Frontiers in bioscience (Landmark edition)最新文献

{"title":"Historical View and Some Unsolved Problems in Red Blood Cell Membrane Research.","authors":"Ingolf Bernhardt, Lars Kaestner","doi":"10.31083/FBL25331","DOIUrl":"https://doi.org/10.31083/FBL25331","url":null,"abstract":"<p><p>The article provides a comprehensive overview of biological membrane lipid composition and distribution and ion transport processes, focusing particularly on red blood cells (RBCs). It begins with a historical perspective, detailing the introduction of the terms 'cell' and 'membrane' in biological sciences, and the development of the fluid-mosaic model of membrane structure. Early findings on ion transport highlighted the non-equilibrium distribution of Na⁺ and K⁺ across cell membranes, leading to the discovery of the Na⁺/K⁺ pump. The article delves into the lipid composition of RBC membranes, emphasising the roles of various lipids, including cardiolipin, and the concept of lipid rafts. These rafts, enriched with sphingolipids and cholesterol, play crucial roles in cellular processes. Variations in RBC shapes are discussed, with biophysical theories explaining transformations and pathological conditions affecting RBC morphology, such as sickle cell anaemia. Na⁺ and K⁺ transporters in RBC membranes are explored, highlighting the almost ubiquitous presence of the Na⁺/K⁺ pump (absent in Carnivora RBCs) and various ion channels, including the Gárdos and Piezo1 channels. The article notes species-specific differences in ion transport mechanisms and the activation or suppression of transporters during RBC maturation. The mechanism of residual ion transport is examined, questioning whether a Na⁺(K⁺)/H⁺ antiporter exists in the human RBC membrane. Residual ion fluxes are mediated by this antiporter, influenced by the fatty acid composition of the RBC membrane. The outlook section underscores the need for further research to fully understand the complexities of RBC membrane structure and function, suggesting that many questions remain unanswered despite significant advances.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 3","pages":"25331"},"PeriodicalIF":3.3,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Scutellarin Attenuates Pro-Inflammatory Foam Cell Formation and Facilitates M2 Polarization in Microglia during Copper Homeostasis Imbalance via the MAPK Signaling Pathway.","authors":"Qiting Zhao, Lingyi Chen, Yantuanjin Ma, Shufen Wang","doi":"10.31083/FBL36255","DOIUrl":"https://doi.org/10.31083/FBL36255","url":null,"abstract":"<p><strong>Background: </strong>Clinical and experimental evidence indicates that copper has the ability to promote the progressive development of demyelinating diseases such as multiple sclerosis. Microglia-mediated neuroinflammation is believed to play a crucial role in this process. Scutellarin, a flavonoid compound, has anti-inflammatory, antioxidative, and neuroprotective effects.</p><p><strong>Aim: </strong>We investigated the effect of scutellarin on copper-induced inflammatory foam cell formation in microglia.</p><p><strong>Methods: </strong>We exposed BV2 murine microglial cells to copper, then collected the conditioned medium and co-cultured it with MO3.13 human glial cells to mimic myelin damage <i>in vitro</i>. The Cell Counting kit-8 assay, quantitative (polymerase chain reaction) PCR, enzyme-linked immunosorbent assay, Luxol fast blue staining, and western blotting were used to detect the cell phenotype. To investigate whether exposure of BV2 cells to copper can cause neurotoxicity and indirect damage to myelin cells, we determined whether BV2 cells promote inflammation through foam cell formation by oil red O staining and detection of malondialdehyde (MDA) content. Finally, we treated cells with scutellarin to investigate its therapeutic effects.</p><p><strong>Results: </strong>Exposure to copper activated the pro-inflammatory phenotype of microglia, as assessed by measuring the transcription of M1/M2-related biomarkers. In addition, increased copper intake by microglia promoted intracellular lipid accumulation and oxidation, facilitating foam cell formation. Rescue experiments showed that copper chelator ammonium tetrathiomolybdate (ATTM) and the lipid oxidation inhibitor ferrostatin-1 (Fer-1) significantly inhibited copper-induced inflammation, reduced intracellular lipid accumulation and MDA levels, and decreased foam cell formation. Moreover, copper-induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) in microglia led to a shift towards the M1 phenotype and foam cell transformation, which were effectively inhibited by ATTM, Fer-1, and the p38 MAPK inhibitor SB203580. Lastly, after treatment with scutellarin, copper-induced foam microglia exhibited inhibited p38 MAPK phosphorylation, increased production of neurotrophic factors, decreased expression of inflammatory mediators, reduced lipid accumulation, and induced polarization towards the M2 phenotype.