{"title":"Liquid biopsy of circulating tumor cells: From isolation, enrichment, and genome sequencing to clinical applications.","authors":"Keqin Tan, Hong Zhu, Xuelei Ma","doi":"10.14670/HH-18-924","DOIUrl":"10.14670/HH-18-924","url":null,"abstract":"<p><p>Circulating tumor cells (CTCs), shed from primary tumors into the bloodstream, play a crucial role in metastasis and hold great potential in cancer diagnosis, prognosis, and treatment monitoring. Conventional CTC detection using epithelial biomarkers like epithelial cell adhesion molecule (EpCAM) for immunocapture overlooks mesenchymal-like CTCs with high metastatic potential, spurring the development of non-immunocapture technologies that use biophysical traits for enrichment. Innovations in microfluidic platforms and multi-parametric sorting improve isolation efficiency and address related challenges. Breakthroughs in single-cell genomic and transcriptomic sequencing enable in-depth molecular characterization of CTCs. Clinically, CTC enumeration and molecular profiling are emerging as real-time tools for assessing therapeutic response and predicting outcomes, especially in metastatic breast, prostate, and colorectal cancers. This review focuses on CTC isolation, enrichment techniques, their applications in different tumors, downstream analysis progress, and potential in precision medicine.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1529-1546"},"PeriodicalIF":2.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063531","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":"Shensiqigui tablets alleviate bleomycin-induced pulmonary fibrosis by inhibiting the hedgehog/wnt-β-catenin pathway.","authors":"Rui Ma, Yupeng Xie, Yuan Dong, Fan Yin, Jiong Yang, Fenghua Xu","doi":"10.14670/HH-18-885","DOIUrl":"10.14670/HH-18-885","url":null,"abstract":"<p><strong>Background: </strong>Pulmonary fibrosis (PF) is a refractory disease characterized by inflammation and fibrosis. Shensiqigui Tablets (SSQGT), a combination of Codonopsis pilosula, Astragalus, and Angelica, is a traditional Chinese medicine with anti-inflammatory and antioxidant properties. Therefore, SSQGT may be a potential therapeutic agent for managing PF. This study aimed to investigate the effects of SSQGT on PF and its potential mechanisms.</p><p><strong>Methods: </strong>This study established a mouse model of PF through a single intratracheal injection of bleomycin (BLM) and used a TGF-β1-induced HFL-1 cell model. The experiment included control, model (BLM/TGF-β1), and treatment groups (pirfenidone, compound Biejiaruangan tablet (BJRGT), low-dose SSQGT, medium-dose SSQGT, and high-dose SSQGT). Histopathological changes and collagen deposition in lung tissues were observed using Hematoxylin-Eosin (HE) and Masson staining. Inflammatory exudation in bronchoalveolar lavage fluid (BALF) was assessed using ELISA, including TNF-α, IL-1β, IL-6, and NO. Oxidative stress markers SOD, GSH, and Malondialdehyde (MDA) were measured using commercial kits. mRNA and protein expression levels in lung tissues and <i>in vitro</i> models, including α-SMA, vimentin, collagen I, caspase-3, TGF-β, and the Hedgehog/Wnt-β-catenin pathway, were evaluated using qRT-PCR and western blot analysis.</p><p><strong>Results: </strong>SSQGT significantly alleviated BLM-induced weight loss and lung injury in mice and reduced HYP levels and collagen deposition. Additionally, SSQGT improved oxidative stress markers (decreased MDA levels and increased SOD and GSH activity) and mitigated inflammatory responses (reduced TNF-α, IL-1β, IL-6, and NO levels) and (downregulated α-SMA, collagen I, caspase-3, and TGF-β). Further mechanistic analysis showed that SSQGT inhibited the Hedgehog/Wnt-β-catenin pathway.</p><p><strong>Conclusion: </strong>SSQGT alleviates BLM- or TGF-β1-induced PF by reducing oxidative stress and inhibiting inflammation through the suppression of the Hedgehog/Wnt-β-catenin pathway, suggesting its potential as a therapeutic agent for PF.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1639-1649"},"PeriodicalIF":2.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482724","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}
Inka Rantala, Hanna-Riikka Teppo, Jonas Händelin, Janette Kemppainen, Riina K Ollikainen, Outi Kuittinen, Milla E L Kuusisto
