Biocell最新文献

{"title":"Epibrassinolide Induces Apoptosis and Inhibits the Migration of Gastric Cancer AGS Cells by Regulating Reactive Oxygen Species-Mediated Signaling Pathways","authors":"Chang Wang, Zhibing Zhang, Wei Sun, Quan Quan, Wen-Shuang Hou, Chenghao Jin","doi":"10.32604/biocell.2025.062155","DOIUrl":"https://doi.org/10.32604/biocell.2025.062155","url":null,"abstract":"Objectives: Epibrassinolide (EBR) is a steroid hormone with anti-tumor properties. Nevertheless, its potential to inhibit gastric cancer (GC) cells remains unknown. The aim of this research was to examine the effects of EBR o... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 3","pages":"465-482"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147903672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pik3cb Antagonizes LPS/ATP-Induced Inflammatory Activation in Cardiomyocytes by Inhibiting the PI3K/AKT/NF-<b>κ</b>B/NLRP3 Signaling Axis","authors":"Xuekun Shao, Cheng Wang, Mengru Zhang, Yi Wang, Zhuoya Qiu, Wen Cai, Rui‐Liang Zhu, Ping Wang","doi":"10.32604/biocell.2025.070859","DOIUrl":"https://doi.org/10.32604/biocell.2025.070859","url":null,"abstract":"Objectives: PI3K plays a pivotal role in the inflammatory response by modulating the production and release of inflammatory factors. Pik3cb is one of the subunits of PI3K, and its specific role in myocardium inflammation remains unelucidated. This study aimed to investigate the role of Pik3cb in the inflammatory response and to elucidate the underlying mechanism. Methods: An inflammation model was established using H9c2 cells treated with LPS and ATP, and Pik3cb expression was evaluated in this model system. Subsequently, an overexpression model was constructed by transfecting cells with a Pik3cb overexpression plasmid, after which the effects of Pik3cb overexpression on the PI3K/AKT and NF-κB/NLRP3 inflammatory signaling pathways were assessed. Results: These analyses revealed that the expression and distribution of Pik3cb were significantly reduced in the LPS/ATP-induced cellular inflammation model group, whereas plasmid-mediated overexpression of Pik3cb significantly inhibited the activation of the PI3K/AKT signaling pathway in response to LPS/ATP stimulation. Additionally, the LPS/ATP-induced activation of the NF-κB/NLRP3 axis was significantly inhibited following Pik3cb overexpression. Conclusion: This study demonstrates that Pik3cb acts as a negative regulator of LPS/ATP-induced inflammation in cardiomyocytes, exerting anti-inflammatory effects by inhibiting the PI3K/AKT/NF-κB/NLRP3 signaling axis. These findings provide a potential therapeutic target for the treatment of myocardial inflammation.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 11","pages":"2181-2194"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147920527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of Lmx1a/NeuroD1 Mediates the Differentiation of Pulmonary Mesenchymal Stem Cells into Dopaminergic Neurons and Repairs Motor Dysfunction in Parkinson’s Disease Rats","authors":"Yiqin He, Cheng‐Hu Hu, Meng Xu, Rundong Ma, Kexin Duan, Yu Guo, Changqing Liu, Caiyun Ma, Gaofeng Liu, Chunjing Wang","doi":"10.32604/biocell.2025.064633","DOIUrl":"https://doi.org/10.32604/biocell.2025.064633","url":null,"abstract":"Background: Mesenchymal stem cells (MSCs) have shown great potential in treating neurodegenerative diseases, including Parkinson’s disease (PD), due to their ability to differentiate into neurons and secrete neurotrophic factors. Genetic modification of MSCs for PD treatment has become a research focus. Methods: In this study, rat pulmonary mesenchymal stem cells (PMSCs) were transduced with lentiviral vectors carrying Lmx1a/NeuroD1 to establish genetically engineered PMSCs (LN-PMSCs) and induce their differentiation into dopaminergic neurons. The LN-PMSCs were then transplanted into the right medial forebrain bundle region of PD model rats prepared using the 6-Hydroxydopamine (6-OHDA) method. Four weeks post-transplantation, the survival and differentiation of the cells in the brain and motor function of the PD rats were evaluated. Results: The results showed that after 12 days of induction, the genetically modified LN-PMSCs had differentiated into a large number of dopaminergic neurons. Four weeks post-transplantation, these cells significantly improved motor dysfunction in PD rats and promoted the expression of neuron marker TUJ1, dopaminergic neuron markers FOXA2 and TH, gamma-aminobutyric acid-ergic (GABAergic) neuron marker GABA, astrocyte marker GFAP, presynaptic marker SYN, and postsynaptic marker PSD95 in the transplantation area. Conclusion: Our findings suggest that the gene-engineered PMSCs cell line overexpressing Lmx1a and NeuroD1 (LN-PMSCs) transplantation could be a potential therapeutic strategy for treating PD.