Cell Biochemistry and Function最新文献

{"title":"Unveiling the Protective Potential of Crocin in Septic Acute Liver Injury via Assessment of TLR4/HGM1/NF-κB Signaling Pathway, Oxidative Stress and Heat Shock Response","authors":"Ali Tugrul Akin,&nbsp;Emin Kaymak,&nbsp;Tayfun Ceylan,&nbsp;Nurhan Kuloglu,&nbsp;Derya Karabulut,&nbsp;Ayse Toluk","doi":"10.1002/cbf.70058","DOIUrl":"https://doi.org/10.1002/cbf.70058","url":null,"abstract":"<div>\u0000 \u0000 <p>Sepsis, defined as a systemic inflammatory response, is one of the conditions with the highest mortality rates. Crosin (CRO) is one of the active ingredients in saffron and known for its various pharmacological effects. It has been reported to have protective and healing effects on liver tissue. In this study, we aimed to investigate the protective role of CRO in lipopolysaccharide (LPS)-induced acute liver injury. 40 male Wistar Albino rats aged 8–12 weeks were randomly divided into 4 groups: Control, CRO (50 mg/kg, intraperitoneal administration for 9 days), LPS (30 mg/kg, single dose), and LPS + CRO (50 mg/kg CRO for 9 days along with a single dose of 30 mg/kg LPS). Following the experimental procedure, liver and blood samples were collected for further analyses. Histopathological analysis revealed a marked increase in liver damage in the LPS group, as evidenced by significant histopathological changes. In contrast, the liver histology in the LPS + CRO group closely resembled that of the Control and CRO groups, exhibiting substantially less damage compared to the LPS group. Immunohistochemical examinations showed a significant increase in the expressions of TLR4, HMGB1, NF-κB, TNF- α, HSP70, and HSP90 in the LPS group. However, in the LPS + CRO group, the levels of these markers were significantly lower compared to the LPS group. ELISA analyses showed a significant increase in MDA, IL-6, and TGF-β and a decrease in SOD, CAT, GSH levels in the LPS group. Conversely, in the LPS + CRO group, CRO applications exhibited a significant protective effect on these alterations. Additionally, AST, ALT, and LDH levels were significantly elevated in the LPS group, while albumin levels were lower in the LPS group. CRO applications in the LPS + CRO group were observed to have a protective effect on these parameters. We believe that CRO holds significant potential in the treatment of acute inflammatory diseases such as septic acute liver injury and should not be overlooked.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143431419","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":"Acute Myeloid Leukemia-Osteoblast Interaction Mediated Autophagy Induction Protects Against Cytarabine Induced Apoptosis","authors":"Kamini Shivhare,&nbsp;Neeraj Kumar Satija","doi":"10.1002/cbf.70055","DOIUrl":"https://doi.org/10.1002/cbf.70055","url":null,"abstract":"<div>\u0000 \u0000 <p>High rate of relapse, following chemotherapy, in acute myeloid leukemia (AML) is a major concern. The chemoprotection conferred by the bone marrow microenvironment has lately been recognized, in addition to autophagy-mediated chemoresistance. Thus, the present study explored the effect of osteoblast on autophagy in AML and its impact on sensitivity to cytarabine (Ara-C) in the context of endosteal niche. Co-culture of KG1-a, HL60, or THP-1 AML cells with osteoblastic Saos-2 cell line induced autophagy in AML cell lines under direct contact. HL60 cells when co-culture with Saos-2 demonstrated more resistance to Ara-C induced apoptosis, which was reversed upon chloroquine treatment. Similarly, inhibition of autophagy in AML cell by knocking down Beclin-1 enhanced HL60 sensitivity to Ara-C. An interesting observation was upregulation of autophagy even in Saos-2 cells upon co-culture with AML cell, and increase in HL60 apoptosis in response to Ara-C on Beclin-1 knockdown in osteoblast cell. This highlights that autophagy plays a chemoprotective role in the endosteal niche in AML against Ara-C.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143389367","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":"Retraction to “LINC00240 Promotes Gastric Cancer Cell Proliferation, Migration and EMT via the MiR-124-3p/DNMT3B Axis”","authors":"","doi":"10.1002/cbf.70054","DOIUrl":"https://doi.org/10.1002/cbf.70054","url":null,"abstract":"<p>Y. Li, J. Yan, Y. Wang, C. Wang, C. Zhang, and G. Li, “LINC00240 Promotes Gastric Cancer Cell Proliferation, Migration and EMT via the MiR-124-3p/DNMT3B Axis,” <i>Cell Biochemistry and Function</i> 38, no. 8 (2020): 1079–1188, https://doi.org/10.1002/cbf.3551.