Cell Biology International最新文献

{"title":"Alagille Syndrome: Unraveling the Complexities of Genotype-Phenotype Relationships and Exploring Avenues for Improved Diagnosis and Treatment.","authors":"Priya Sharma, Deepti Abbey","doi":"10.1002/cbin.70009","DOIUrl":"https://doi.org/10.1002/cbin.70009","url":null,"abstract":"<p><p>Alagille syndrome (ALGS) is a rare genetic disorder caused by mutations in the JAG1 and NOTCH2 genes, leading to a wide range of clinical manifestations. This review explores the complex genetic and clinical landscape of ALGS, emphasizing the challenges in understanding genotype-phenotype relationships due to its rarity and the lack of suitable research models. The review projects a clinical overview of the disease, emphasizing the influence of potential gene modifiers on its clinical presentation and the lack of mechanistic studies for over 100 mutations identified in the last 24 years from various populations, representing a significant gap in our current knowledge and advocating for further exploration. The review addresses the diagnostic challenges posed by the variable expressivity and overlapping symptoms of ALGS. It summarizes current treatment options and discusses emerging approaches such as antisense oligonucleotides (ASOs) and gene therapies. Further, the need for improved diagnostic tools, a deeper understanding of the underlying mechanisms, and the development of targeted therapies are emphasized using zebrafish and mice models, as well as genome editing for variant analysis and stem cell organoid models for disease modeling and drug discovery. The importance of cohort-based studies in understanding the natural history and outcomes of ALGS in diverse populations is highlighted. The review concludes by emphasizing the need for multi-disciplinary collaborative research to address the challenges in ALGS diagnosis, prognosis, and treatment, particularly for underrepresented populations.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556009","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Different In Vitro Models of Chronic Myeloid Leukemia Show Different Characteristics: Biological Replicates Are Not Biologically Equivalent.","authors":"Alessia Cavalleri, Besjana Xhahysa, Silvia Mutti, Rosalba Monica Ferraro, Elena Laura Mazzoldi, Mirko Farina, Alessandro Leoni, Luca Garuffo, Federica Trenta, Federica Re, Vera Radici, Eugenia Accorsi Buttini, Enrico Morello, Gabriele Magliano, Valeria Cancelli, Silvia Clara Giliani, Michele Malagola, Domenico Russo, Simona Bernardi","doi":"10.1002/cbin.70007","DOIUrl":"https://doi.org/10.1002/cbin.70007","url":null,"abstract":"<p><p>Chronic Myeloid Leukemia (CML) is characterized by the BCR::ABL1 fusion gene, driving uncontrolled myeloid cell proliferation. Furthermore, metabolic dysregulation contributes to disease progression. Despite the efficacy of tyrosine kinase inhibitors (TKIs), unresolved clinical needs persist, necessitating refined preclinical models. This study compared responses of three commonly used CML cell lines (K562, LAMA84, KCL22) to five TKIs (imatinib, nilotinib, dasatinib, bosutinib, ponatinib) and a Specifically Targeting the ABL Myristoyl Pocket (STAMP) inhibitor commonly used in clinical settings. Using morphological assessments, viability and metabolic activity assays, glutamate intake evaluations, and gene expression analyses we observed distinct responses among cell lines. TKIs and STAMP inhibitor treatments showed varying impacts on morphological features, cell viability, metabolic activity, and gene expression profiles, highlighting significant differences in cellular responses. This emphasizes the necessity of considering cellular heterogeneity in CML research. This comprehensive comparison provides valuable insights for refining preclinical models and enhancing translational relevance in CML research and treatment development. Understanding the diverse responses of CML cell lines to TKIs and STAMP inhibitor facilitates the selection of appropriate models for specific research questions, ultimately improving the accuracy and reliability of preclinical studies in CML.