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Trends in noninvasive ocular nanoparticle drug delivery: A bibliometric analysis (2004-2023). 无创眼部纳米颗粒给药趋势:文献计量学分析(2004-2023)。
Biomolecules & biomedicine Pub Date : 2025-08-05 DOI: 10.17305/bb.2025.11772
Dan Li, Qing Ye, Chao Li
{"title":"Trends in noninvasive ocular nanoparticle drug delivery: A bibliometric analysis (2004-2023).","authors":"Dan Li, Qing Ye, Chao Li","doi":"10.17305/bb.2025.11772","DOIUrl":"10.17305/bb.2025.11772","url":null,"abstract":"<p><p>This study presents a bibliometric analysis of research on noninvasive nanoparticle drug delivery systems for the transocular surface from 2004 to 2023. Relevant publications were retrieved from the Web of Science Core Collection. VOSviewer and CiteSpace were used to map contributions by countries/regions, authors, institutions, journals, keywords, keyword clusters, and timeline trends. A total of 695 articles were analyzed, showing a steady year-by-year increase in publications. China, the United States, and Spain were the leading contributors. Among authors, Alvarez-Lorenzo, Carmen was the most prolific, while Chanhan, Anuj's work received the most citations among the top 10 prolific researchers. The International Journal of Pharmaceutics published the highest number of articles in this field, whereas the Journal of Controlled Release was the most frequently cited among the top 10 most productive journals. The University of Santiago de Compostela and the University of Florida were among the most active institutions in this research area. Keyword analysis identified recent key themes, such as controlled release, cell interaction, dry eye, mechanisms, gene expression, and ocular drug delivery. The growing interest in transocular surface nanoparticle drugs is driven by their advantages, including increased solubility, improved stability, reduced administration frequency, sustained therapeutic concentrations, enhanced corneal penetration, and prolonged ocular surface residence time.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1949-1960"},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12450095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The impact of MITF expression on tumor-infiltrating lymphocytes in melanoma: Insights into immune microenvironment dynamics. MITF表达对黑色素瘤中肿瘤浸润淋巴细胞的影响:免疫微环境动力学的见解。
Biomolecules & biomedicine Pub Date : 2025-08-05 DOI: 10.17305/bb.2025.12125
Damir Vučinić, Matea Lekić, Gordana Žauhar, Gordana Zamolo
{"title":"The impact of MITF expression on tumor-infiltrating lymphocytes in melanoma: Insights into immune microenvironment dynamics.","authors":"Damir Vučinić, Matea Lekić, Gordana Žauhar, Gordana Zamolo","doi":"10.17305/bb.2025.12125","DOIUrl":"10.17305/bb.2025.12125","url":null,"abstract":"<p><p>Melanoma progression is influenced by complex interactions between tumor cells and the immune microenvironment. This study examined the relationship between microphthalmia-associated transcription factor (MITF) expression and the immune microenvironment in primary melanoma using a modified classification of tumor-infiltrating lymphocytes (TILs) based on conventional BRISK categories. Archival formalin-fixed, paraffin-embedded tissue samples from 81 primary melanoma patients were analyzed via tissue microarray immunohistochemistry to assess MITF protein levels. TIL patterns were categorized into six groups, refining the traditional BRISK classification to distinguish between continuous and discontinuous infiltration, as well as peripheral vs intratumoral distribution. The analysis revealed that melanomas classified under the BRISK B category exhibited the highest MITF expression, often exceeding 50%. In contrast, tumors in the NON-BRISK and ABSENT TIL groups showed significantly lower MITF expression (mean values: 32.73% ± 16.98% and 22.00% ± 10.54%, respectively), with statistically significant differences (Kruskal-Wallis test, P = 0.027; modified classification, P = 0.011). Additionally, the presence of CD20+ B lymphocytes correlated with increased MITF expression (P = 0.009). MITF gene amplification was detected in 29% of cases, though its association with protein expression showed only a trend (P = 0.058). These findings highlight the complex interplay between MITF expression and TIL distribution in melanoma, suggesting that refined TIL classification may offer deeper insights into tumor immunobiology and help predict responses to immunotherapy.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"2050-2057"},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12450080/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
