Biomedicine & Pharmacotherapy最新文献

{"title":"Eriocitrin and its derivatives against Alzheimer’s disease: Cumulative accounts of in vitro and in vivo studies","authors":"Kritika ,&nbsp;Sanjay ,&nbsp;Hae-Jeung Lee","doi":"10.1016/j.biopha.2025.118362","DOIUrl":"10.1016/j.biopha.2025.118362","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease (ND), and its adversities are not limited to the brain. Due to complex and interconnected pathologies with other NDs, an effective treatment for multidimensional AD-related adversities has yet to be reported. Several phytoconstituents have been reported and are currently being studied for their bioactive potential in AD. Eriocitrin, a dihydroflavonoid compound present in citrus fruits, such as lemons, limes, lemon peels, grapefruit, and vegetables, and processed items, such as beverages and wine, along with its derivatives hesperetin, hesperidin, eriodictyol, and homoeriodictyol, has been reported to possess various neuroprotective bioactivities, including anti-inflammatory, anti-oxidative, anti-amyloidogenic, anti-tau phosphorylation, and anti-apoptotic properties, in several <em>in vitro</em> and <em>in vivo</em> models. However, a comprehensive review summarizing and correlating the multidimensional bioactive potentials of eriocitrin and its derivatives against AD has yet to be compiled. This review extensively discusses the in-depth role of eriocitrin and its derivatives in ameliorating different AD-related signaling pathways both <em>in vitro</em> and <em>in vivo</em>, and summarizes the incorporation of eriocitrin like different plant-based flavonoids in long-term dietary practice to combat AD and other similar NDs. Additionally, this review suggests examining various nano-formulations of eriocitrin and its derivatives for their anti-AD effects in comparison to the parent compound. Furthermore, in-depth <em>in vitro</em> and <em>in vivo</em> studies, along with different clinical trials, should be conducted to fully elucidate the true potential of eriocitrin and its derivatives in AD pathology.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":"190 ","pages":"Article 118362"},"PeriodicalIF":6.9,"publicationDate":"2025-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144670197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Riboceine and N-acetylcysteine protect normal prostate cells from chemotherapy-induced oxidative stress while selectively modulating the cytotoxicity of methotrexate and docetaxel in prostate (PC-3) and breast cancer (MCF-7) cells","authors":"Trudy J. Philips ,&nbsp;Benoit Banga N’guessan ,&nbsp;Eunice Dotse ,&nbsp;Joseph Kofi Abankwah ,&nbsp;Regina Appiah-Opong","doi":"10.1016/j.biopha.2025.118355","DOIUrl":"10.1016/j.biopha.2025.118355","url":null,"abstract":"<div><h3>Background</h3><div>Cancer chemotherapy often results in severe side effects due to its non-selective cytotoxicity toward rapidly dividing normal cells. These adverse effects are largely driven by oxidative stress resulting from elevated reactive oxygen species (ROS) production. Riboceine (RIB), a synthetic precursor of glutathione (GSH), and N-acetylcysteine (NAC), a clinically used antioxidant, hold promise in mitigating oxidative damage; however, their impact on chemotherapy efficacy and the molecular mechanisms involved remain incompletely understood.</div></div><div><h3>Aim</h3><div>This study aimed to evaluate the cytoprotective potential of RIB and NAC against methotrexate (MET)- and docetaxel (DOC)-induced toxicity in normal and cancer cells, and to explore mechanistic pathways using integrative network pharmacology and molecular docking approaches.</div></div><div><h3>Methodology</h3><div>Cytotoxic effects of MET and DOC, alone or in combination with RIB or NAC, were assessed in normal prostate epithelial (PNT-2), prostate cancer (PC3), and breast cancer (MCF-7) cell lines using the Resazurin assay. Intracellular ROS and GSH levels were quantified using DCF and OPA fluorescence assays, respectively. Network pharmacology, protein–protein interaction (PPI) analysis, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and molecular docking were conducted using SwissTargetPrediction, STRING, ShinyGO, Cytoscape, and AutoDock Vina platforms.