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chlorogenic Acid Enhances Beta-Lapachone-Induced Cell Death by Suppressing Autophagy in NQO1-Positive Cancer Cells.","authors":"Sahib Zada, Md Entaz Bahar, Wanil Kim, Deok Ryong Kim","doi":"10.1002/cbin.70006","DOIUrl":"https://doi.org/10.1002/cbin.70006","url":null,"abstract":"<p><p>Resistance to apoptosis-inducing drugs frequently occurs in cancer cells, limiting their usefulness in ongoing cancer treatment. Despite ongoing efforts to overcome drug resistance, a definitive solution remains elusive. However, autophagy inhibition has been shown to enhance the effectiveness of some anticancer drugs and is a possible strategy for overcoming drug resistance. In this study, we demonstrate that chlorogenic acid (CGA), a natural antioxidant, significantly enhances beta-lapachone (β-Lap)-induced cell death in cancer cells. The augmented apoptosis induced by CGA is associated with activation of protein kinase A (PKA) in β-Lap-treated cells, independent of the antioxidant properties of CGA. As a result, PKA activation in cancer cells co-treated with β-Lap and CGA effectively inhibits autophagy. Notably, PKA activation leads to phosphorylation of microtubule-associated protein 1 A/1B-light chain 3 (LC3) at the serine 12 residue, causing autophagy suppression irrespective of mTORC activity. Importantly, the cell death induced by β-Lap and CGA in NQO1-overexpressing breast or lung cancers is closely linked to autophagy inhibition. These findings suggest that combining β-Lap and CGA might be a novel strategy for cancer therapy, particularly for overcoming drug resistance caused by autophagy induction in cancer cells.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of Glutamate Excitotoxicity in Glioblastoma Growth and Its Implications in Treatment.","authors":"Colin Moriarty, Natasha Gupta, Debanjan Bhattacharya","doi":"10.1002/cbin.70005","DOIUrl":"https://doi.org/10.1002/cbin.70005","url":null,"abstract":"<p><p>Glioblastoma is a highly malignant and invasive type of primary brain tumor that originates from astrocytes. Glutamate, a neurotransmitter in the brain plays a crucial role in excitotoxic cell death. Excessive glutamate triggers a pathological process known as glutamate excitotoxicity, leading to neuronal damage. This excitotoxicity contributes to neuronal death and tumor necrosis in glioblastoma, resulting in seizures and symptoms such as difficulty in concentrating, low energy, depression, and insomnia. Glioblastoma cells, derived from astrocytes, fail to maintain glutamate-glutamine homeostasis, releasing excess glutamate into the extracellular space. This glutamate activates ionotropic N-methyl-D-aspartate (NMDA) receptors and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors on nearby neurons, causing hyperexcitability and triggering apoptosis through caspase activation. Additionally, glioblastoma cells possess calcium-permeable AMPA receptors, which are activated by glutamate in an autocrine manner. This activation increases intracellular calcium levels, triggering various signaling pathways. Alkylating agent temozolomide has been used to counteract glutamate excitotoxicity, but its efficacy in directly combating excitotoxicity is limited due to the development of resistance in glioblastoma cells. There is an unmet need for alternative biochemical agents that can have the greatest impact on reducing glutamate excitotoxicity in glioblastoma. In this review, we discuss the mechanism and various signaling pathways involved in glutamate excitotoxicity in glioblastoma cells. We also examine the roles of various receptor and transporter proteins, in glutamate excitotoxicity and highlight biochemical agents that can mitigate glutamate excitotoxicity in glioblastoma and serve as potential therapeutic agents.