EPAS1 amplifies asthma pathogenesis through JAK2/STAT3-mediated ferroptosis and inflammation. EPAS1通过JAK2/ stat3介导的铁下垂和炎症放大哮喘发病机制。
Biomolecules & biomedicine Pub Date : 2025-08-05 DOI: 10.17305/bb.2025.11334
Lili Liu, Cheng Yang, Yan Li, Hao Zhou, Mei Shi, Tiantian Shi, Weibing Shi
{"title":"EPAS1 amplifies asthma pathogenesis through JAK2/STAT3-mediated ferroptosis and inflammation.","authors":"Lili Liu, Cheng Yang, Yan Li, Hao Zhou, Mei Shi, Tiantian Shi, Weibing Shi","doi":"10.17305/bb.2025.11334","DOIUrl":"10.17305/bb.2025.11334","url":null,"abstract":"<p><p>Asthma is a chronic respiratory disorder marked by airway hyperresponsiveness and inflammation, yet the specific molecular mechanisms driving these processes remain only partially understood. This study aims to better understand how the JAK2/STAT3/EPAS1 axis regulates inflammation and ferroptosis in asthma. Asthma-related datasets were retrieved from the Gene Expression Omnibus (GEO) database, and differentially expressed genes (DEGs) were identified. Weighted Gene Co-expression Network Analysis (WGCNA) was used to detect gene modules associated with asthma. A protein-protein interaction (PPI) network was then constructed by intersecting WGCNA-derived genes with ferroptosis-related genes to identify key hub genes. The diagnostic value of these ferroptosis-associated genes was evaluated using Receiver Operating Characteristic (ROC) curve analysis. Additionally, immune cell infiltration in asthma patients was analyzed using the Immune Cell AI database in relation to ferroptosis-related genes. Functional experiments at the cellular level were conducted to assess the effects of key genes on cell viability, inflammation, and ferroptosis. Bioinformatics analysis identified 1,698 DEGs linked to asthma. Five hub genes with clinical diagnostic value- Endothelial PAS Domain Protein 1 (EPAS1), STAT3, G6PD, CYBB, and CBS-were identified. Immune analysis revealed that EPAS1 is closely associated with immune cell infiltration in asthma. Functional experiments further demonstrated that the JAK2/STAT3 axis promotes ferroptosis and inflammatory responses by upregulating EPAS1 expression. Notably, these findings highlight the JAK2/STAT3/EPAS1 axis as a potential therapeutic target for asthma, offering new insights into its molecular mechanisms and identifying novel biomarkers for diagnosis and treatment.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"2092-2113"},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12450083/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Jianpi Yiqi Busui prescription alleviates myasthenia gravis by regulating Th17 through the TAK1/P38 MAPK/eIF-4E signaling pathway. 健皮益气布水方通过TAK1/P38 MAPK/eIF-4E信号通路调节Th17,从而缓解肌无力。
Biomolecules & biomedicine Pub Date : 2025-08-05 DOI: 10.17305/bb.2025.11546
Zhuming Chen, Jing Lu, Tianying Chang, Dongmei Zhang, Yibin Zhang, Miao Liu, Tong Wu, Peng Xv, Jian Wang
{"title":"Jianpi Yiqi Busui prescription alleviates myasthenia gravis by regulating Th17 through the TAK1/P38 MAPK/eIF-4E signaling pathway.","authors":"Zhuming Chen, Jing Lu, Tianying Chang, Dongmei Zhang, Yibin Zhang, Miao Liu, Tong Wu, Peng Xv, Jian Wang","doi":"10.17305/bb.2025.11546","DOIUrl":"10.17305/bb.2025.11546","url":null,"abstract":"<p><p>Jianpi Yiqi Busui Prescription (JYBP), a traditional Chinese medicine formula (TCM), is used in the treatment of myasthenia gravis (MG). However, its mechanisms of action still require further clarification. In this study, an experimental autoimmune MG (EAMG) rat model was established for research. Changes in body weight, forelimb grip strength, Lennon clinical score, and antifatigue ability of EAMG model rats were recorded to evaluate the effectiveness of JYBP. Flow cytometry was utilized to count Th17, Th1, Th2, and Treg cells in lymphocytes. ELISA and RT-qPCR were used to measure acetylcholine receptor antibody (AChR-Ab) and Th17-related cytokines, including IL-17, IL-21, IL-23, TNF-α, TGF-β, IL-1β, and IL-6. Western blot and immunofluorescence staining were used to detect the expression levels of key proteins and their phosphorylated forms, such as transforming growth factor beta-activated kinase 1 (TAK1), P38 mitogen-activated protein kinase (P38 MAPK), and eukaryotic initiation factor 4E (eIF-4E). The results indicate that JYBP can increase the body weight of EAMG model rats, improve grip strength and antifatigue ability, and reduce the Lennon clinical score and AChR-Ab concentration. Mechanistic studies indicate that JYBP can inhibit the differentiation of CD4+ T cells into Th17 and Th1, promote their differentiation into Th2 and Treg, and regulate the expression of Th17-related cytokines. Further research shows that JYBP can reduce the expression of related proteins in the TAK1/P38 MAPK/eIF-4E signaling pathway. In conclusion, JYBP can alleviate the condition of EAMG model rats, positively affecting MG treatment. The inhibitory effect of JYBP on the differentiation of CD4+ T cells into Th17 may be related to the TAK1/P38 MAPK/eIF-4E signaling pathway.