{"title":"Oxidative stress markers 8-OHdG, Trx-1, and Prx6 are expressed in seminoma and are connected to TXNDC2, 3, and 6 expression levels.","authors":"Inka Rantala, Hanna-Riikka Teppo, Jonas Händelin, Janette Kemppainen, Riina K Ollikainen, Outi Kuittinen, Milla E L Kuusisto","doi":"10.14670/HH-18-898","DOIUrl":"10.14670/HH-18-898","url":null,"abstract":"<p><p>Testis-specific thioredoxins (TXNDCs) and oxidative stress have not been studied before in seminoma. We studied the immunohistochemical (IHC) expression of 8-OHdG, Prx6, Trx-1, TXNDC2, 3, and 6 in 25 testicular seminoma and 24 control samples. We retrospectively collected patient details and treatments from hospital records and combined them with IHC results. In normal testis, IHC expression of 8-OHdG, Prx6, TXNDC2, and 3 was higher than in seminoma samples (<i>p</i><0.001 each), and the absence of n8-OHdG (<i>p</i>=0.002) and nTXNDC2 expression (<i>p</i>=0.044) was clinically associated with elevated lactate dehydrogenase levels. On the contrary, Trx-1 and TXNDC6 were overexpressed in seminoma samples (<i>p</i>=0.035 and <i>p</i><0.001, respectively), and TXNDC6 was negatively associated with age over 40 (<i>p</i>=0.036). Concordant with the IHC expression, <i>PRDX6</i> mRNA levels were downregulated with a fold change of -2517.4 (<i>p</i><0.001), and <i>TXN</i> mRNA levels were upregulated with a fold change of 11637.4 (<i>p</i>=0.008) in seminoma samples compared with healthy controls. The oxidative stress markers studied had a correlation between the nuclear and cytoplasmic localization, a mutual correlation in expression between different markers, and mutual protein-protein interactions according to STRING Enrichment analysis. Our results show that oxidative stress markers and their expression in seminoma differ from that in normal testis tissue. Trx-1 and cTXNDC6 are seemingly overexpressed in seminoma, which might indicate their relevance in seminoma biology.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1607-1615"},"PeriodicalIF":2.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648420","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":"PIP5K3 upregulation correlates with unfavorable prognosis in patients with nasopharyngeal carcinoma.","authors":"Szu-Chi Yao, Hung-Chang Wu, Ching-Chieh Yang, Yun-Tzu Lin, Chien-Feng Li, Shih-Lun Chang, Yu-Hsuan Kuo","doi":"10.14670/HH-18-996","DOIUrl":"https://doi.org/10.14670/HH-18-996","url":null,"abstract":"<p><strong>Background: </strong>Nasopharyngeal carcinoma (NPC) is prevalent in East and Southeast Asia, with metastasis and recurrence leading to poor prognosis. Identifying prognostic biomarkers is essential.</p><p><strong>Methods: </strong>We analyzed differentially expressed genes involved in the phosphatidylinositol metabolic process (GO: 0046488) and tumorigenesis (GSE12452) in NPC. Associations between PIP5K3 expression and clinicopathological features were assessed using chi-square tests and Cox proportional hazards models.</p><p><strong>Results: </strong>PIP5K3 was significantly upregulated in NPC tissues, correlating with advanced stage (<i>p</i>=0.001) and nodal metastasis (<i>p</i><0.001). High PIP5K3 expression was associated with worse disease-specific survival (DSS), distant metastasis-free survival (DMeFS), and local recurrence-free survival (LRFS). Multivariate analysis confirmed its association with poor prognosis (DSS: HR=4.321, DMeFS: HR=2.883, LRFS: HR=2.249; all <i>p</i><0.001).</p><p><strong>Conclusions: </strong>PIP5K3 upregulation is associated with unfavorable clinical outcomes in NPC and may serve as a novel prognostic biomarker and potential therapeutic target.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18996"},"PeriodicalIF":2.0,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191650","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":"UCHL1 enhances <i>TSC1</i> transcription by stabilizing FOXO1 through deubiquitination in knee osteoarthritis.","authors":"Yu Wang, Jiawei Lu, Chonghao Gu, Zikang Xie, Zhongyu Xia, Bingqing Guo, Tao Jiang","doi":"10.14670/HH-18-995","DOIUrl":"https://doi.org/10.14670/HH-18-995","url":null,"abstract":"<p><p>Ferroptosis has been shown to play a significant role in the pathophysiological progression of knee osteoarthritis (KOA). In this study, we sought to investigate the biological role of Ubiquitin C-terminal hydrolase 1 (UCHL1) in KOA and elucidate its underlying molecular mechanisms. An <i>in vitro</i> KOA cell model was established by stimulating C28/I2 chondrocytes with IL-1β, and UCHL1 expression was decreased in IL-1β-treated chondrocytes. Notably, overexpression of UCHL1 significantly alleviated IL-1β-induced ferroptosis and extracellular matrix (ECM) degradation. Mechanistically, UCHL1 facilitated the deubiquitination and stabilization of FOXO1. Knockdown of FOXO1 partially reversed the inhibitory effects of UCHL1 on ferroptosis and ECM degradation. Furthermore, FOXO1 was found to bind to the Tuberous Sclerosis Complex 1 (<i>TSC1</i>) promoter, enhancing <i>TSC1</i> transcription. Intriguingly, knockdown of FOXO1 counteracted the inhibitory effects of UCHL1 overexpression on ferroptosis and ECM degradation, while these effects were rescued by TSC1 overexpression. <i>In vivo</i> experiments demonstrated that UCHL1 alleviated cartilage damage in KOA rats by inhibiting ferroptosis and ECM degradation through the FOXO1/TSC1 axis. These findings demonstrate the pivotal role of UCHL1 in regulating ferroptosis and maintaining ECM homeostasis, offering novel insights into the molecular mechanisms driving KOA progression.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18995"},"PeriodicalIF":2.0,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145185791","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}
Yawei Zhao, Yiwei Hao, Chen Li, Haoying Li, Xue Han, Hefei Wang, Xi Chu, Zhiwei Su, Shijiang Sun
{"title":"Cardioprotective mechanisms of Jiangfu Decoction against myocardial ischemia may involve regulation of the AMPK/PINK1/Parkin mitochondrial autophagy pathway.","authors":"Yawei Zhao, Yiwei Hao, Chen Li, Haoying Li, Xue Han, Hefei Wang, Xi Chu, Zhiwei Su, Shijiang Sun","doi":"10.14670/HH-18-994","DOIUrl":"https://doi.org/10.14670/HH-18-994","url":null,"abstract":"<p><strong>Background: </strong>Jiangfu Decoction (JFD) is a classical traditional herbal medicine used to clinically treat ischemic heart disease (IHD). Nonetheless, the influence of JFD on myocardial ischemia (MI), along with its precise underlying mechanism, is still unclear. The objective of this research was to investigate the potential mechanisms by which JFD exerts cardioprotective effects on MI induced by isoproterenol (ISO).</p><p><strong>Methods: </strong>An acute MI model was established by subcutaneous injection of ISO (85 mg/kg/d). To evaluate alterations in myocardial structure, electrocardiogram recordings and heart histology examinations were employed. The myocardial ultrastructure was observed by transmission electron microscopy (TEM). Using specific kits, the levels and activities of oxidative stress markers as well as inflammatory cytokines were separately assessed. Western blotting was employed to assess the expression levels of proteins related to adenosine monophosphate-activated protein kinase (AMPK), PTEN-induced putative kinase 1 (PINK1), Parkin, Nod-like receptor protein 3 (NLRP3), and Caspase-1.</p><p><strong>Results: </strong>The findings show that JFD treatments markedly diminished heart rate, pathological alterations in cardiac tissue, chondriosome injury, and serum concentrations of creatine kinase, creatine kinase-myocardial band, lactate dehydrogenase, malondialdehyde, interleukin-1β, and interleukin-18. Concurrently, these treatments augmented the activation of superoxide dismutase, catalase, and glutathione peroxidase in the serum of animals subjected to ISO treatment. Additionally, JFD also reversed the ISO-induced changes in the levels of AMPK, PINK1, Parkin, NLRP3, and Caspase-1.</p><p><strong>Conclusion: </strong>JFD exhibits a notable safeguarding influence on MI via a mechanism that involves regulation of the AMPK/PINK1/Parkin mitochondrial autophagy pathway, inhibition of pyroptosis, and reduction of oxidative stress and inflammation.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18994"},"PeriodicalIF":2.0,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148935","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":"Unraveling key molecules mediating the mechanisms of YAP deletion or inhibition in liver fibrosis regression through a multi-omics approach.","authors":"Siyuan Wang, Shihui Liu, Hejing Ruan, Yuzhe Cheng, Yan Qiao, Jiawei Wang, Xiaojun Liu, Chuanmiao Liu, Wen Zhao","doi":"10.14670/HH-18-993","DOIUrl":"https://doi.org/10.14670/HH-18-993","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to identify key molecules that potentially mediate the mechanisms by which YAP deletion or inhibition attenuates liver fibrosis.