Histology and histopathology最新文献

{"title":"Clomiphene and dexamethasone inhibit apoptosis and autophagy via the ROS-JNK/MAPK-P21 signaling pathway in PCOS.","authors":"Ruxia Liu, Yuxiang Tang, Xiangjun Chen, Xintong Shang","doi":"10.14670/HH-18-800","DOIUrl":"10.14670/HH-18-800","url":null,"abstract":"<p><strong>Background: </strong>Polycystic ovarian syndrome (PCOS) is a complicated endocrine and metabolic disease, which seriously affects women's health. However, the etiology and genetic basis of PCOS are complex, and the pathogenesis remains unclear. In this study, we aimed to explore the effects of clomiphene and dexamethasone on PCOS and their potential mechanisms.</p><p><strong>Methods: </strong>Sprague-Dawley (SD) rats were injected with dehydroepiandrosterone (DHEA) to establish a PCOS model. After treatment with clomiphene, dexamethasone, and their combination, ovarian tissue of rats was collected. The morphological changes in the ovary were observed by hematoxylin and eosin (HE) staining and Electron microscopy. The levels of oxidative stress and hormones were determined by ELISA. Apoptosis was assessed by TUNEL assay. The mechanism of clomiphene and dexamethasone effects on PCOS was explored by Immunohistochemical staining, real-time PCR, and western blotting.</p><p><strong>Results: </strong>Clomiphene and dexamethasone could improve the morphology of the ovary in PCOS. TUNEL assay and ELISA showed that clomiphene, dexamethasone, and their combination could inhibit apoptosis and significantly reverse the levels of ROS, T-SOD, CAT, T, and E2 in the ovary. Immunohistochemical staining revealed that clomiphene and dexamethasone could remarkably reduce the protein levels of Bax, Caspase-3, LC3II, p-JNK, p-P38 MAPK, and P21, and increase P62 and Bcl-2 protein expression. The mRNA levels of Bax, Bcl-2, and Caspase-3 were also modulated in the PCOS model with clomiphene and dexamethasone treatment. Additionally, western blotting indicated that clomiphene and dexamethasone significantly regulated the levels of Bax, Bcl-2, Caspase-3, LC3I, LC3II, P62, p-JNK, JNK, p-P38 MAPK, P38 MAPK, and P21 in PCOS rats.</p><p><strong>Conclusions: </strong>Clomiphene and dexamethasone can not only reduce oxidative damage, and inhibit apoptosis and autophagy, but they can also regulate the ROS-JNK/MAPK-P21 signaling pathway in PCOS rats. It provides an experimental basis for the clinical application of clomiphene and dexamethasone in PCOS.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"555-570"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142286029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of T cell-related proteins in breast ductal carcinoma <i>in situ</i>.","authors":"Eunah Shin, Hye Min Kim, Ja Seung Koo","doi":"10.14670/HH-18-805","DOIUrl":"10.14670/HH-18-805","url":null,"abstract":"<p><p>This study aims to explore the expression of T cell subtype markers within the immune cells constituting the tumor microenvironment of ductal carcinoma <i>in situ</i> (DCIS) and to assess its implications. A tissue microarray comprising 191 cases of breast DCIS was created, and immunohistochemistry staining for T cell subtype markers (STAT3, STAT4, STAT-6, and FOXP3) was conducted. The DCIS cases were categorized into luminal, HER-2, and TNBC (Triple-negative breast cancer) types based on ER, PR, HER-2, and Ki-67 results. Additionally, they were classified as low-TIL (tumor-infiltrating lymphocytes) (<10%) or high-TIL (≥10%) types according to stromal TIL. Results revealed that 54.6% were luminal, 39.5% HER-2, and 5.9% TNBC. STAT3 exhibited a high positivity rate in luminal-type tumor cells, while STAT3, STAT4, STAT6, and FOXP3 showed elevated positivity rates in TNBC immune cells (<i>p</i><0.05). Furthermore, a higher positivity rate was observed in high-TIL immune cells compared with low-TIL (<i>p</i><0.001). The strongest agreement between T cell subtype markers in immune cells was found between STAT3 and STAT4 (OA=83.7%, κ=0.658), whereas the lowest was between STAT4 and FOXP3 (OA=71.7%, κ=0.370). In immune cells, STAT3 and STAT4 positivity correlated with necrosis (<i>p</i><0.001), and the absence of positivity in all immune cell-related proteins in DCIS with necrosis was associated with poor prognosis (<i>p</i>=0.013). In conclusion, the immune cells in DCIS exhibit positivity for diverse T cell subtype markers, with TNBC and high-TIL DCIS displaying heightened positivity.