</p><p>The above article, published online on 11 June 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors, the journal Editors-in-Chief, Raphael Gaudin and Robert Heath; and John Wiley &amp; Sons Ltd. An investigation by the publisher revealed several flaws and inconsistencies between the results presented and the experimental methods described. Furthermore, the article reports major results in the cell lines BGC-823 and SGC-7901, reported as contaminated [1, 2]. Accordingly, the article is retracted as the editors consider the conclusions of this article to be invalid.</p><p><b>References</b></p><p>[1] F. Ye, C. Chen, J. Qin, J. Liu, and C. Zheng, “Genetic Profiling Reveals an Alarming Rate of Cross-Contamination Among Human Cell Lines Used in China,” <i>FASEB Journal</i> 29, no. 10 (2015): 4268–4272, https://doi.org/10.1096/fj.14-266718.</p><p>[2] X. Bian, Z. Yang, H. Feng, H. Sun, and Y. Liu, “A Combination of Species Identification and STR Profiling Identifies Cross-Contaminated Cells From 482 Human Tumor Cell Lines,” <i>Scientific Reports</i> 7, no. 1 (2017): 9774, https://doi.org/10.1038/s41598-017-09660-w.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70054","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143380844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective Effect of Carvedilol Against Oxidative Stress Induced by Palmitic Acid in Primary Rat Hepatocytes","authors":"Sandra A. Serna Salas,&nbsp;Turtushikh Damba,&nbsp;Manon Buist-Homan,&nbsp;Han Moshage","doi":"10.1002/cbf.70057","DOIUrl":"https://doi.org/10.1002/cbf.70057","url":null,"abstract":"<p>Hepatocyte lipotoxicity (HL) is an important factor in the pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD). It is defined as the detrimental effects of exposure to (excessive) amounts of toxic lipid species, leading to increased mitochondrial β-oxidation, oxidative stress (OxS), and organellar dysfunction. Carvedilol (CV) is a β-adrenergic blocker with antioxidant properties. To elucidate whether CV protects hepatocytes against lipotoxicity induced by palmitic acid (PA) by reducing OxS and endoplasmic reticulum (ER) stress. Primary rat hepatocytes (rHep) were used. Lipotoxicity was induced by PA (1 mmol/L). Cell damage was evaluated by Sytox Green staining. Mitochondrial generation of reactive oxygen species (mROS) was assessed by MitoSox. mRNA and protein expression were measured by qPCR and Western blot, respectively. Lipid accumulation was measured by Oil Red O staining and triglyceride (TG) content. PA induced cell death in &gt; 80% of cells and increased mROS generation. PA increased mRNA expression of ER stress markers CHOP and sXBP1 and slightly increased lipid accumulation. Expression of the β-oxidation-related gene Cpt1a was increased. CV (10 µmol/L) significantly reduced PA-induced cell death to control levels (&lt; 8% of total cells), and mROS generation and expression of the mitochondrial antioxidant enzymes Sod2 and Cat were increased by 40% by CV in the presence of PA. CV did not change the expression of ER stress markers. CV, added before PA, protects rHep against PA-induced cytotoxicity by reducing OxS and increasing the expression of antioxidant enzymes without any additional protective effect on ER stress or lipid accumulation.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbf.70057","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143380087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigallocatechin-Gallate: Unraveling Its Protective Mechanisms and Therapeutic Potential","authors":"Xiang-Wen Dong,&nbsp;Wen-Lan Fang,&nbsp;Yun-Hang Li,&nbsp;Yu-Rong Chai","doi":"10.1002/cbf.70056","DOIUrl":"https://doi.org/10.1002/cbf.70056","url":null,"abstract":"<div>\u0000 \u0000 <p>Epigallocatechin-gallate (EGCG), the predominant catechin in green tea, is a key constituent of tea polyphenols. Due to the EGCG's diverse biological activities of anti-inflammatory, antioxidant, and so forth, green tea is believed to exert a positive influence on a variety of diseases. And extensive research had uncovered a range of protective effects attributed to EGCG, indicating its potential to mitigate various pathological conditions. The precise mechanisms through which EGCG operates remain a subject of ongoing discussion among researchers. Reactive oxygen species (ROS), a primary culprit in oxidative stress, have been demonstrated to be reduced by EGCG. Furthermore, nuclear factor kappa-B (NF-κB), a pivotal signal molecular of inflammation progress, has been observed to be suppressed by EGCG. Sirtuins1 (Sirt1) is a histone deacetylase, the obligate substrate of which is NAD+. Evidence suggests that EGCG can enhance the activities of Sirt1 to induce autophagy to protect inflammation injury and oxidative stress in tissues and organs. Despite the promising protective effects of EGCG, its clinical use is constrained by its limited bioavailability. This review aims to consolidate the existing evidence and elucidate the mechanisms that support EGCG's protective role, as well as to explore the challenges and potential strategies for its clinical application.