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"2004-2019"},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12450089/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143400866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Methylene blue mitigates lung injury in HCA rats by regulating macrophage pyroptosis via Nrf2/HO-1 and NLRP3 pathways. 亚甲蓝通过 Nrf2/HO-1 和 NLRP3 通路调节巨噬细胞的脓毒症,减轻 HCA 大鼠的肺损伤。
Biomolecules & biomedicine Pub Date : 2025-08-05 DOI: 10.17305/bb.2025.11851
Fuyan Ding, Hong Wang, Gang Qiao, Zhidong Zhang
{"title":"Methylene blue mitigates lung injury in HCA rats by regulating macrophage pyroptosis via Nrf2/HO-1 and NLRP3 pathways.","authors":"Fuyan Ding, Hong Wang, Gang Qiao, Zhidong Zhang","doi":"10.17305/bb.2025.11851","DOIUrl":"10.17305/bb.2025.11851","url":null,"abstract":"<p><p>Methylene blue (MB) has antioxidant properties, yet its role in acute lung injury (ALI) induced by hypothermic circulatory arrest (HCA) remains unexplored. This study investigates MB's effects and underlying regulatory mechanisms in an HCA rat model. Rats received an intravenous bolus of MB (1 mg/kg) 15 min before HCA induction. Physiological parameters were monitored, and bronchoalveolar lavage fluid (BALF) was collected 2 h postoperatively to assess total protein levels, inflammatory cells, and cytokines. Histopathological lung damage was evaluated using hematoxylin-eosin (H&E) and TUNEL staining. Inflammatory markers and oxidative stress indicators were measured via ELISA and dihydroethidium (DHE) staining. Alveolar macrophages (AMs) were isolated to analyze polarization using flow cytometry and immunofluorescence double staining. Pyroptosis in AMs was detected with Yo-Pro-1 and Hoechst 33342 staining. Additionally, Western blotting was performed to examine the nuclear factor erythroid-2 related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, Nod-like receptor protein 3 (NLRP3) inflammasome, and pyroptosis-related proteins. Following HCA, rats exhibited significant blood gas abnormalities, structural lung damage, increased pathological scores, and higher apoptosis rates. However, MB mitigated these effects, improving physiological parameters and reducing lung histopathology scores. MB also lowered proinflammatory cytokine levels, increased SOD and GSH-Px activity, promoted AM polarization toward the M2 phenotype, and decreased pyroptosis. Mechanistically, MB activated the Nrf2/HO-1 pathway while inhibiting NLRP3 inflammasome activation. Notably, Nrf2 inhibitors and NLRP3 agonists weakened MB's protective effects by promoting inflammasome activation and pyroptosis, whereas Nrf2 agonists and NLRP3 inhibitors enhanced MB's beneficial impact. In conclusion, MB attenuates HCA-induced ALI by modulating AM polarization and pyroptosis via Nrf2/HO-1 pathway activation and NLRP3 inflammasome inhibition.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"2020-2034"},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12450078/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Function and mechanism of miRNAs during the process of Klebsiella pneumoniae infection: A review. 肺炎克雷伯氏菌感染过程中 miRNA 的功能和机制。
Biomolecules & biomedicine Pub Date : 2025-08-05 DOI: 10.17305/bb.2025.11421
Chuhan Zhang, Ge Li, Safi Ullah, Liang Liu, Huajie Zhao, Fan Yang, Liwei Guo, Duan Li
{"title":"Function and mechanism of miRNAs during the process of <i>Klebsiella pneumoniae</i> infection: A review.","authors":"Chuhan Zhang, Ge Li, Safi Ullah, Liang Liu, Huajie Zhao, Fan Yang, Liwei Guo, Duan Li","doi":"10.17305/bb.2025.11421","DOIUrl":"10.17305/bb.2025.11421","url":null,"abstract":"<p><p>Klebsiella pneumoniae (K. pneumoniae), a Gram-negative bacterium, is a major cause of nosocomial infections and can lead to severe, widespread infections. The rise of hypervirulent and multidrug-resistant K. pneumoniae presents significant challenges to public health. Diseases associated with K. pneumoniae, such as pneumonia, lung injury, peritonitis, and sepsis, have garnered increasing attention. MicroRNAs (miRNAs) are a class of short, endogenously expressed non-coding RNAs that regulate gene expression by inhibiting translation or promoting mRNA