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"467-475"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression pattern, immune signature, and prognostic value of RBM10 in human cancers.","authors":"Xi Sun, Dexin Jia, Yan Yu","doi":"10.14670/HH-18-790","DOIUrl":"10.14670/HH-18-790","url":null,"abstract":"<p><strong>Background: </strong>RNA-binding motif protein 10 (RBM10) regulates the expression of genes involved in immune responses and is associated with a wide spectrum of cancers. Meanwhile, immunotherapy is the most promising cancer treatment of our time; nevertheless, the pan-cancer role of RBM10 remains to be elucidated.</p><p><strong>Methods: </strong>Data from multiple online databases, including ONCOMINE, UALCAN, GEPIA2, Kaplan-Meier Plotter, cBioPortal, STRING, and TIMER were analyzed. The protein expression levels of RBM10 in various tumor types were verified by immunohistochemistry (IHC).</p><p><strong>Results: </strong>RBM10 is upregulated in multiple tumors compared with the corresponding normal tissues. In addition, RBM10 is highly mutated in various cancers. We also compared the levels of phosphorylated RBM10 between normal and primary tumor tissues. We found that the expression of RBM10 was positively correlated with Programmed cell death 1 (PD-L1) and Cytotoxic lymphocyte antigen 4 (CTLA4) in most cancers, except Thyroid carcinoma (THCA). Moreover, the expression of RBM10 was significantly related to immune cell infiltration in many cancers, suggesting that it is a promising target for cancer immunotherapy.</p><p><strong>Conclusions: </strong>RBM10 expression is closely related to tumor prognosis and the immune microenvironment. Our findings provide new insights into the role of RBM10 in cancer diagnosis and treatment.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"493-508"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141758419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ACAT2 negatively modulated by FOXA2 suppresses ferroptosis to expedite the aggressive phenotypes of endometrial cancer cells.","authors":"Xin Xiao, Tingyun Huang, Bin Chen, Jinshu Zhu, Qingbang Xiao, Yuxin Bao","doi":"10.14670/HH-18-793","DOIUrl":"10.14670/HH-18-793","url":null,"abstract":"<p><p>Endometrial cancer (EC) remains a prevalent gynecological disease with a continuously rising incidence and fatality rate. Acyl coenzyme A: cholesterol acyltransferase 2 (ACAT2) has been commonly perceived as a tumor promoter in multiple human malignancies. This study was conducted to specify the role and mechanism of ACAT2 in EC, which has not been covered. The expression and prognostic significance of ACAT2 in EC samples were respectively analyzed by the ENCORI and Kaplan-Meier plotter databases. RT-qPCR and western blot examined ACAT2 and forkhead box protein A2 (FOXA2) expression in EC cells. The CCK-8 method, colony formation, and EdU staining assays detected cell proliferation. The cell cycle was detected by flow cytometry analysis. Wound healing and Transwell assays, respectively, estimated cell migration and invasion. The thiobarbituric acid reactive species (TBARS) method and BODIPY 581/591 C11 probe detected lipid peroxidation levels. FerroOrange staining estimated intracellular iron level. Western blot examined the expression of epithelial-mesenchymal transition (EMT) and ferroptosis-associated proteins. The human TFDB database predicted the binding of FOXA2 with the ACAT2 promoter, which was substantiated by ChIP and luciferase reporter assays. As a result, ACAT2 expression was increased in EC tissues and cells and associated with poor survival outcomes in EC patients. ACAT2 deletion might hinder EC cell proliferation, migration, invasion, and EMT while stimulating cell cycle arrest. Moreover, ACAT2 silencing promoted the ferroptosis of EC cells. Also, FOXA2 inactivated the transcription of ACAT2 through binding with the ACAT2 promoter. FOXA2 interference could promote the proliferation, migration, invasion, EMT, cell cycle, and inhibit the ferroptosis of ACAT2-silenced EC cells, which was partially reversed by the ferroptosis activator erastin. Conclusively, ACAT2 transcriptionally inactivated by FOXA2 might contribute to the malignant progression of EC via the inhibition of ferroptosis.