</p><p><strong>Conclusions: </strong>Here, we demonstrated that copper can induce microglia to damage myelinating cells, with the key mechanism involving the phosphorylation of p38 MAPK. Scutellarin partially reversed the positive effects of copper on promoting microglial M1 polarization, lipid deposition, and lipid oxidation by mediating the p38 MAPK signaling pathway. Taken together, these results suggest that scutellarin may be a promising drug for the treatment of demyelinating diseases such as multiple sclerosis.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 3","pages":"36255"},"PeriodicalIF":3.3,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of Atoh8 Affects Neurocranial and Axial Skeleton Development in Zebrafish.","authors":"Ninfa Fragale, Satya Srirama Karthik Divvela, Victoria Clare Williams-Ward, Beate Brand-Saberi","doi":"10.31083/FBL26806","DOIUrl":"https://doi.org/10.31083/FBL26806","url":null,"abstract":"<p><strong>Background: </strong>The basic helix-loop-helix (bHLH) transcription factor atonal homologue 8 (Atoh8) has been implicated in various developmental and physiological processes by means of transient knockdown and conditional knockout approaches in zebrafish, chick and mouse. Despite its demonstrated involvement in multiple tissues, the role of Atoh8 remains elusive in zebrafish. A recent permanent knockout study in zebrafish investigated the role of Atoh8 on the background of previous morpholino studies which demonstrated various developmental defects but could not find any of the morpholino-based effects in the mutant. In mice, a knockout study demonstrated involvement of the transcription factor in skeletal development, showing that disruption of the <i>atoh8</i> gene results in reduction of skeletal size. We investigated a mutant fish line generated using clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) (CRISPR/Cas9)-technology for possible phenotypic effects on zebrafish skeletogenesis.</p><p><strong>Methods: </strong>Here, we present a CRISPR/Cas9-generated <i>atoh8</i> permanent zebrafish mutant and investigate the phenotypic effects of the knockout on the developing zebrafish craniofacial and axial skeleton. We investigated the expression pattern of the gene in wildtype and conducted detailed morphometric analysis for a variety of bone and cartilage elements of the developing skeleton at 12 days post fertilisation (dpf) in zebrafish siblings from a heterozygous mating using detailed morphometric measurements and statistical analysis of the results.</p><p><strong>Results: </strong>Homozygous mutants are viable into late adulthood and show no overt morphological phenotype. Despite the prominent appearance of <i>atoh8</i> signal in various embryonic and larval craniofacial and axial skeletal structures, detailed morphometric analysis revealed only subtle phenotypic effects of the mutation on skeletal development in zebrafish. We found the formation of the orbital cartilages of the developing neurocranium and the progress of chordacentra mineralisation to be negatively affected by loss of the transcription factor.</p><p><strong>Conclusions: </strong>Despite the very subtle phenotypic effect of our mutation, we were able to show involvement of <i>atoh8</i> in the skeletal development of zebrafish. We attribute the mild phenotype to a compensatory mechanism induced by nonsense-mediated degradation of messenger ribonucleic acid (mRNA) as suggested in the recent literature. The effect of <i>atoh8</i>-disruption on zebrafish skeletal development suggests that the loss of <i>atoh8</i> cannot be compensated for at interfaces where more than one embryonic cell lineage contributes to bone and cartilage formation.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 3","pages":"26806"},"PeriodicalIF":3.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"cGAS/STING/NLRP3 Signaling Pathway-Mediated Pyroptosis in Hypertrophic Cardiomyopathy Radiotherapy.","authors":"Huiyang Li, Xin Wang, Xinping Luo, Haiming Shi, Jian Li","doi":"10.31083/FBL26084","DOIUrl":"https://doi.org/10.31083/FBL26084","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Radiotherapy is a commonly employed treatment modality for cancer; however, its radiobiological effects in hypertrophic cardiomyopathy (HCM) remain unclear. Radiation exposure activates the cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) synthase (cGAS)-stimulator of interferon genes (STING) pathway, which is functionally associated with the activation of NOD-like Receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasomes, known mediators of pyroptotic cell death. Nonetheless, the underlying mechanism requires further investigation. Therefore, the objective of this study is to elucidate the role of the cGAS/STING/NLRP3 pathway in the process of cardiomyocyte pyroptosis during radiotherapy for HCM.