</p><p><strong>Materials and methods: </strong>C57BL/6 mice were divided into four groups: control, carbon tetrachloride (CCl4), CCl4-YAP<sup>-HKO</sup>, and CCl4-verteporfin (VP). RNA sequencing (RNA-seq) and proteomic analysis were conducted. Immunohistochemistry and western blotting were also performed to verify the differentially expressed genes (DEGs) identified through the multi-omics approach. Human subjects were enrolled to further assess the identified DEGs.</p><p><strong>Results: </strong>In comparison with the CCl4 group, both the CCl4-YAP<sup>-HKO</sup> and CCl4-VP groups exhibited liver fibrosis regression. RNA-seq and proteomic analyses identified 12 commonly differentially expressed molecules. Immunohistochemistry and western blotting validated that heat shock protein 27 (HSP27), heat shock protein 70 (HSP70), and p62 expression were significantly reduced, and milk fat globule-epidermal growth factor 8 (MFGE8) expression was elevated in both the CCl4-YAP<sup>-HKO</sup> and CCl4-VP groups compared with the CCl4 group. Furthermore, plasma p62, HSP27, and HSP70 levels were increased with the occurrence of chronic hepatitis B and HBV-related cirrhosis, whereas MFGE8 levels were decreased. Spearman's correlation analysis further illustrated a significant association between these biomarkers and YAP levels.</p><p><strong>Conclusions: </strong>This study identified HSP27, HSP70, p62, and MFGE8 as crucial YAP-related molecules involved in liver fibrosis.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18993"},"PeriodicalIF":2.0,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137307","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":"Crumbs3: Expression and biological significance in normal and neoplastic tissues.","authors":"Hidekazu Iioka, Akane Kitta-Kunihiro, Chiemi Ikude, Eisaku Kondo","doi":"10.14670/HH-18-992","DOIUrl":"10.14670/HH-18-992","url":null,"abstract":"<p><p>Cellular polarity plays a fundamental role in tissue organization and homeostasis, and its disruption is closely linked to tumorigenesis. Crumbs3 (CRB3), a conserved polarity protein, is essential for epithelial morphogenesis, tight-junction formation, and barrier function. This review summarizes current knowledge regarding CRB3 expression in normal and malignant human tissues and its dual roles in cancer progression. Systematic immunohistochemical analyses revealed strong CRB3 expression in non-neoplastic glandular epithelia of the gastrointestinal, hepato-pancreato-biliary, renal, and respiratory tracts, as well as in fetal tissues, suggesting its importance in organ development and maintenance. In neoplastic tissues-represented by colorectal adenocarcinoma and oral squamous cell carcinoma-CRB3 expression is preserved or even enhanced compared with normal tissues, which promotes tumor cell migration, triggering invasion/metastasis as well as cellular proliferation through signaling pathways involving FGFR and RhoA activation. Conversely, previous studies reported that CRB3 functions as a tumor suppressor, based on findings that CRB3 expression induces loss of epithelial-mesenchymal transition, whereas loss of CRB3 expression attenuates the integrity of tight junctions, resulting in significantly poorer prognosis in certain cancers. Current data thus suggest that the biological role of CRB3 in tumors is complex. Whether CRB3 acts as a tumor accelerator or suppressor may depend on the individual-specific, unique characteristics of tumor cells. Understanding these dual functions may contribute to the development of novel polarity-targeted therapeutic strategies for cancers of differing origin.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18992"},"PeriodicalIF":2.0,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130569","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}
Dongfang Ji, Mingxin Cui, Chao Tian, Kaili Chen, Jing Shao