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 6","pages":"1037-1055"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147896943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophage polarization in cardiac transplantation: Insights into immune modulation and therapeutic approaches","authors":"Fang Chen, Yueping Li, Guoxing Ling, BAOSHI ZHENG, Cheng Luo, Jingwei Jiang, Bo Jia, Chuan Wang","doi":"10.32604/biocell.2024.056981","DOIUrl":"https://doi.org/10.32604/biocell.2024.056981","url":null,"abstract":"The role and regulatory mechanisms of macrophage polarization in cardiac transplantation have gained significant attention. Macrophages can polarize into either the M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotype in... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 1","pages":"61-78"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://cdn.techscience.press/files/biocell/2025/TSP_BIOCELL-49-1/Biocell-49-01-56981/Biocell-49-56981.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147900708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetramethylpyrazine Alleviates Pancreatitis Progression by Regulating Inflammation and Autophagy through the YAP-RIPK1-NF-<b>κ</b>B Axis","authors":"Hong Wu, Yang Liu","doi":"10.32604/biocell.2025.069527","DOIUrl":"https://doi.org/10.32604/biocell.2025.069527","url":null,"abstract":"Background: Acute pancreatitis (AP) is a serious gastrointestinal disorder. Tetramethylpyrazine (TMP), a bioactive alkaloid extracted from Ligusticum chuanxiong, exhibits various pharmacological effects, but its protective mechanisms against AP remain unclear. This study aimed to investigate the protective effects and underlying mechanisms of TMP in AP. Methods: The study utilized Cerulein (CER) to model pancreatitis across experimental systems. Cellular responses were characterized through functional assays (CCK-8 viability, EdU proliferation, Transwell migration, flow cytometric apoptosis, Fluo-3/AM calcium imaging) and inflammatory profiling (ELISA for trypsin, CRP, TNF-α, IL-1β, IL-6). Autophagy was monitored via mRFP-GFP-LC3 flux and LysoTracker staining, with parallel LDH measurements. Mechanistic studies examined autophagy-related proteins (LAMP-1, p62, LC3) and YAP-RIPK1-NF-κB signaling intermediates by Western blot, supported by YAP genetic manipulation. In vivo assessments included HE-stained histology, TUNEL apoptosis detection, and MPO-based neutrophil evaluation. Results: TMP dose-dependently improved CER-induced cell viability and ATP levels, inhibited cell apoptosis, reduced Ca2+ concentration, LDH release, and inflammatory responses (trypsin, CRP, TNF-α, IL-1β, IL-6, and NLRP3). TMP also upregulated LAMP-1 protein expression, downregulating p62, Beclin-1, Atg5, LC3 protein levels, promoting autophagosome-lysosome fusion, and enhancing lysosomal activity, thus alleviating pancreatic damage. Additionally, TMP inhibited YAP, RIPK1, and NF-κB p65 phosphorylation, with YAP knockdown enhancing TMP effects while YAP overexpression partially counteracted TMP actions. In the rat AP model, TMP significantly improved tissue pathological changes, reduced inflammatory infiltration and cell apoptosis, decreased serum inflammatory marker levels, and inhibited YAP-RIPK1-NF-κB axis activation. Conclusion: This study reveals that TMP alleviates AP progression by inhibiting YAP-RIPK1-NF-κB axis activation, achieving dual effects of anti-inflammation and promoting autophagy.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"0 0","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147909733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eosinophils in Rheumatoid Arthritis: A Multifaceted Role in the Pathogenesis of the Disease.","authors":"Alexander Blagov, Michael Bukrinsky, Aleksandra Utkina, Gulalek Babayeva, Vasily Sukhorukov, Alexander Orekhov","doi":"10.32604/biocell.2025.062821","DOIUrl":"10.32604/biocell.2025.062821","url":null,"abstract":"<p><p>Eosinophils are multifunctional granulocytes that contribute to the initiation and modulation of inflammation. Accumulating evidence suggests that eosinophils are adaptable leukocytes that orchestrate the resolution of inflammatory responses. The most prevalent chronic inflammatory illness, rheumatoid arthritis (RA), is typified by persistent synovitis that makes it hard for the disease to go away on its own. Interestingly, a unique subset of eosinophils known as regulatory eosinophils has been found in RA patients' synovium, especially while the disease is in remission. Pro-resolving signatures of regulatory eosinophils in the synovium are distinct from those of their lung counterparts. The most recent research on eosinophils and their function in this disease pathogenesis is compiled in this review. Based on the role of regulatory eosinophils, a new pathological model of inflammation resolution in RA is proposed, and potential therapeutic strategies aimed at enhancing the action of regulatory eosinophils in RA are proposed.