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Transverse aortic constriction surgery was conducted to establish a mouse model of pressure overload-induced HCM, followed by the administration of 30 Gray (Gy) radiation one-week post-surgery. Cardiac morphology and function were evaluated through echocardiographic techniques. Hematoxylin & Eosin staining, along with Wheat Germ Agglutinin (WGA) staining, were utilized to quantify the cross-sectional area of cardiomyocytes and the degree of left ventricular hypertrophy. The HL-1 mouse cardiac muscle cell line was subjected to 40 Gy of radiation using an X-ray irradiator to establish an &lt;i&gt;in vitro&lt;/i&gt; model of HCM, with or without the application of the NLRP3 inhibitor MCC950 and cGAS overexpression. Various assays, including the Cell Counting Kit-8 (CCK8), enzyme-linked immunosorbent assay (ELISA), and 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimi- dazolylcarbocyanine iodide (JC-1) probe assays, were performed to assess cell viability, the concentrations of Interleukin (IL)-1β, IL-18, and cGAMP, as well as mitochondrial membrane potential. The morphology of cell membranes and mitochondria was analyzed using scanning electron microscopy (SEM) and fluorescence &lt;i&gt;in situ&lt;/i&gt; hybridization (FISH) dual labelling techniques. The expression levels of cGAS, STING, and NLRP3 were evaluated through by western blot analysis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Radiotherapy reduced cardiac hypertrophy, improved cardiac function, and decreased fibrotic changes in HCM mice when compared to control groups. The application of radiation resulted in pyroptosis in HL-1 cells and a reduction in cell viability; this effect that was alleviated by the inhibition of NLRP3, while overexpression of cGAS exacerbated the situation. Furthermore, radiation led to a decline in mitochondrial membrane potential and the leakage of mitochondrial DNA into the cytoplasm, which activated the cGAS-STING signaling pathway, thereby initiating pyroptosis. This activation was corroborated by elevated levels of pyroptosis-associated proteins, including cGAS, STING, NLRP3, caspase-1, Gasdermin D (GSDMD), cGAMP, IL-18, and IL-1β. Notably, the inhibition of NLRP3 effectively abolished the upregulation of IL-1","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 3","pages":"26084"},"PeriodicalIF":3.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD47 Contributes to the Proliferation of Breast Cancer.","authors":"Junbin Wang, Xia Wu, Xuejian Liu, Ying Xu","doi":"10.31083/FBL28210","DOIUrl":"https://doi.org/10.31083/FBL28210","url":null,"abstract":"<p><strong>Background: </strong>The <i>CD47</i> molecule (<i>CD47</i>) performs a novel role in regulating immunoreactions by binding to signal-regulatory protein alpha (<i>SIRPα</i>), resulting in the tumorigenesis of multiple malignant neoplasms. However, its effects and mechanisms in breast cancer (BC) remain unknown.</p><p><strong>Methods: </strong>To explore the molecular mechanisms and explicit impacts of CD47, we screened two databases for <i>CD47</i>-associated signaling pathways and cellular functions. BC samples and patients' basic information were collected to identify the statistical significance of <i>CD47</i> expression. We also constructed experiments to validate the regulatory role of <i>CD47</i> in BC cell proliferation.</p><p><strong>Results: </strong>Analysis of the TCGA-BRCA, GSE42568, and GSE15852 datasets demonstrated an elevated level of <i>CD47</i> in BC tissues. A Venn diagram revealed 11,194 co-expressed genes, and pathway analysis linked elevated <i>CD47</i> levels to critical signaling pathways, such as cytokine-receptor interactions and Janus kinase/signal transducer and activator of transcription (<i>JAK/STAT</i>) signaling, which are integral to cell proliferation and invasiveness. Clinical data from 108 BC specimens showed that <i>CD47</i> localization was primarily membranous, with higher levels correlating with proliferation marker Ki-67 (<i>Ki-67</i>) expression (<i>p</i> < 0.0001) and advanced tumor/node/metastasis (TNM) stage (<i>p</i> < 0.0001). Additionally, functional assays demonstrated that <i>CD47</i> depletion reduced cell viability (<i>p</i> < 0.01), migration (<i>p</i> < 0.001), and invasion (<i>p</i> < 0.05 in 4T1 cells; <i>p</i> < 0.001 in MDA-MB-231 cells) <i>in vitro</i> and led to smaller tumor volumes (<i>p</i> < 0.0001) <i>in vivo</i>.