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Differentiation Abilities of Hair Follicle and Dental Pulp Stem Cells Into Islet Like Cells.","authors":"Avinash Kharat, Kalyani Bhate, Avinash Sanap, Supriya Kheur, Murtuza Contractor, Poonam Suryawanshi, Ramesh Bhonde","doi":"10.1002/cbin.70010","DOIUrl":"https://doi.org/10.1002/cbin.70010","url":null,"abstract":"<p><p>This study aimed to compare the differentiation potential of dental pulp-derived mesenchymal stem cells (DP-MSCs) and hair follicle-derived mesenchymal stem cells (HF-MSCs), which originated from the ectoderm. Dental pulps were separated from the extracted wisdom teeth during dental surgery, and Hair follicles were extracted from the scalp of patients undergoing hair transplantation. We cultivated the cell in cell culture media, supplemented with additional nutrients. After the fourth passage, the homogeneous population of DP-MSCs and HF-MSCs was analyzed for the surface markers (CD73, CD90, and CD105) by fluorescence-activated cell sorting. In vitro, the multi-lineage differentiation potential for both the MSCs was tested with respective induction media such as osteogenic, chondrogenic, adipogenic, and insulin-producing cells. Following the fourth passage, identical fibroblast-like cells were noted in each culture plate. Mesenchymal stem cell marker was expressed in both DP-MSCs and HF-MSCs. Both the DP-MSCs and HF-MSCs exhibited similar differentiation potential toward osteogenic, chondrogenic, and adipogenic differentiation. However, there was a difference in the differentiation potential into IPCs. HF-MSCs showed higher C-peptide and insulin secretion response to glucose, PDX1, and Insulin gene expression compared to DP-MSCs. These findings suggest that although DP-MSCs and HF-MSCs showed similar stemness properties, they differ in their differentiation potential towards insulin-producing cells (IPCs). This is the first report showing the potential of HF-MSCs to generate IPCs, revealing hair follicles as a novel and promising source for autologous stem cell therapy in diabetes. The generated islet organoids can be used for diabetic drug toxicity testing and screening.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hinokitiol Prevents Diabetic Acute Kidney Injury by Mitigating ER Stress.","authors":"Tahib Habshi, Hrushikesh Kulkarni, Neha Dagar, Vishwadeep Shelke, Anil Bhanudas Gaikwad","doi":"10.1002/cbin.70008","DOIUrl":"https://doi.org/10.1002/cbin.70008","url":null,"abstract":"<p><p>Acute kidney injury (AKI) in diabetic conditions often advances to chronic kidney disease (CKD), exacerbated by ischemia-reperfusion injury (IRI) through pathomechanisms such as endoplasmic reticulum (ER) stress and inflammation. Currently, available treatment options for diabetic AKI are not uniformly effective, highlighting the need for novel interventions. This study aimed to examine the renoprotective effects of hinokitiol, a natural tropolone compound, against diabetic AKI with its capability to decrease ER stress and inflammation, along with apoptosis. This study involved NRK-52E cells grown in-vitro under high-glucose conditions subjected to 10 mM sodium azide to elicit hypoxia/reperfusion injury (HRI). The expression of key ER stress markers like binding immunoglobulin binding protein (BiP), R/PKR-like ER kinase (PERK), and eukaryotic initiation factor-2 (eIF2α) as well as inflammatory proteins was markedly diminished by hinokitiol pretreatment (50 μM). Hinokitiol further reduced apoptosis in the NRK-52E cells. Similarly, in the in-vivo study, male Wistar rats with STZ-induced Type 1 diabetes (55 mg/kg, i.p.) were treated with hinokitiol 50 and 100 mg/kg/day i.p. for 5 days, followed by AKI induction via bilateral IRI. Hinokitiol pretreatment significantly reduced the elevated plasma blood urea nitrogen (BUN), creatinine, and urinary kidney injury molecule-1 (KIM-1) levels and tubular damage in diabetic AKI rats. Hinokitiol also reduced the respective ER stress protein expressions in diabetic AKI rats, as demonstrated by immunohistochemical analysis and immunoblotting. These findings suggest that hinokitiol alleviates diabetic AKI by modulating the PERK/CHOP/NF-κB axis, highlighting the likeliness of hinokitiol as a viable therapeutic technique for alleviating diabetic AKI.