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"509-521"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141792350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morphologic and molecular diagnostic criteria of malignancies in biliary strictures.","authors":"Elisa Albertini, Lucia Miranda, Thais Maloberti, Dario de Biase, Francesco Vasuri","doi":"10.14670/HH-18-811","DOIUrl":"10.14670/HH-18-811","url":null,"abstract":"<p><p>The differential diagnosis of benign and malignant biliary strictures is not always feasible and still represents a major diagnostic challenge, mainly due to the scarcity of the tissue retrieved for proper cytological or histopathological diagnosis. The present review focuses on morphological criteria in the diagnosis of biliary strictures, in the course of primary sclerosing cholangitis and other pathologies, starting from the limits of the cytological and histological evaluation, as well as the ancillary methodologies currently available in Pathology laboratories The current guidelines suggest fluorescence <i>in situ</i> hybridization for the analysis of chromosomes 3, 7, and 17 polysomies and deletion of the 9p21 locus; however, other more promising techniques are on the horizon for both patient care and research purposes, such as Next-Generation Sequencing, able to analyze multiple genes simultaneously in a cost-effective fashion. Lastly, the most recent approaches proposed in the literature for the differential diagnosis of biliary stricture are described, such as circulating tumor DNA, miRNAs, and DNA methylation, among others.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"443-452"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL1 aggravates sepsis-acute kidney injury by promoting m7G methylation of NLRP3-mediated pyroptosis.","authors":"Lu Wang, Yuexuan Chen, Ming Fang, Jingjing Hu","doi":"10.14670/HH-18-910","DOIUrl":"https://doi.org/10.14670/HH-18-910","url":null,"abstract":"<p><p>Sepsis is a major cause of acute kidney injury (AKI). Dysregulation of N7-methyladenosine (m7G) methylation is a pathogenic mechanism of sepsis. However, the role of m7G methylation in renal damage remains poorly understood. In this study, we investigated the regulation of METTL1, an m7G &quot;writer&quot;, on pyroptosis in sepsis-induced AKI. HK-2 cells were treated with lipopolysaccharide (LPS), and pyroptosis was assessed using enzyme-linked immunosorbent assays and western blotting. The m7G methylation status of NLRP3 was analyzed through methylated-RNA immunoprecipitation (Me-RIP), RNA immunoprecipitation (RIP), and dual-luciferase reporter assays. Renal injury in mice subjected to cecal ligation and puncture (CLP) was evaluated using hematoxylin and eosin (H&E) staining. Our results demonstrated that METTL1 expression was significantly upregulated in both LPS-treated HK-2 cells and the CLP-induced mouse model. Interfering with METTL1 suppressed LPS-induced pyroptosis <i>in vitro</i> and attenuated kidney damage and pyroptosis <i>in vivo</i>. Furthermore, METTL1 knockdown inhibited m7G methylation of NLRP3, thereby reducing its stability. Overexpression of NLRP3 abrogated the inhibition of pyroptosis caused by METTL1 knockdown. In conclusion, silencing of METTL1 alleviates sepsis-induced AKI by inhibiting m7G methylated NLRP3-mediated pyroptosis in renal tubular epithelial cells. These findings suggest that targeting METTL1 may represent a promising therapeutic strategy for managing sepsis-associated AKI.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18910"},"PeriodicalIF":2.5,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143779861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deregulation and delocalization of the m⁶A demethylase FTO and aberrant m⁶A levels in ccRCC tissue samples.","authors":"Claudia Tito, Paolo Rosa, Veronica Sorrentino, Martina Magnanti, Angelica Innocenti, Lorenzo Zaccaria, Manuela Costantini, Alessia Iaiza, Daniela Bastianelli, Silvia Masciarelli, Antonio Luigi Pastore, Giuseppe Simone, Antonio Carbone, Alessandro Fatica, Vincenzo Petrozza, Francesco Fazi","doi":"10.14670/HH-18-909","DOIUrl":"https://doi.org/10.14670/HH-18-909","url":null,"abstract":"<p><p>N6-methyladenosine (m⁶A) is one of the most abundant mRNA modifications established by the activity of three classes of enzymes: writers, readers, and erasers. The relevance of m⁶A in the regulation of gene expression implies