hayder Naji Sameer, Ahmed Yaseen, Rasim M. Salih, Mohaned Adil","doi":"10.1002/cbin.70203","DOIUrl":"https://doi.org/10.1002/cbin.70203","url":null,"abstract":"<div>\u0000 \u0000 <p>Gastric cancer (GC) remains a leading cause of cancer-related mortality, with chemoresistance posing a critical barrier to effective treatment. Tumor-associated macrophages (TAMs), particularly the immunosuppressive M2-polarized subset, are emerging as pivotal mediators of chemoresistance within the tumor microenvironment (TME). TAMs promote resistance through multifaceted mechanisms, including activation of pro-survival signaling pathways, induction of epithelial–mesenchymal transition (EMT), and enhancement of angiogenesis. For instance, M2-like TAMs secrete CXCL5, which activates the PI3K/AKT/mTOR axis in GC cells, thereby conferring resistance to 5-fluorouracil (5-FU). Similarly, TMEM, a transmembrane protein overexpressed in cisplatin-resistant GC, drives M2 polarization of TAMs via the Wnt/β-catenin pathway, further amplifying drug resistance and tumor progression. Clinical studies reveal that high TAM infiltration correlates with poor chemotherapy response and reduced survival in GC patients. This review synthesizes current evidence on TAM-driven chemoresistance in GC, highlighting the molecular interplay between TAMs, tumor cells, and stromal components. It underscores the potential of TAM-centric therapies—including checkpoint inhibitors, epigenetic modulators, and combination regimens—to overcome resistance and improve clinical outcomes. By integrating preclinical insights and clinical data, this work provides a roadmap for developing precision therapies that exploit TAM biology to enhance chemosensitivity in GC.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 9","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148811178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mitoxyperiosis: A Novel Mitochondria-Driven Cell Death Mechanism in Immunometabolic Stress 线粒体坏死：免疫代谢应激中线粒体驱动细胞死亡的新机制。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-08-17 DOI: 10.1002/cbin.70200

Suyeol Im, Daram Yang, Wanil Kim, Jong-Won Kim

{"title":"Mitoxyperiosis: A Novel Mitochondria-Driven Cell Death Mechanism in Immunometabolic Stress","authors":"Suyeol Im, Daram Yang, Wanil Kim, Jong-Won Kim","doi":"10.1002/cbin.70200","DOIUrl":"10.1002/cbin.70200","url":null,"abstract":"<div>\u0000 \u0000 <p>Wang et al. recently proposed mitoxyperiosis as a previously uncharacterized, mitochondria-dependent form of lytic cell death triggered by immunometabolic stress. Unlike apoptosis, pyroptosis, necroptosis, or ferroptosis, mitoxyperiosis is driven by sustained oxidative stress and prolonged mitochondria-plasma membrane contact, culminating in localized oxidative membrane damage and non-caspase-dependent rupture, termed mitoxyperilysis. Central to this mechanism is the activation of mechanistic target of rapamycin complex 2 (mTORC2), which suppresses actin cytoskeletal remodeling and inhibits lamellipodia formation, thereby retaining mitochondria at the cell periphery. Remarkably, mTORC2 inhibition or the restoration of cytoskeletal dynamics prevents membrane rupture despite persistent oxidative stress. This review synthesizes mechanistic insights and experimental evidence underlying mitoxyperiosis and examines its implications for tumor biology and inflammatory disease. We further discuss how this pathway may expand current understanding of spatial control in regulated cell death and may provide therapeutic opportunities targeting mitochondrial positioning and mTORC2 signaling in immunometabolic disorders.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RETRACTION: USP44 Suppresses Proliferation and Enhances Apoptosis in Colorectal Cancer Cells by Inactivating the Wnt/β-catenin Pathway via Axin1 Deubiquitination 撤回：USP44通过Axin1去泛素化使Wnt/β-catenin通路失活，从而抑制结直肠癌细胞增殖并增强凋亡

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-08-15 DOI: 10.1002/cbin.70198

{"title":"RETRACTION: USP44 Suppresses Proliferation and Enhances Apoptosis in Colorectal Cancer Cells by Inactivating the Wnt/β-catenin Pathway via Axin1 Deubiquitination","authors":"","doi":"10.1002/cbin.70198","DOIUrl":"https://doi.org/10.1002/cbin.70198","url":null,"abstract":"<p><b>RETRACTION:</b> T. Huang, Q. Zhang, W. Ren, B. Yan, L. Yi, T. Tang, H. Lin, and Y. Zhang “USP44 Suppresses Proliferation and Enhances Apoptosis in Colorectal Cancer Cells by Inactivating the Wnt/β-catenin Pathway via Axin1 Deubiquitination,” <i>Cell Biology International</i> 44, no. 8 (2020): 1651-1659, https://doi.org/10.1002/cbin.11358.</p><p>The above article, published online on 14 April 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editorial Board; and John Wiley & Sons Ltd. The retraction has been agreed upon following concerns raised by a third party. An investigation identified a duplication between the oeUSP44 HT29 and HCT116 flow cytometry panels presented in Figure 2B. Additional duplications were identified between bands presented in the western blot shown in Figures 3 and 4 and bands published in other articles, where the duplicated bands were used to represent different proteins. Further duplication involving the data presented in Figure 6 C was also identified in other articles representing a different scientific context. The authors did not respond to invitations to comment on the concerns and provide their data. Therefore, the editors consider the results and conclusions of this article to be compromised. The authors did not respond to the retraction notice.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70198","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148753952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RETRACTION: Downregulation Of Tripartite Motif Protein 11 Attenuates Cardiomyocyte Apoptosis After Ischemia/Reperfusion Injury Via Dusp1-JNK1/2 撤回：三方基序蛋白11的下调通过Dusp1-JNK1/2减弱缺血/再灌注损伤后心肌细胞凋亡