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bryophyllum pinnatum Induces p53-Dependent Apoptosis of Colorectal Cancer Cells via Increased Intracellular ROS and G2/M Cell-Cycle Arrest In Vitro and Validated in Silico by Molecular Docking.","authors":"Sumoyee Mukherjee, Sheuli Kangsa Banik, Sourio Chakraborty, Tanya Das, Manabendra Dutta Choudhury, Anusri Tripathi","doi":"10.1002/cbin.70004","DOIUrl":"https://doi.org/10.1002/cbin.70004","url":null,"abstract":"<p><p>Chemotherapy, radiotherapy and surgical treatments of cancer having several limitations and toxic side-effects, have led researchers to focus towards development of alternative natural plant-based therapeutics that can reduce disease severity. The present research work is mainly focussed towards identifying molecular mechanisms of apoptosis of colorectal cancer cells (HCT116) by perennial herb Bryophyllum pinnatum leaf-extract via both in vitro experimentations and in silico analysis. B. pinnatum leaf extract induced highest cytotoxicity at lowest dose (IC₅₀:0.01 mg/mL) against HCT116 cells with 49.5% (p < 0.0001) cellular death, in comparison to other cancer cell lines. It has arrested HCT116 cell populations at G2/M cell-cycle phase and led to 10 folds (p < 0.0001) and 5.5 folds (p < 0.0001) increased intracellular ROS production in treated groups. ROS production might have led to significant 34.23% and 21.03% (p < 0.0001) apoptosis in treated cells, proved in vitro and in silico, with significant upregulation of p53 (p < 0.0001), BAX (p = 0.0252), CASPASE3 (p < 0.0001) and downregulation of BCL2 (p = 0.0058), leading to increased nuclear p53 (p = 0.0002) accumulation in treated cells, suggesting that the leaf-extract might have induced p53-dependent apoptosis of colorectal cancer cells. The phyto-extract also possess significant gene-modulatory potential as evident from qRT-PCR analysis of oncogenes and tumor suppressor genes. Leaf's bioactive phyto-constituents were elucidated by GC-MS and HPLC-ESI/MS analysis. In silico STITCH analysis provided significant network interactions between these bioactive phyto-compounds and studied proteins. Further Molecular Docking studies revealed strong binding between such docked complexes. Also, predicted major bioactive phyto-constituents of B. pinnatum leaf-extract such as Quercetin, Morin and β-Sitosterol have induced significant (p < 0.0001) apoptosis and increased intracellular ROS, validating their in silico interactions with studied proteins of HCT116 cells. All these studies together demonstrated ability of B. pinnatum to be used as a suitable natural phyto-therapeutic agent for development of chemo-preventive medications against colorectal cancer.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143490981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Caveolae Modulate the Activity of LRRC8-Mediated VRAC by the Structural Membrane Protein Caveolin-1.","authors":"Yan Liu, Xing Li, Cong Huo, Liming Hou, Xin Jia, Rong Xu, Jie Yang, Xiaoming Wang","doi":"10.1002/cbin.70001","DOIUrl":"https://doi.org/10.1002/cbin.70001","url":null,"abstract":"<p><p>The volume-regulated anion channel (VRAC) plays a critical role in cell volume regulation and other fundamental physiological processes. However, the mechanism of how VRAC is activated and modulated has not been completely clarified. Caveolin-1 (Cav-1), as an important ion channel binding protein, forms complexes with channel proteins and exchangers to regulate channel activity and function. The purpose of this study was to explore the importance and value of Cav-1 in cardiac VRAC activation and regulation. In the study, we proved that the membrane protein LRRC8A was detected in the same caveolae-enriched fractions, as the same as Caveolin-1 in ventricular myocytes. The intracellular Cl^- concentration increased and the cell volume decreased dramatically after caveolae being destroyed in cardiomyocytes. Moreover, we found that I_Cl,vol decreased not only in LRRC8A silencing cardiomyocytes but also in Cav-1 silencing cardiomyocytes, which indicated that caveolin-1 may affect the function of VRAC. Then we further explore the physical relationship between LRRC8A and Cav-1 in cell membrane. We observed that the fluorescence label of LRRC8A was overlapping with Cav-1 in the cell plasma membrane and caveolin-1 co-immunoprecipitated with LRRC8A, which demonstrated that Cav-1 is the basis of VRAC channel activation by acting on LRRC8A. The whole study provides further evidence of the relevance of Cav-1 on the activation and modulation of endothelial LRRC8A-mediated VRAC.