</div></div><div><h3>Results</h3><div>MET and DOC showed dose-dependent cytotoxicity in PNT-2 and PC3 cells, but limited efficacy in chemoresistant MCF-7 cells. RIB and NAC significantly reduced ROS and restored GSH levels in PNT-2 cells, protecting them against oxidative injury. These antioxidants preserved anticancer effects in PC3 cells but reduced chemotherapy efficacy in MCF-7 cells, likely due to elevated redox buffering and transporter expression. Network analyses identified BCL-2, MAPK8, and SOD among key antioxidant and apoptotic targets. However, no direct experimental validation of these mechanisms was performed, and apoptotic markers such as Annexin V or caspase-3 were not assessed.</div></div><div><h3>Conclusion</h3><div>RIB and NAC provide selective cytoprotection to normal prostate cells during chemotherapy while maintaining anticancer effects in sensitive prostate cancer cells. However, their concurrent use in resistant cancers like MCF-7 may reduce drug efficacy, warranting cautious clinical application. Time-shifted antioxidant administration (e.g., post-chemotherapy) could be explored as a strategy to balance protection and efficacy. Future studies should include <em>in vivo</em> validation, apoptosis profiling, and protein-level mechanistic assays to confirm the predicted pathways.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":"190 ","pages":"Article 118355"},"PeriodicalIF":6.9,"publicationDate":"2025-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harnessing the potential of CAR-NK cell therapy in gastrointestinal cancers: From bench to bedside","authors":"Ahmad Ghorbani Vanan ,&nbsp;Mohammad Reza Askari ,&nbsp;Kamyar Bagheri ,&nbsp;Mohammad Reza Arghand ,&nbsp;Farid Ghorbaninezhad ,&nbsp;Safa Tahmasebi ,&nbsp;Milad Taghizadeh-Anvar ,&nbsp;Samaneh Nouri ,&nbsp;Elham Safarzadeh","doi":"10.1016/j.biopha.2025.118380","DOIUrl":"10.1016/j.biopha.2025.118380","url":null,"abstract":"<div><div>Cancer is one of the leading causes of mortality worldwide, with gastrointestinal (GI) malignancies being among the most prevalent and lethal types. Traditional treatments for GI cancers, such as chemotherapy and radiotherapy, often result in severe side effects due to their lack of specificity. Among the various therapeutic strategies, immunotherapy has emerged as a promising and highly specific approach for treating GI cancers. Immunotherapeutic methods include the use of monoclonal antibodies with diverse specificities, as well as cell-based therapies. Engineered cell therapies, particularly those utilizing chimeric antigen receptor (CAR) T cells and natural killer (NK) cells, represent a forefront in innovative cancer treatment. While CAR-T cells have shown promise, CAR-NK cells offer distinct advantages, such as the ability to kill tumor cells independently of CAR signaling and their suitability for safe allogeneic transplantation.Given these benefits, CAR-NK cells have gained attention as either a complementary or alternative strategy to CAR-T cell therapy in GI cancers. Despite this potential, a comprehensive review specifically focused on CAR-NK therapy in GI malignancies has been lacking. The present study aims to address this gap by exploring the application of CAR-NK therapy in various GI cancers, including colorectal, pancreatic, hepatocellular, esophageal, gastric, and tongue cancers, highlighting the targeted tumor antigens and recent advancements in the field.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":"190 ","pages":"Article 118380"},"PeriodicalIF":6.9,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144665735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protein post-translational modifications: Novel molecular switches and strategies for targeted therapy in ischemic heart disease","authors":"Yuanyuan Chen ,&nbsp;Gaojie Xin ,&nbsp;Xiaoshan Cui ,&nbsp;Jiaming Gao ,&nbsp;Huiyu Zhang ,&nbsp;Fan Guo ,&nbsp;Zixin Liu ,&nbsp;Shujuan Xu ,&nbsp;Ce Cao ,&nbsp;Lanlan Li ,&nbsp;Hao Guo ,&nbsp;Jianhua Fu","doi":"10.1016/j.biopha.2025.118357","DOIUrl":"10.1016/j.biopha.2025.118357","url":null,"abstract":"<div><div>Protein post-translational modifications (PTMs), serving as crucial molecular switches regulating protein function and signaling pathways, have emerged as a research hotspot for elucidating the pathogenesis of Ischemic heart disease (IHD) and devising targeted therapeutic approaches. This review provides a comprehensive overview of the principal PTM types associated with IHD, encompassing phosphorylation, acetylation, ubiquitination, SUMOylation, glycosylation, lactylation and succinylation. It also delves into the molecular mechanisms and key targets of PTMs in IHD pathology, primarily involving myocardial energy metabolism, calcium homeostasis, inflammatory responses, cell death, and myocardial fibrosis. Additionally, this paper evaluates the prospective applications of specific kinase modulators, PTM-targeting modifiers, and gene editing technologies in the treatment of IHD, and proposes a “modificatomics”-oriented precision intervention strategy, which offers a novel perspective for the management of IHD.