its key role in normal biological processes and cancer development. Given the little knowledge about the involvement of m⁶A in clear cell Renal Carcinoma (ccRCC), our analysis should be regarded as a pilot study aimed at investigating the expression of m⁶A enzymes in tissues and urine specimens of ccRCC patients. The expression of m⁶A enzymes was validated by quantitative reverse-transcription PCR and immunohistochemistry, comparing normal and tumoral tissues. Quantification of m⁶A levels in urine specimens of healthy and cancer patients was performed by colorimetric Urine m⁶A assay. We observed the upregulation and nuclear localization of the m⁶A demethylase FTO in tumoral tissues compared with their respective normal counterparts. The nuclear expression of FTO decreases with an increase in tumor grade. Moreover, we identified a decrease in m⁶A levels in cancer samples. These findings might represent novel evidence to further investigate the issue, to reveal new diagnostic markers for tumorigenesis, leading to a potential m⁶A-targeted therapy in ccRCC.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18909"},"PeriodicalIF":2.5,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772157","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histological and transcriptomic analysis of paravaginal and central defects in anterior vaginal wall prolapse: Insights from DeLancey's pelvic floor theory.","authors":"Chun Zhang, Qingxia Tang, Yan Zhou, Xuemei Fu, Pan Hu, Lubin Liu","doi":"10.14670/HH-18-908","DOIUrl":"10.14670/HH-18-908","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to preliminarily explore the differences between paravaginal and central defect types of anterior vaginal wall prolapse based on DeLancey's pelvic floor theory.</p><p><strong>Methods: </strong>Seventy-eight patients with normal, paravaginal, or central defect vaginal wall tissues were collected and stained using hematoxylin and eosin (HE) and immunofluorescence staining to analyze and identify the expression of vimentin and phosphohistone H3 (PH3). Ribonucleic acid from fresh tissues was extracted for transcriptome sequencing to analyze differences between paravaginal and central defect types of anterior vaginal wall prolapse.</p><p><strong>Results: </strong>Significant differences were found in age, menopausal status, body mass index, pregnancy, and delivery among the control, paravaginal, and central defect groups. Histological analysis revealed that the distribution of interstitium in the normal HE staining group was compact and continuous. In the paravaginal defect interstitium, fiber morphology was altered, while central defect interstitial fibers were fragmented. PH3 expression was significantly lower in the central defect type than in the normal and paravaginal defect groups, suggesting degenerative lesions in the vaginal mucosa with central defects. Vimentin distribution in the normal group was tightly packed and continuous, whereas, in the paravaginal defect interstitium, vimentin filaments were fragmented into small spots and micro-aggregates. In the central defect interstitium, vimentin micro-aggregates exhibited altered coalescence and cell shape, appearing punctate. These findings indicated degenerative lesions in the anterior vaginal interstitium of both paravaginal and central defect types. KEGG enrichment analysis of differential genes revealed their involvement in proteinaceous extracellular matrix (ECM)-related signaling pathways, with increased expression of matrix metalloproteinase 13 (MMP13), MMP3, MMP12, and MMP7 in the paravaginal defect type compared with the central defect type.</p><p><strong>Conclusion: </strong>The differences between paravaginal and central defect types of anterior vaginal wall prolapse may be related to the expression of MMP-related proteins; KEGG enrichment analysis of differential genes indicated that they were closely related to the protein ECM pathway. Moreover, delineative lesions appeared in the paravaginal defect interstitium, and degenerative lesions appeared in the central defect mucosa and interstitium, which further enriched the DeLancey three-level theory.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18908"},"PeriodicalIF":2.