{"title":"Asiatic acid alleviates dexamethasone-induced muscle atrophy through regulating the Sirt1/PGC-1α/FOXO3 pathway.","authors":"Dongfang Ji, Mingxin Cui, Chao Tian, Kaili Chen, Jing Shao","doi":"10.14670/HH-18-991","DOIUrl":"https://doi.org/10.14670/HH-18-991","url":null,"abstract":"<p><strong>Background: </strong>Skeletal muscle atrophy, which results in muscular dysfunction and weakness, is associated with various factors, including aging, sepsis, chronic diseases, and long-term glucocorticoid therapy. Although asiatic acid exhibits multiple biological activities and can activate the Sirt1 signaling pathway, an important regulator of skeletal muscle function,itsrole in muscle atrophy remains unclear.</p><p><strong>Methods: </strong>C2C12 myotubes were treated with 10 μM dexamethasone,with or without designated concentrations of asiatic acid. Subsequently, cell viability, apoptosis, differentiation markers (MyHC and myogenin), levels of atrophy-related proteins (MAFbx, MuRF1), and the Sirt1/PGC-1α/FOXO3 pathway were analyzed. Moreover,the underlyingmechanismswere further explored through inhibition of Sirt1 using the selective inhibitor EX-527 or short hairpin RNA <i>in vitro</i>. <i>In vivo</i>, muscle atrophy was induced via intraperitoneal injections of 20 mg/kg dexamethasone, and 50 mg/kg asiatic acid was administered by oral gavage. Body weight, muscle strength, gastrocnemius muscle mass, histological changes, and atrophy- and Sirt1/PGC-1α/FOXO3 pathway-associated proteins were assessed.</p><p><strong>Results: </strong>Asiatic acid elevated cellviability, inhibited apoptosis, increased MyHC and myogeninprotein contents, and suppressed MAFbx and MuRF1 proteinlevels in dexamethasone-treated C2C12 myotubes. Moreover, asiatic acid activated the Sirt1/PGC-1αp athwayand inactivated FOXO3. Inhibition of Sirt1 attenuated the influence of asiatic acid in a muscle atrophy cell model. <i>In vivo</i>, asiatic acid increased body weight and gastrocnemius muscle mass, improved muscle strength and structural damage of gastrocnemius muscles, suppressed MAFbx and MuRF1 protein contents, and regulated the Sirt1/PGC-1α/FOXO3 pathway.</p><p><strong>Conclusions: </strong>Asiatic acid can improve dexamethasone-induced muscle atrophy via regulating the Sirt1/PGC-1α/FOXO3 pathway. Therefore, asiatic acid might be a potential therapeutic agent for muscle atrophy.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18991"},"PeriodicalIF":2.0,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124588","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":"Penning decoction ameliorated pyroptosis in mice with lipopolysaccharide-induced endometritis through inhibition of the TLR4/NF-κB/NLRP3 pathway.","authors":"Jiani Shi, Chen Chen, Yuqiong Yuan, Zhihui Liu, Qianru Zhou","doi":"10.14670/HH-18-990","DOIUrl":"https://doi.org/10.14670/HH-18-990","url":null,"abstract":"<p><strong>Objectives: </strong>Endometritis, stemming from bacterial infection, manifests as persistent inflammation and may cause infertility. Penning decoction (PND) has been approved for clinical treatment of patients with endometritis. However, the mechanism by which it prevents endometritis remains unknown. This study aimed to examine the impact of PND on lipopolysaccharide (LPS)-induced endometritis and elucidate the underlying mechanisms involved.</p><p><strong>Methods: </strong>Firstly, ultra-performance liquid chromatography‒quadrupole‒time‒of‒flight mass spectrometry (UPLC‒Q‒TOF‒MS) analysis, in which both positive and negative ion modes were used to identify the chemical compounds in PND, was performed. The antipyroptotic effects of PND were validated in LPS-induced endometritis mice. Additionally, mouse endometrial epithelial cells (MEECs) were used to explore the molecular mechanism of PND in serum <i>in vitro</i>.</p><p><strong>Results: </strong>A total of 145 chemical compounds, including flavones, saponins, polysaccharides, alkaloids, and glycosides, were identified in positive and negative ion modes. The results showed that LPS could induce pyroptosis in endometritis <i>in vivo</i> and <i>in vitro</i>. Treatment with PND or serum containing PND could significantly ameliorate LPS-induced pyroptosis by inhibiting the activation of the TLR4/NF-κB/NLRP3 signaling pathway.</p><p><strong>Conclusion: </strong>Our results demonstrated that PND may improve LPS-induced endometritis by inhibiting the TLR4/NF-κB/NLRP3 pathway, which provides a potentially effective drug for the clinical treatment of endometritis.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18990"},"PeriodicalIF":2.0,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145113119","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}