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":"190 ","pages":"Article 118357"},"PeriodicalIF":6.9,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144662876","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of KMH-45, a novel MRGPRX2 inhibitor with enhanced anti-pruritic properties","authors":"Babina Sanjel ,&nbsp;Mahesh kumar Teli ,&nbsp;Surendra Kumar ,&nbsp;Ji-Hoon Oh ,&nbsp;Han-Joo Maeng ,&nbsp;Won-Sik Shim ,&nbsp;Mi-hyun Kim","doi":"10.1016/j.biopha.2025.118371","DOIUrl":"10.1016/j.biopha.2025.118371","url":null,"abstract":"<div><div>Pruritus, or itch, is a common complaint in dermatology, adversely affecting patient’s well-being and becoming unbearable when severe. Histamine induces itch by binding to the histamine receptor and antihistamines alleviate itch symptoms by blocking this action in many cases. However, the insufficient relief provided by antihistamines in various chronic conditions necessitates the development of anti-pruritic agents beyond the histamine mechanisms. In this study, we screened our in-house compounds with anti-inflammatory properties to assess their therapeutic potential in pruritus. In particular, protein-ligand interaction pattern of MRGPRX2 was investigated for the screening and KMH-45 was identified as a non-peptide inhibitor through molecular simulations of MRGPRX2 rotamer models, followed by calcium flux assay. Molecular mechanism study for pruritus targets revealed anti-pruritic efficacy of KMH-45 along with the regulation of anti-pruritic targets histamine receptor 1 and TRPA1 ion channel as well as MRGPR family. Moreover, KMH-45 dose-dependently inhibited peritoneal mast cell degranulation and demonstrated <em>in vivo</em> efficacy in the scratching behavior test. For further progression and application to clinical studies, the developability of KMH-45 and feature analysis of the MRGPRX2-ligand interaction pattern using GPCR-IPL Score was addressed.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":"190 ","pages":"Article 118371"},"PeriodicalIF":6.9,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144666026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-associated changes in type I collagen promote the invasion of BRAFV600E mutated melanoma cells and their resistance to targeted therapies within three-dimensional matrix models","authors":"Laetitia Florent ,&nbsp;Charles Saby ,&nbsp;Marie-Pierre Courageot ,&nbsp;Christine Terryn ,&nbsp;Laurence Van Gulick ,&nbsp;Jade Vanmansart ,&nbsp;Florian Slimano ,&nbsp;Hamid Morjani","doi":"10.1016/j.biopha.2025.118351","DOIUrl":"10.1016/j.biopha.2025.118351","url":null,"abstract":"<div><div>Melanoma represents the most aggressive form of skin cancer, with the highest rate of mortality. Anti-mutated BRAF^V600E therapies, such as vemurafenib, has improved the prognosis for melanoma patients; however, resistance to these targeted therapies frequently emerges. Type I collagen—a key element of the tumor microenvironment—contributes to tumor progression and therapeutic resistance. With aging, type I collagen undergoes structural remodeling that alters its fibrillar organization and mechanical properties. Although these changes have been documented, their impact on BRAF^V600E-mutated melanoma cell behavior and drug response remains unclear. In this study, we utilized both <em>in vitro</em> and <em>in vivo</em> models to fill this critical gap by investigating how collagen remodeling associated with advanced age modulates BRAF^V600E-mutated melanoma response to vemurafenib. Our findings indicate that <em>in vitro</em>—using a 3D culture matrix model—old collagen promotes increased proliferation of 1205Lu cells and protects both 1205Lu and SKMEL28 cells from vemurafenib effects. This was associated with elevated YAP expression, suggesting a role for mechanotransduction in drug resistance. The 3D collagen matrix spheroid model revealed that aged collagen enhances the invasive properties of 1205Lu cells, which correlated with an upregulation of the AXL receptor. <em>In vivo</em>, vemurafenib reduced tumor growth in athymic mice xenografted with melanoma cells embedded in young collagen matrices, but not in those with aged collagen. Collectively, our data suggest that age-related alterations in type I collagen contribute to reduced efficacy of anti-BRAF^V600E therapies in BRAF^V600E-mutated melanoma.