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Licochalcone A ameliorates lipid accumulation in metabolic dysfunction-associated steatotic liver disease via upregulating PPARα/CPT1α.","authors":"Wenrui Zhu, Hongfeng Xu, Rui Yan, Luqi Qiu, Guojun Wang, Yantao Zhu","doi":"10.14670/HH-18-907","DOIUrl":"https://doi.org/10.14670/HH-18-907","url":null,"abstract":"<p><strong>Background: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent hepatic disorder with high morbidity and mortality. Licochalcone A (LiA) exhibits significant therapeutic efficacy in obesity through diverse pharmacological mechanisms. This study aimed to explore the efficacy and underlying mechanism of LiA in attenuating MASLD, which requires further investigation.</p><p><strong>Methods: </strong>Male C57BL/6 mice were fed a high-fat diet (HFD) for 12 weeks to establish a MASLD mouse model. The lipid level and liver function of mice were evaluated by the levels of TG, TC, ALT, and AST. H&E staining and Oil Red O staining were used to evaluate the pathological changes and lipid deposits in the liver. Lipid metabolism and PPARα/CPT1α signaling pathway-related genes were detected.</p><p><strong>Results: </strong>LiA effectively reduced weight and improved glucose tolerance and insulin resistance in MASLD mice. LiA treatment significantly reduced lipid accumulation in HFD-induced mice. In addition, bioinformatics analysis, molecular docking, and cellular thermal shift assays further indicated that LiA alleviated MASLD by upregulating PPARα. Furthermore, the protective effect of LiA on lipid accumulation and hepatic steatosis was abolished by PPARα inhibitor (GW7461) pretreatment in MASLD mice.</p><p><strong>Conclusion: </strong>This study demonstrated that LiA ameliorates the lipid metabolism disorder in MASLD mice by upregulating the PPARα/CPT1α signaling pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18907"},"PeriodicalIF":2.5,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sheng-Jiang-Yi-You decoction inhibits the inflammatory response by down-regulating the p38MAPK signaling pathway to alleviate <i>Helicobacter pylori</i>-associated gastritis.","authors":"Ze Li, Ruirui Chen, Weihong Tang, Xiaoya Zheng, Xuefeng Jin, Zhongmin Wang, Qiao Wu","doi":"10.14670/HH-18-906","DOIUrl":"10.14670/HH-18-906","url":null,"abstract":"<p><strong>Background: </strong><i>Helicobacter pylori</i> (HP)-associated gastritis is an important factor in development of stomach cancer. Components of Sheng-Jiang-Yi-You decoction (SJYYD) exert gastroprotective effects. However, the effects and mechanism of SJYYD in HP-associated gastritis remain uncertain.</p><p><strong>Methods: </strong>HP bacterial solution (1×10⁹ CFU/mL) was gavaged every other day for 14 days to construct an HP-associated gastritis mouse model. Male BALB/c mice were randomized into Sham, HP, HP+Standardized triple therapy (HP+Triplet), HP+SJYYD (0.4 mL/20 g), HP+Triplet+SJYYD, HP+anisomycin (ANI) (2.5 mg/kg/d, p38MAPK agonist, HP+ANI), and HP+SJYYD+ANI groups (<i>n</i>=6). Gastric mucosal injury detection and rapid urease test for HP infection were conducted. HE staining for pathological damage and ELISA for pro-inflammatory factors and immunoglobulin G (IgG) content were performed. Measurement of p38 mitogen-activated protein kinase (p38MAPK) pathway-related factor expression was performed by qRT-PCR and western blot.</p><p><strong>Results: </strong>The increased IgG content and HP colonization rate indicated successful modeling. SJYYD caused attenuated gastric mucosal damage, with decreased ulcer index (UI), HP colonization rate, inflammatory cell infiltration, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β levels in HP-associated gastritis mice. Moreover, SJYYD reduced p38MAPK, c-Jun N-terminal kinase (JNK), and extracellular regulated protein kinase (ERK) mRNA expression, as well as p-p38MAPK/p38MAPK, p-JNK/JNK, and p-ERK/ERK protein expression in gastric mucosa tissues of HP-associated gastritis mice. The above effects were reversed by further ANI treatment.</p><p><strong>Conclusion: </strong>SJYYD may attenuate HP-associated gastritis by inhibiting inflammatory response by down-regulating p38MAPK pathway, providing scientific evidence for clinical application of SJYYD in HP-associated gastritis treatment and promoting the development of therapeutic approaches in HP-associated gastritis.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18906"},"PeriodicalIF":2.5,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}