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-08-15 DOI: 10.1002/cbin.70199

引用次数: 0

Murine T Cell-Dependent Response Affects Leishmania amazonensis Amastigote Survival and Virulence 小鼠T细胞依赖性反应影响亚马逊利什曼原虫的存活和毒力。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-08-12 DOI: 10.1002/cbin.70197

Gustavo Henrique Corrêa Soares, Gustavo Rolim Barbosa, Beatriz Simonsen Stolf

{"title":"Murine T Cell-Dependent Response Affects Leishmania amazonensis Amastigote Survival and Virulence","authors":"Gustavo Henrique Corrêa Soares, Gustavo Rolim Barbosa, Beatriz Simonsen Stolf","doi":"10.1002/cbin.70197","DOIUrl":"10.1002/cbin.70197","url":null,"abstract":"<p>Our group has previously described the infection course of <i>Leishmania amazonensis</i> in BALB/c and BALB/c<sup>nu/nu</sup> mice, which have distinct T-cell dependent responses. In this study, lesion-derived amastigotes exhibited differential protein expression in a host-dependent manner. Herein, we evaluate the impact of the immune system of these two mouse strains on parasite survival and virulence. For this, BALB/c and BALB/c<sup>nu/nu</sup> mice were infected with promastigotes of the LV79 strain, and after 13-weeks of infection, amastigotes were isolated from the lesion footpads. The amastigotes recovered from BALB/c mice were more viable, generating cultures with a higher number of promastigotes than those from BALB/c nude mice. Accordingly, lesion-derived amastigotes from BALB/c mice displayed higher infectivity, induced larger parasitophorous vacuoles in vitro, and exhibited greater virulence in vivo than those from BALB/c<sup>nu/nu</sup> mice. These findings demonstrate that the mouse immune environment can shape the biological phenotype of the parasite, directly impacting its survival and virulence.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70197","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Piwei Peiyuan Pill Ameliorates Chronic Atrophic Gastritis and Intestinal Metaplasia at Least in Part by Inhibiting the Pellino1/IRAK1/NF-κB Signaling Axis 脾胃培元丸通过抑制Pellino1/IRAK1/NF-κB信号轴部分改善慢性萎缩性胃炎和肠化生。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-08-12 DOI: 10.1002/cbin.70195

Cheng Zhang, Fei Lu, Ting Ye, Yueping Jin, Yunpeng Qin, Kairui Wu, Kai Liu, Xuncui Wang, Hang Song, Xuejun Li

{"title":"Piwei Peiyuan Pill Ameliorates Chronic Atrophic Gastritis and Intestinal Metaplasia at Least in Part by Inhibiting the Pellino1/IRAK1/NF-κB Signaling Axis","authors":"Cheng Zhang, Fei Lu, Ting Ye, Yueping Jin, Yunpeng Qin, Kairui Wu, Kai Liu, Xuncui Wang, Hang Song, Xuejun Li","doi":"10.1002/cbin.70195","DOIUrl":"10.1002/cbin.70195","url":null,"abstract":"<div>\u0000 \u0000 <p>Chronic atrophic gastritis (CAG) with intestinal metaplasia (IM) is a key precancerous lesion that may progress to intestinal-type gastric adenocarcinoma. Piwei Peiyuan Pill (PPP) has shown significant clinical efficacy in ameliorating CAG with IM, but its active components and underlying mechanisms remain unclear. High-performance liquid chromatography (HPLC) and ultra-high performance liquid chromatography coupled with high-resolution mass spectrometry (UHPLC-HRMS) were used to identify the components of PPP and the active ingredients in PPP-containing serum. The therapeutic efficacy and potential mechanisms of PPP were further investigated via transcriptomic sequencing and experimental validation. UHPLC-HRMS analysis of PPP-containing serum identified several bioactive components, including esculin, lithospermic acid, and atractylenolide III. In CAG rats, PPP significantly ameliorated gastric mucosal damage and reduced serum IL-6 and TNF-α levels. Transcriptomic results showed that IRAK1 was highly expressed in CAG patients with IM and associated with activation of the NF-κB pathway. PPP intervention dose-dependently suppressed hyperactivation of the Pellino1/IRAK1/NF-κB axis and decreased the expression of intestinal metaplasia markers CDX1 and MUC2. Additionally, PPP improved immune function by increasing the proportion of CD4<sup>+</sup> T cells and decreasing the proportion of CD8<sup>+</sup> T cells in CAG model rats. Taken together, these findings suggest that PPP mitigates CAG and attenuates IM at least in part by suppressing the Pellino1/IRAK1/NF-κB signaling pathway, indicating that it may serve as a promising therapeutic strategy for reducing inflammation-associated gastric carcinogenesis.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0