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":"190 ","pages":"Article 118351"},"PeriodicalIF":6.9,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144663027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methanol extract of Euphorbia cotinifolia L. leaf attenuates inflammation and oxidative stress in RAW 264.7 macrophages via TAK1-mediated suppression of NF-κB/MAPK and activation of Nrf2 pathways","authors":"Junho Lee ,&nbsp;Salah Uddin ,&nbsp;Chohee Jeong ,&nbsp;Sang Beom Han ,&nbsp;Sayeon Cho","doi":"10.1016/j.biopha.2025.118372","DOIUrl":"10.1016/j.biopha.2025.118372","url":null,"abstract":"<div><div><em>Euphorbia cotinifolia</em> L. (<em>E. cotinifolia</em> L.) is distributed in temperate and tropical regions. It exhibits various biological activities, including antioxidant, antimicrobial, and antiviral properties. Although its antioxidant properties have been described, its regulatory molecular mechanisms remain poorly understood and its anti-inflammatory effects have not been studied yet. This study investigated the effects of methanol extract of <em>E. cotinifolia</em> L. (MECL) on inflammation and oxidative stress in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. MECL significantly suppressed the production of inflammatory mediators, including nitric oxide (NO) and prostaglandin E₂ (PGE₂), by downregulating inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). In addition, MECL inhibited the production of key pro-inflammatory cytokines, including interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α), by suppressing of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. It suppressed TAK1 phosphorylation, thereby inhibiting IKKα/β. Consequently, IκBα was stabilized, preventing its degradation and thereby suppressing NF-κB p65 phosphorylation and nuclear translocation. Additionally, MECL attenuated the activation of JNK, ERK, and p38 MAPK signaling. It also activated nuclear factor erythroid 2-related factor 2 (Nrf2), which is a key antioxidant transcription factor, upregulating its target genes, heme oxygenase-1 and NAD(P)H quinone dehydrogenase 1, which are essential for oxidative stress defense. These findings suggested that MECL mitigated inflammation and oxidative stress by regulating TAK1-mediated NF-κB/MAPK signaling and Nrf2 activation. Therefore, it showed potential as a natural therapeutic candidate for inflammatory diseases.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":"190 ","pages":"Article 118372"},"PeriodicalIF":6.9,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144655066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic challenges in breast cancer: Navigating the impact of oxidative stress on treatment efficacy and toxicity","authors":"Dariush Haghmorad ,&nbsp;Fatemeh Tavassoli Razavi ,&nbsp;Yasamin Eivazzadeh ,&nbsp;Esmaeil Yazdanpanah ,&nbsp;Niloufar Orooji","doi":"10.1016/j.biopha.2025.118364","DOIUrl":"10.1016/j.biopha.2025.118364","url":null,"abstract":"<div><div>Breast cancer remains one of the most prevalent and challenging malignancies worldwide, necessitating a multifaceted therapeutic approach. Although current treatments- including chemotherapy, radiotherapy, targeted therapy, and hormone therapy- have significantly improved patient outcomes, they are often associated with substantial adverse effects and therapeutic resistance. Emerging evidence underscores the critical role of oxidative stress in mediating both the efficacy and toxicity of these treatments. Reactive oxygen species (ROS), generated either endogenously or as a byproduct of anticancer therapies, contribute to cellular damage, inflammation, and impaired redox homeostasis, ultimately influencing treatment outcomes. This review systematically explores the mechanisms by which oxidative stress modulates the biological response to anthracyclines, taxanes, and ionizing radiation, and highlights its involvement in treatment-induced cardiotoxicity, neurotoxicity, fibrosis, and immune dysregulation. Additionally, we examine the role of oxidative stress in resistance to HER2-targeted and hormone-based therapies. The article further discusses combination therapy-induced synergistic toxicity and outlines current and emerging antioxidant-based strategies- ranging from natural compounds and synthetic agents to nanomedicine and gene modulation- that may mitigate oxidative damage. Understanding the complex interplay between redox biology and therapeutic response offers new opportunities for improving treatment efficacy, minimizing adverse effects, and advancing personalized interventions in breast cancer care.