</p>","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 7","pages":"1135-1140"},"PeriodicalIF":1.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12333626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144818363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic actions of terpenes in neurodegenerative disorders and their correlations with the regulation and remodeling of the extracellular matrix","authors":"Renata da Silva Carneiro, Mateus Henrique de Almeida da Costa, José Maria Santos, Anderson Nogueira Mendes, Valdiléia Teixeira Uchôa, LUCIANO DA SILVA LOPES","doi":"10.32604/biocell.2024.058405","DOIUrl":"https://doi.org/10.32604/biocell.2024.058405","url":null,"abstract":"Neurodegenerative diseases are a major public health challenge, mainly affecting the elderly population and compromising their cognitive, sensory, and motor functions. Currently, available therapies focus on alleviating symp... | Find, read and cite all the research you need on Tech Science Press","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 1","pages":"109-125"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147917104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect and Mechanism of Thalidomide in Ameliorating Crohn’s Disease-Related Intestinal Fibrosis","authors":"Xiaoyue Feng, Yu Liu, Ying Kang, Juan Wei, Bei Yuan, Kang Jiang, Weijun Xu, Xinyi Xia, Fangyu Wang","doi":"10.32604/biocell.2025.066504","DOIUrl":"https://doi.org/10.32604/biocell.2025.066504","url":null,"abstract":"Objectives: A common side effect of inflammatory bowel disease (IBD) is intestinal fibrosis, which frequently leads to intestinal blockage and stricture formation. Although Thalidomide (THD) has shown anti-fibrotic benefits in hepatic and renal models, little is known about how it affects intestinal fibrosis and the underlying processes. The present research examines the molecular targets of THD and its potential as a treatment for intestinal fibrosis brought on by colitis. Methods: Clinical samples from Crohn’s disease (CD) patients with intestinal strictures treated with infliximab (IFX) and THD combined with IFX were collected. Dextran sulfate sodium (DSS) was used to develop a mouse model of intestinal fibrosis in C57BL/6 mice. Anti-tumor necrosis factor-alpha (Anti-TNFα), THD, or a combination of the two were administered to the mice. Body weight, colon length, histology, and disease activity index were used to evaluate the disease’s severity. In vitro, THD was tested on colonic fibroblast lines (CCD-18Co and MPF) to assess its effects on cell proliferation, motility, and transdifferentiation. To examine changes in gene expression and signaling pathway modifications, namely in the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway, RNA sequencing, qRT-PCR, and Western blotting were carried out. Results: In DSS-induced colitis, THD therapy lowered fibrosis, as seen by downregulated fibrotic markers (α-smooth muscle actin (α-SMA), collagen I, and collagen III) and decreased collagen deposition. Mechanistically, THD prevented fibroblasts from transdifferentiating and decreased their vitality. Furthermore, THD inhitited the PI3K/AKT/mTOR pathway in vivo and in vitro. Conclusion: THD inhibits the PI3K/AKT/mTOR signaling cascade and suppresses colonic fibroblast transdifferentiation, which protects against DSS-induced colitis-associated fibrosis, especially when combined with anti-TNFα therapy.