</p><p><strong>Conclusion: </strong><i>CD47</i> is a key regulator of BC cell proliferation and invasiveness and serves as a potential marker for assessing tumor aggressiveness and guiding therapeutic strategies.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 3","pages":"28210"},"PeriodicalIF":3.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune Imbalance in Primary Membranous Nephropathy at Single-cell Resolution.","authors":"Xuan Tie, Zhiang Chen, Shulei Yao, Binxin Wu, Bingjuan Yan, Huifang Zhai, Xi Qiao, Xiaole Su, Lihua Wang","doi":"10.31083/FBL36332","DOIUrl":"https://doi.org/10.31083/FBL36332","url":null,"abstract":"<p><strong>Background: </strong>Primary membranous nephropathy (pMN) often progresses to end-stage renal disease (ESRD) in the absence of immunosuppressive therapy. The immunological mechanisms driving pMN progression remain insufficiently understood.</p><p><strong>Methods: </strong>We developed a single-cell transcriptomic profile of peripheral blood mononuclear cells (PBMCs) from 11 newly-diagnosed pMN patients and 5 healthy donors. Through correlation analysis, we identified potential biomarkers for disease stratification and poor prognosis.</p><p><strong>Results: </strong>Expression levels of several proinflammatory factors were significantly increased in patients compared to healthy donors, such as interleukins (<i>IL1B</i>, <i>IL8</i>, and <i>IL15</i>) and interferon G (<i>IFNG</i>). Multiple pattern recognition receptors involved in proinflammatory signaling were also upregulated in patients, including NOD-like receptors (NLRs) (<i>NLRP1</i>, <i>NLRP3</i>, and <i>NLRC5</i>), RNA helicases (<i>DDX58</i>, <i>IFIH1</i>, <i>DHX9</i>, and <i>DHX36</i>), <i>cGAS</i> (cyclic GMP-AMP synthase) and <i>IFI16</i> (interferon gamma inducible protein 16). Additionally, human leukocyte antigen molecules <i>HLA-DQA1</i> and <i>HLA-DRB1</i> enriched in memory B cells were upregulated in patients. More importantly, we found that the genes for antiviral defense response were significantly elevated in high-risk patients relative to the low-risk group. More than twenty genes were negatively correlated with estimated glomerular filtration rate (eGFR), such as <i>BST2</i> (bone marrow stromal cell antigen 2) and <i>SLC35F1</i> (solute carrier family 35 member F1). Their predicted values were confirmed in a larger population with nephrotic syndrome or other chronic kidney diseases from a public database. Furthermore, we developed a series of scoring systems for distinguishing high-risk patients from low- and moderate-risk individuals.</p><p><strong>Conclusions: </strong>Our study provides insight into the immunological mechanism of pMN and identifies numerous biomarkers and signaling pathways as potential therapeutic targets for managing the progression of high-risk pMN.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"36332"},"PeriodicalIF":3.3,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Innovative Gastrointestinal Drug Delivery Systems: Nanoparticles, Hydrogels, and Microgrippers.","authors":"Haiming Chen, Waliul Islam, Jessica El Halabi, Ling Li, Florin M Selaru","doi":"10.31083/FBL25281","DOIUrl":"https://doi.org/10.31083/FBL25281","url":null,"abstract":"<p><p>Over the past decade, new technologies have emerged to increase intrinsic potency, enhance bioavailability, and improve targeted delivery of drugs. Most pharmaceutical formulations require multiple dosing due to their fast release and short elimination kinetics, increasing the risk of adverse events and patient non-compliance. Due to these limitations, enormous efforts have focused on developing drug delivery systems (DDSs) for sustained release and targeted delivery. Sustained release strategies began with pioneering research using silicone rubber embedding for small molecules and non-inflammatory polymer encapsulation for proteins or DNA. Subsequently, numerous DDSs have been developed as controlled-release formulations to deliver systemic or local therapeutics, such as small molecules, biologics, or live cells. In this review, we discuss the latest developments of DDSs, specifically nanoparticles, hydrogels, and microgrippers for the delivery of systemic or localized drugs to the gastrointestinal (GI) tract. We examine innovative DDS design and delivery strategies tailored to the GI tract's unique characteristics, such as its extensive length and anatomical complexity, varying pH levels and enzymatic activity across different sections, and intrinsic peristalsis. We particularly emphasize those designed for the treatment of inflammatory bowel disease (IBD) with <i>in vivo</i> preclinical studies.