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macrophage-to-Myofibroblast Transition Contributes to Cutaneous Scarring Formation Through the TGF-β/Smad3 Signaling Pathways.","authors":"Yuan Jia, Yi Qin, Feng-Lai Yuan, Jie-Hong Shen","doi":"10.1002/cbin.70002","DOIUrl":"https://doi.org/10.1002/cbin.70002","url":null,"abstract":"<p><p>Cutaneous scarring typically arises after surgery, trauma, and infection, occurring when normal skin tissue is replaced by fibrous tissue during the healing process. Myofibroblasts have been identified as a significant contributor to this scarring. While the differentiation of fibroblasts into myofibroblasts is well-recognized as essential for wound healing and tissue repair, the mechanisms underlying the macrophage-myofibroblast transition (MMT) remain largely unexplored. This study aimed to investigate the role and potential mechanisms of MMT in cutaneous scarring. In specimens of hypertrophic scars, keloid and scleroderma, we confirmed the coexistence of MMT markers CD68 and α-smooth muscle actin (α-SMA) in areas of skin fibrosis. Additionally, most MMT cells in human cutaneous scar co-expressed the M2-type macrophage marker CD206. Fate-mapping in Lyz2-Cre/Rosa26-tdTomato mice further demonstrated that the majority of myofibroblasts in cutaneous scars were derived from bone marrow macrophages. Furthermore, higher levels of TGF-β were released from scar fibroblasts, which contributed to MMT through the Smad3 pathways. In vivo studies inhibiting Smad3 reduced MMT and scarring. Macrophage depletion with clodronate liposomes also reduced cutaneous scar formation. Our findings indicate that MMT plays a pivotal role in cutaneous scarring through the TGF-β/Smad3 pathways. Consequently, inhibiting MMT may be a novel strategy for the treatment of cutaneous scarring.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Alleviative Effect of Sodium Butyrate on Dexamethasone-Induced Skeletal Muscle Atrophy.","authors":"Xingchen Zhao, Mingqiang Zhu, Zifan Wang, Ming Gao, Yifei Long, Shuo Zhou, Wei Wang","doi":"10.1002/cbin.70003","DOIUrl":"https://doi.org/10.1002/cbin.70003","url":null,"abstract":"<p><p>Skeletal muscle mass is significantly negatively regulated by glucocorticoids. Following glucocorticoid administration, the balance between protein synthesis and breakdown in skeletal muscle is disrupted, shifting towards a predominance of catabolic metabolism. Short-chain fatty acids like sodium butyrate have been found to regulate inflammatory reactions and successively activate signaling pathways. The preventive benefits of sodium butyrate against dexamethasone-induced skeletal muscle atrophy and myotube atrophy models were examined in this work, and the underlying mechanism was clarified. A total of 32 6-week-old C57BL/6 inbred male mice were randomly assigned to one of four groups and treated with dexamethasone to induce muscle atrophy and sodium butyrate. We found that sodium succinate alleviated dexamethasone-induced myotube atrophy in the myotube atrophy model by lowering the gene expression of two E3 ubiquitin ligases, Atrogin-1 and MURF1, and activating the AKT/mTOR signaling pathway. Pertussis toxin reversed this effect, indicating that G protein-coupled receptors were involved in sodium butyrate's action as a mediator. Additionally, pre-treatment with sodium butyrate lowered weight and muscle mass loss in a mouse model of skeletal muscle atrophy, dramatically decreased the MURF1 gene expression and decreased the nuclear translocation of the glucocorticoid receptor. In conclusion, this study shows that sodium butyrate inhibits the expression of atrophy genes, thus preventing the breakdown of proteins and the loss of muscle mass, while also inhibiting weight loss, in animal models.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398475","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}