degradation. As key regulators of gene expression, miRNAs play a crucial role in K. pneumoniae infections by modulating host inflammatory pathways, suppressing inflammasome activity, regulating cytokine secretion, and facilitating post-translational modifications. Understanding miRNA alterations and their mechanisms during K. pneumoniae infections is of great significance. This comprehensive review explores the functions and mechanisms of miRNAs in K. pneumoniae-induced lung injury, peritonitis, and sepsis. By analyzing differential miRNA expression during infection, we aim to provide new insights and potential directions for future clinical diagnosis and treatment strategies for K. pneumoniae infections.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1919-1927"},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12450076/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Lymphocyte subsets predict mortality in acute paraquat poisoning. 淋巴细胞亚群预测急性百草枯中毒的死亡率。
Biomolecules & biomedicine Pub Date : 2025-08-05 DOI: 10.17305/bb.2025.11891
Qian Dong, Huan Xu, Pengjie Xu, Jiang Liu
{"title":"Lymphocyte subsets predict mortality in acute paraquat poisoning.","authors":"Qian Dong, Huan Xu, Pengjie Xu, Jiang Liu","doi":"10.17305/bb.2025.11891","DOIUrl":"10.17305/bb.2025.11891","url":null,"abstract":"<p><p>Paraquat (PQ) is a highly effective herbicide widely used in agricultural production, known for its strong herbicidal power, rapid action, and minimal environmental pollution. However, it is also highly toxic to humans and animals, with acute lung injury (ALI) being the primary cause of death. While the toxic mechanisms of PQ have been studied from various perspectives, its effects on lymphocytes and their subsets remain unclear. This study aimed to explore the relationship between lymphocyte dysfunction and mortality in acute PQ poisoning. A total of 92 patients with PQ poisoning who visited the emergency department of The Affiliated Lihuili Hospital of Ningbo University between January 1, 2016, and September 30, 2021, were included. Basic demographic and laboratory data within 24 h of admission were collected. Peripheral blood lymphocyte subsets were analyzed using flow cytometry. To identify independent risk factors for mortality, patients were followed up for 90 days. COX proportional hazards models and LASSO regression were applied to screen for predictive variables and develop a predictive model. All participants provided informed consent, and the study was approved by the relevant ethics committee. Among the 92 patients, 36 died. Compared with the survival group, the death group showed significantly higher white blood cell and neutrophil counts, lymphocyte counts, and CD4+/CD8+ T cell ratios, while the percentage of natural killer (NK) cells was significantly lower (P < 0.001). COX regression analysis identified these factors as independent risk factors for mortality: lymphocyte count: hazard ratio (HR) = 1.59; 95% confidence interval (CI), 1.02-2.47; P = 0.04 neutrophil count: HR = 1.12; 95% CI, 1.06-1.18; P = 0.04 CD4+/CD8+ T cell ratio: HR = 2.01; 95% CI, 1.03-3.92; P = 0.04 NK cell percentage: HR = 0.88; 95% CI, 0.82-0.95; P = 0.002. These findings suggest that lymphocyte count, neutrophil count, CD4+/CD8+ T cell ratio, and NK cell percentage are all associated with mortality in PQ poisoning cases.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"2058-2066"},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12450086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143460892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Enhanced membrane protein production in HEK293T cells via ATF4 gene knockout: A CRISPR-Cas9 mediated approach. 通过敲除ATF4基因增强HEK293T细胞膜蛋白的产生:CRISPR-Cas9介导的方法
Biomolecules & biomedicine Pub Date : 2025-08-05 DOI: 10.17305/bb.2024.11519
Byung-Jo Choi, Ba Reum Kim, Ho Joong Choi, Ok-Hee Kim, Say-June Kim
{"title":"Enhanced membrane protein production in HEK293T cells via <i>ATF4</i> gene knockout: A CRISPR-Cas9 mediated approach.","authors":"Byung-Jo Choi, Ba Reum Kim, Ho Joong Choi, Ok-Hee Kim, Say-June Kim","doi":"10.17305/bb.2024.11519","DOIUrl":"10.17305/bb.2024.11519","url":null,"abstract":"<p><p>HEK293T cells are extensively utilized for therapeutic protein production due to their human origin, which enables accurate post-translational modifications. This study aimed to enhance membrane protein production in HEK293T cells by knocking out the ATF4 gene using CRISPR-Cas9 technology. The ATF4 gene was edited by infecting HEK293T cells with a lentivirus carrying optimized single-guide RNA (ATF4-KO-3) and Cas9 