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143362543","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 Microbiota-Derived Metabolites in Prostate Cancer Inflammation and Progression","authors":"Pradeep Kumar,&nbsp;Anil Kumar,&nbsp;Virendra Kumar","doi":"10.1002/cbf.70050","DOIUrl":"10.1002/cbf.70050","url":null,"abstract":"<div>\u0000 \u0000 <p>Prostate cancer (PCa) is the most commonly detected malignancy in men worldwide. PCa is a slow-growing cancer with the absence of symptoms at early stages. The pathogenesis has not been entirely understood including the key risk factors related to PCa development like diet and microbiota derived metabolites. Microbiota may influence the host's immunological responses, inflammatory responses, and metabolic pathways, which may be crucial for the development and metastasis. Similarly, short-chain fatty acids, methylamines, hippurate, bile acids, and other metabolites generated by microbiota may have potential roles in cancer inflammation and progression of cancer. Most studies have focused on the role of metabolites and their pathways involved in chronic inflammation, tumor initiation, proliferation, and progression. In summary, the review discusses the role of microbiota and microbial-derived metabolite-built strategies in inflammation and progression of the PCa.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073770","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":"Super-Enhancer Protects Cells From Toxicity of C9orf72 Poly(proline–arginine) by Inducing the Expression of KPNA2/KPNB1","authors":"Miaomiao Chen,&nbsp;Henglu Cui,&nbsp;Xiaoyu Zhang,&nbsp;Shuyan Ma,&nbsp;Jinjing Guo,&nbsp;Zhaoxiu Liu,&nbsp;Donghua Gu,&nbsp;Yihui Fan","doi":"10.1002/cbf.70053","DOIUrl":"10.1002/cbf.70053","url":null,"abstract":"<div>\u0000 \u0000 <p>Hexanucleotide repeat expansions in C9orf72 are the most common genetic mutation associated with amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) (C9-ALS/FTD). Dipeptide repeat (DPR) proteins, such as poly(proline–arginine) (polyPR) generated from G4C2 repeat expansions, have been shown to be highly toxic. In this study, PR20 was labeled with fluorescein isothiocyanate (FITC) to track its cellular localization. Several cell lines demonstrated survival under PR20 treatment by sequestering PR20 in the cytoplasm. Treatment with JQ-1 or Ivermectin (Iver) translocated PR20 into the nucleus, leading to cell death. Mechanistically, KPNA2/KPNB1 interacted with PR20 in the cytoplasm and hindered PR20 from entering the cell nucleus. Genetic silencing of KPNA2/KPNB1 converted PR20-resistant cells into PR20-sensitive cells. Treatment with JQ1 significantly reduced the protein levels of KPNA2/KPNB1, allowing PR20 to enter the nucleus. Overexpression of KPNA2 or KPNB1 effectively blocked cell death induced by co-treatment with JQ-1 and PR20. Our results indicate that super-enhancers shield cells from PR20 toxicity by upregulating the expression of KPNA2/KPNB1.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073771","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":"Suppression of Fibroblast Growth Factor 23 in UMR106 Osteoblast-Like Cells and MC3T3-E1 Cells by Adipokine Chemerin","authors":"Julia Vogt,&nbsp;Kim Daferner,&nbsp;Michael Föller","doi":"10.1002/cbf.70051","DOIUrl":"10.1002/cbf.70051","url":null,"abstract":"<p>Endocrine fibroblast growth factor 23 (FGF23) derived from bone governs phosphate and vitamin D metabolism. Paracrine FGF23 has additional functions in different organs. Moreover, plasma FGF23 is correlated with outcomes in chronic kidney disease. FGF23 regulation is complex depending on a plethora of different factors and conditions including AMP-dependent kinase (AMPK), inflammation, and adipokines leptin and adiponectin. Chemerin is an adipokine implicated in proinflammatory processes in adipose tissue and other organs and an activator of AMPK. Here, we investigated whether chemerin is a regulator of FGF23. UMR106 osteoblast-like cells and MC3T3-E1 osteoblasts were studied. Gene expression was assessed by qRT-PCR, FGF23 protein by ELISA, and AMPK activity by western blotting. Both cell lines expressed <i>Cmklr1</i> encoding chemerin chemokine-like receptor 1. Chemerin slightly but significantly reduced <i>Fgf23</i> expression. Chemerin reduced FGF23 protein abundance in the cell culture supernatant, and RNAi-mediated <i>Cmklr1</i> silencing upregulated <i>Fgf23</i> expression in UMR106 cells. In the presence of AMPK inhibitor compound C, chemerin failed to suppress <i>Fgf23</i> in UMR106 cells. In conclusion, chemerin-dependent <i>Cmklr1</i> signaling downregulates FGF23 in bone cell lines. This effect requires, at least partly, AMPK.