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"25281"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of scRNA-seq in Dental Research: Seeking Regenerative Clues From the Structure of Tooth and Periodontium in Physical or Pathological States.","authors":"Xixi Miao, Yufen Huang, Kelsey Xingyun Ge, Yunlong Xu","doi":"10.31083/FBL26200","DOIUrl":"https://doi.org/10.31083/FBL26200","url":null,"abstract":"<p><p>This review presents a comprehensive overview of single-cell RNA sequencing (scRNA-seq) analyses used to study tooth and periodontal tissues. The intricate cellular composition of both teeth and periodontium are revealed, leading to the identification of new cell types and tracing lineage profiles for each cell type. Herein, we summarize the progression of dental and periodontal tissue formation, tooth homeostasis, and regenerative mechanisms. scRNA-seq analyses have demonstrated that the cellular constituent ratio of dental and periodontal tissues transforms homeostasis or injury repair. Importantly, single-cell data in the diseased tissue demonstrated a change in both cell types and intercellular communication patterns compared to the normal state. These findings provide valuable insights into the underlying disease mechanisms at the cellular level in the context of single-cell vision, thereby facilitating the investigation of potential therapeutic interventions.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"26200"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of PI3K/AKT/GLUT1 Signaling Pathway by Quercetin in the Treatment of Psoriasis.","authors":"Jie Ma, Feifei Wang, Lei Wang, Ying Wang, Doudou Wu, Wenbo Jiang, Nuo Li, Yanping Bai","doi":"10.31083/FBL26884","DOIUrl":"https://doi.org/10.31083/FBL26884","url":null,"abstract":"<p><strong>Background: </strong>Psoriasis is an enduring inflammatory skin disorder defined by recurring attacks, distinguished primarily by red patches and scaly skin. Quercetin, a kind of natural flavonoid compound, is widely found in various vegetables, fruits, and Chinese herbs. Quercetin is a multifaceted compound with a wide range of potential health benefits. In addition to antioxidant, cardiovascular protection, and anti-tumor effects, quercetin has shown potential in regulating immune and inflammation effects. In the initial stages, <i>in vivo</i> studies have demonstrated that quercetin positively affects psoriasis and is connected with the phosphatidylinositol 3-kinase (PI3K)/Protein Kinase B (AKT)/glucose transporter 1 (GLUT1) signaling. Nevertheless, the precise mechanism by which quercetin influences the PI3K/AKT/GLUT1 signaling cascade in the context of psoriasis remains uncertain.</p><p><strong>Objective: </strong>The aim of this study was to investigate the potential therapeutic influence of quercetin on psoriasis and the relationship with the PI3K/AKT/GLUT1 signaling pathway.</p><p><strong>Methods: </strong>A mouse model for psoriasis induced by imiquimod was employed to assess alterations in the morphology of skin lesions and their histopathological characteristics. Cell Counting kit-8 (CCK-8) assay was used to assess the impact of proliferation of HaCaT human keratinocyte cells. HaCaT cells were examined using flow cytometry for the influence of quercetin on apoptosis. Additionally, Western blot analysis was used to evaluate the protein expression levels in the PI3K/AKT/GLUT1 signaling pathway.</p><p><strong>Results: </strong>concerning pathological alterations, the mice in the model group exhibited characteristic alterations associated with psoriasis. The extent of excessive keratinization in the epidermis and hypertrophy of the spinous layer observed in each quercetin dosage group was less pronounced compared to the model group. The CCK-8 assay laid out that quercetin can suppress the proliferation of HaCaT cells. Furthermore, it was found that quercetin facilitates the apoptosis of these cells. Analysis of immunoblotting demonstrated that the intervention of quercetin in HaCaT cells led to modifications in the proteins related to the PI3K/AKT/GLUT1 signaling pathway.</p><p><strong>Conclusion: </strong>Through <i>in vivo</i> and <i>in vitro</i> experiments, this study shows that quercetin may play a therapeutic role in psoriasis and inhibit the PI3K/AKT/GLUT1 signaling pathway.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"26884"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction: Gu <i>et al.</i> Lonicerin prevents inflammation and apoptosis in LPS-induced acute lung injury. Frontiers in Bioscience (Landmark Edition). 2020; 25: 480-497.","authors":"","doi":"10.31083/FBL38385","DOIUrl":"https://doi.org/10.31083/FBL38385","url":null,"abstract":"","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 2","pages":"38385"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}