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 8","pages":"1505-1528"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147892679","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BMP-2 Inhibits the Inflammatory Response and Promotes Bone Formation in Rats with Femoral Fracture by Activating the AMPK Signaling Pathway","authors":"Yong Huang, Xiandeng Li, Qingling Jing, Qin Zhang, Chungui Huang","doi":"10.32604/biocell.2025.072716","DOIUrl":"https://doi.org/10.32604/biocell.2025.072716","url":null,"abstract":"Objective: Mesenchymal stem cells (MSCs) are important cells in bone tissue engineering. Bone morphogenetic protein-2 (BMP-2) effectively treats bone defects and nonunion. The purpose of this study is to investigate whether BMP-2 promotes bone formation and femoral fracture healing by inhibiting inflammation and promoting osteogenic differentiation of MSCs, in order to provide an experimental basis for developing more efficient fracture treatment strategies. Methods: Bone marrow-derived MSCs (BMSCs) were isolated from rats and treated with OE-BMP-2, the 5′-adenosine monophosphate-activated protein kinase (AMPK) signal agonist 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), and the inhibitor Compound C. Osteogenic differentiation was evaluated through an alkaline phosphatase (ALP) kit, Western blot, and Alizarin Red S (ARS) staining. A rat model of femoral fracture was constructed, and fracture healing in the rats was detected by X-ray, microcomputed tomography (CT), and pathological staining. The AMPK signaling pathway and inflammation levels in the BMSCs and fracture model rats were measured by Western blot and enzyme-linked immunosorbent assay (ELISA) kits. Results: After BMP-2 overexpression, the ALP activity in osteogenic BMSCs was significantly increased (increased to 253.64%), the levels of osteogenic differentiation proteins (Osterix and osteocalcin) and p-AMPK Thr172 protein were significantly increased, and the concentrations of inflammatory factors were decreased. In rat fracture tissues, BMP-2 overexpression promoted the expression of p-AMPK Thr172 protein and bone callus formation, increased bone volume (increased to 22.22%), reduced the number of fibrous components in the cartilage matrix, increased the numbers of osteoblasts and chondrocytes, increased the expression of osteogenic differentiation proteins, and reduced the content of inflammatory factors in the serum. After AICAR intervention, ALP activity and the expression of osteogenic differentiation proteins in BMSCs and fracture tissues further increased, and the level of inflammation decreased. However, the changes in osteogenic differentiation and inflammation levels were significantly reversed after Compound C intervention. Conclusion: BMP-2 activated the AMPK signaling pathway, inhibited the inflammatory response, and effectively promoted the osteogenic differentiation of BMSCs and femoral fracture healing in rats.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"49 11","pages":"2195-2216"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147909898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Curcumin inhibits colorectal cancer development by blocking the YAP/TAZ signaling axis","authors":"Fei Sha, DAISHAN XIN, Jun Xu, ZHIWEI ZHENG, Wen Qing Lin, XIAORUI CAI, Fei Lin, Minghao Zheng, JIAOLING CHEN","doi":"10.32604/biocell.2023.029188","DOIUrl":"https://doi.org/10.32604/biocell.2023.029188","url":null,"abstract":"Background: Curcumin is a plant polyphenol with antitumor properties and inhibits the development of colorectal cancer (CRC). However, as the molecular mechanism associated is still unclear, our study aimed to explore the underlying molecular mechanisms by which curcumin inhibits CRC. Methods: HT29 and SW480 cells were treated with curcumin or/and Doxycycline (DOX), and cell viability, colony forming ability, migration and invasion were confirmed by cell counting kit-8 (CCK-8), colony forming, Transwell assays. And Yes-associated protein 1 (YAP) and PDZ-binding motif (TAZ) signaling-related genes or proteins were analyzed using reverse transcription quantitative real-time PCR (RT-qPCR), western blot, and immunofluorescence assays. Then nude mice xenograft tumor model was constructed, YAP and Ki67 expressions were tested by immunohistochemistry (IHC) staining. Results: In our study, we proved that curcumin significantly inhibited the CRC cell viability, cell migration, and cell invasion abilities. In addition, curcumin inhibited YAP and Transcriptional coactivator with TAZ or the YAP/TAZ signaling axis in CRC cells. Further, in the nude mice model, curcumin treatment significantly decreased the size and weight of xenotransplant tumors. Conclusion: Therefore, curcumin significantly inhibited CRC development and invasion by regulating the YAP/TAZ signaling axis.","PeriodicalId":55384,"journal":{"name":"Biocell","volume":"48 3","pages":"443-451"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.techscience.com/biocell/online/detail/20035/pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147894614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}