</p>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11782926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063933","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin Prevents Thymic Atrophy but Does Not Protect Against Disruption of T Cell Maturation Related to Cyclophosphamide Exposure","authors":"Gustavo F. Pimenta,&nbsp;Thales M. H. Dourado,&nbsp;Kayse D. B. de Souza,&nbsp;Jefferson Elias-Oliveira,&nbsp;Vanessa F. Rodrigues,&nbsp;Daniela Carlos,&nbsp;Carlos R. Tirapelli","doi":"10.1002/cbf.70052","DOIUrl":"10.1002/cbf.70052","url":null,"abstract":"<div>\u0000 \u0000 <p>Increased oxidative stress and apoptosis are key mechanisms of thymic atrophy induced by cyclophosphamide (CYP). Atrophy leads to changes in the thymic microenvironment and disrupts T cell maturation. The hormone melatonin displays antioxidant and antiapoptotic effects. Here, we tested the hypothesis that melatonin would act as a cytoprotective agent against the harmful effects of CYP in the thymus. A single dose of CYP (300 mg/kg; ip) was injected in male C57BL/6 mice pretreated or not with melatonin (10 mg/kg/day, ip) for 4 days. Atrophy, oxidative stress and apoptosis markers, and T cell subpopulations were evaluated in the thymus 24 h after CYP injection. Melatonin partially prevented atrophy and the increase in caspase 3 activity induced by CYP. Augmented lipoperoxidation and generation of NADPH-oxidase derived superoxide (O₂^•−), as well as decreased superoxide dismutase (SOD) activity, were detected in the thymus of CYP-injected mice. Pretreatment with melatonin abrogated these responses. CYP reduced the number of double-positive (CD4⁺CD8⁺) cells, activated single-positive (CD8⁺ and CD4⁺) cells, and regulatory CD4⁺FoxP3⁺ (Treg) cells in the thymus. None of these effects were reversed by melatonin. In conclusion, melatonin partially prevented thymic atrophy, possibly by reducing apoptosis and oxidative stress. However, melatonin did not abrogate the immunomodulatory effect of CYP on T cell populations. The lack of effect of melatonin on CYP-induced reduction in Treg cells may be of interest since these cells reduce antitumor immunity.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063929","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":"Evaluating the Effectiveness of a Novel Pongamia pinnata Derived Herbal Mouth-Dissolving Film for Treating Oral Disorders and Evaluating Its Anticancer Properties","authors":"Devang Prajapati,&nbsp;Masuma Hakim,&nbsp;Margi Patel,&nbsp;Mohammad Javed Ansari,&nbsp;Saleh Alfarraj,&nbsp;Sanjay Chauhan,&nbsp;Vaibhav Bhatt,&nbsp;Virendra Kumar Yadav,&nbsp;Dipak Kumar Sahoo,&nbsp;Kashyap Thummar,&nbsp;Ashish Patel","doi":"10.1002/cbf.70049","DOIUrl":"10.1002/cbf.70049","url":null,"abstract":"<div>\u0000 \u0000 <p>The present study aimed to optimize a mouth-dissolving film (MDF) made from <i>Pongamia pinnata</i> stem bark extract to increase patient compliance and accelerate oral disease therapy. Several stem bark extracts were prepared, and karanjin was used as an herbal marker for the extracts. The ethanolic extract showed the maximum yield (12.10% ± 0.09%) and cytotoxic activity against human oral cancer (KB 3-1) and embryonic kidney cell lines. The MDF formulation was focused on incorporating a fixed amount of the extract and varying concentrations of HPMC E5 polymer, along with evaluating the performance of plasticizers like PEG 400 and propylene glycol (PG). An optimized formulation was determined based on disintegration time, wetting time, and folding endurance. The formulation consisted of HPMC E5 as a film-forming polymer, PG as a superior plasticizer, ascorbic acid as an antioxidant, and other ingredients contributing to solubility, dispersion, sweetening, and appearance. High-performance thin-layer chromatography-mass spectrometry analysis confirmed higher levels of karanjin in the optimized formulation, ensuring its successful incorporation and stability. Taste masking evaluations indicate a favorable taste profile and a high potential for patient compliance. The stability study displayed no significant changes in the physical characteristics of the film, affirming its stability and quality. In conclusion, the developed herbal-based optimized MDF presents a promising drug delivery system, offering enhanced patient compliance, taste masking, and stability. The MDF holds great potential for effective treatment and management of oral diseases, providing convenience and improved therapeutic outcomes.</p></div>","PeriodicalId":9669,"journal":{"name":"Cell Biochemistry and Function","volume":"43 2","pages":""},"PeriodicalIF":2.8,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058311","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}