genes. Comparative evaluations were conducted using all-in-one and two-vector systems. Genome sequencing and membrane protein productivity of ATF4-knockout (KO) cells were compared to wild-type (WT) cells using next-generation sequencing (NGS) and a membrane protein isolation kit, respectively. Single-cell analysis confirmed gene editing patterns, with NGS verifying the intended deletions. Membrane protein production was also assessed indirectly via flow cytometry, analyzing cells expressing Membrane-GFP. Compared to WT cells, ATF4-KO cells exhibited a significant increase in membrane protein production, with a 52.2 ± 19.0% improvement. Gene editing efficiency was compared between the two delivery systems, with the two-vector system demonstrating higher efficiency based on T7 endonuclease I assays. Western blot analysis confirmed ATF4 suppression and increased expression of membrane proteins, including E-cadherin and CD63. Quantitative analysis via PAGE revealed a 77.2 ± 30.6% increase in purified membrane protein yields, consistent with the observed enhancements. Flow cytometry using Membrane-GFP further demonstrated a 22.9 ± 9.7% increase in productivity. In summary, ATF4 knockout significantly enhances membrane protein production in HEK293T cells, offering potential improvements in biopharmaceutical manufacturing by enabling more efficient protein synthesis.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"1961-1971"},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12450088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048932","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
miR-542-3p attenuates corticosterone-induced hippocampal neuronal damage in depressive mice by modulating PTEN/AKT/GSK3β/β-catenin pathway. miR-542-3p 通过调节 PTEN/AKT/GSK3β/β-catenin 通路,减轻皮质酮诱导的抑郁小鼠海马神经元损伤。
Biomolecules & biomedicine Pub Date : 2025-08-05 DOI: 10.17305/bb.2025.11523
Ningbo Yang, Jie Li, Hongxia Hu, Xujiang Wang
{"title":"miR-542-3p attenuates corticosterone-induced hippocampal neuronal damage in depressive mice by modulating PTEN/AKT/GSK3β/β-catenin pathway.","authors":"Ningbo Yang, Jie Li, Hongxia Hu, Xujiang Wang","doi":"10.17305/bb.2025.11523","DOIUrl":"10.17305/bb.2025.11523","url":null,"abstract":"<p><p>Depression is a common psychological disease, and nerve injury is the key link of depression. The molecular mechanism involved in this link needs to be explored. miR-542-3p can reduce the degree of hippocampal neuronal damage in rats, but its mechanism in the neural damage of depression is still unclear. HT-22 cell injury was induced by corticosterone (CORT). After overexpression or knockdown of miR-542-3p, CORT-induced HT-22 cell injury was tested by cell counting kit-8 (CCK-8) assay, lactate dehydrogenase (LDH) assay and flow cytometry. Inflammatory and oxidative stress indicator levels were analyzed by kit and flow cytometry. The target genes of miR-542-3p were obtained by database analysis, and the targeting relationship between miR-542-3p and phosphatase and tensin homolog (PTEN) was explored based on dual luciferase assay. After PTEN overexpression or application of AKT pathway agonist MK-2206, the degree of cell damage, inflammation, and oxidative stress were detected again. CORT was used to induce depression in mice. Pathological changes of brain tissue structure and neuronal survival were observed by pathological staining. The miR-542-3p, PTEN, and AKT/GSK3β/β-catenin pathway protein levels in vivo and in vitro were detected by qRT-PCR and Western blot. Overexpression/knockdown of miR-542-3p alleviated/aggravated CORT-induced cell injury, inflammation, and oxidation levels in HT-22 cells (P < 0.05). Meanwhile, overexpressed miR-542-3p can reduce neurological damage of mice. miR-542-3p can target PTEN, and it can trigger the AKT/GSK3β/β-catenin pathway by targeting PTEN expression to reduce CORT-induced nerve injury (P < 0.05). miR-542-3p can reduce CORT-induced hippocampal neuronal damage by targeting PTEN and activating the AKT/GSK3β/β-catenin pathway.</p>","PeriodicalId":72398,"journal":{"name":"Biomolecules & biomedicine","volume":" ","pages":"2067-2082"},"PeriodicalIF":0.0,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12450084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Clinical profile and risk factors for respiratory failure in children with Mycoplasma pneumoniae infection. 肺炎支原体感染患儿呼吸衰竭的临床特点及危险因素
Biomolecules & biomedicine Pub Date : 2025-08-05 DOI: 10.17305/bb.2024.11641
Yanfei Wang, Limin Huang, Junjie Qian, Kelei Deng, Zihao Yang, Zhenjie Chen, Wei Li, Linhua Tan
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