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":"190 ","pages":"Article 118364"},"PeriodicalIF":6.9,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144655051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating neuroprotection, antioxidative effects, and precision medicine in glaucoma management with bioactive compounds","authors":"Yan Zhu,&nbsp;Laxmi Moksha,&nbsp;Rebecca Salowe,&nbsp;Vrathasha Vrathasha,&nbsp;Kenneth Pham,&nbsp;Marine-Ayan Ibrahim Aibo,&nbsp;Roy Lee,&nbsp;Mina Halimitabrizi,&nbsp;Isabel Di Rosa,&nbsp;Joan M. O’Brien","doi":"10.1016/j.biopha.2025.118319","DOIUrl":"10.1016/j.biopha.2025.118319","url":null,"abstract":"<div><div>Glaucoma is a group of progressive optic neuropathies characterized by the degeneration of retinal ganglion cells (RGCs) and their axons, leading to irreversible vision loss or blindness if left untreated. Current glaucoma treatments primarily focus on lowering intraocular pressure (IOP), the only proven method to slow disease progression. However, these treatments do not effectively address RGC loss or promote optic nerve regeneration. Emerging research into both natural and synthetic bioactive compounds offers promising new avenues for glaucoma management. This review explores the multifaceted therapeutic potential of bioactive compounds in glaucoma treatment, focusing on their mechanisms of action in IOP reduction and neuroprotection, as well as antioxidant and anti-inflammatory effects. We further review ongoing clinical trials and discuss significant challenges to clinical translation, including the issues of bioavailability, standardization, long-term safety, and regulatory challenges. Furthermore, this paper highlights the potential of integrating precision medicine into bioactive treatments, emphasizing the value of personalized care based on genetic and phenotypic profiles. Finally, the review discusses the role of combination therapies, which leverage the complementary mechanisms of bioactive compounds and conventional treatments. As research progresses, the development of targeted, bioactive-based therapies could transform glaucoma management, offering more comprehensive and effective options for patients with this vision-threatening disease.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":"190 ","pages":"Article 118319"},"PeriodicalIF":6.9,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144655411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HA-PAs hydrogel for enhanced cartilage repair in early osteoarthritis: A novel minimally invasive treatment strategy","authors":"Guangjie Li ,&nbsp;Jianbao Feng ,&nbsp;Fei He ,&nbsp;Ge Xu ,&nbsp;Chengye Wu ,&nbsp;Xiaoming Ma ,&nbsp;Yufei Qiao ,&nbsp;Zeyu Luo ,&nbsp;Pengcheng Du","doi":"10.1016/j.biopha.2025.118356","DOIUrl":"10.1016/j.biopha.2025.118356","url":null,"abstract":"<div><div>Osteoarthritis (OA) is a degenerative joint disease characterized by joint inflammation, progressive degeneration and destruction of articular cartilage, ultimately resulting in irreversible damage. The treatment of OA is costly, has significant side effects, and yields limited efficacy. To improve OA therapy, we used 3-aminobenzoboronic acid (PBA) as a binding site for proanthocyanidins (PAs), with hyaluronic acid (HA) serving as a drug carrier. A simple method was employed to develop an injectable, biocompatible hydrogel (HA-PAs hydrogel) with sustained-release functionality, aimed is to promote the <em>in vivo</em> repair of cartilage and ligaments by enhancing the expression of collagen and glycosaminoglycans. Characterization results confirmed that HA and PAs crosslinked to form hydrogels through amide and borate ester bonds in PBA. The controlled release function of PAs was further validated through in vitro drug release experiments. The good biocompatibility of HA-PAs hydrogel was further confirmed by CCK-8 assay and cellular live/dead staining. More importantly, compared with PAs alone, the HA-PAs hydrogel exhibited superior ability to promote the expression of collagen and glycosaminoglycans. In a rat enzymatic OA model, the HA-PAs hydrogel significantly reduced joint inflammation in the early stages of cartilage destruction and accelerated cartilage formation. This work provides an inexpensive and efficacious strategy for minimally invasive treatment of early osteoarthritis.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":"190 ","pages":"Article 118356"},"PeriodicalIF":6.9,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144655067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}