Archives of Pharmacal Research最新文献

{"title":"Associations between the gut microbiota and the metabolism rate of tacrolimus in kidney transplant recipients during the early posttransplant period.","authors":"Nahathai Dukaew, Kajohnsak Noppakun, Patcharawadee Thongkumkoon, Mingkwan Na Takuathung, Ratchanon Inpan, Nattharinee Kongta, Naruemon Suyayai, Chalongrat Manoree, Nut Koonrungsesomboon","doi":"10.1007/s12272-025-01549-x","DOIUrl":"https://doi.org/10.1007/s12272-025-01549-x","url":null,"abstract":"<p><p>The use of tacrolimus (TAC), a critical immunosuppressant post transplantation, is complicated by its high pharmacokinetic variability. While the gut microbiota has gained attention as a potential contributor, few studies have assessed its role in TAC metabolism variability. This study investigated the associations between the gut microbiota and TAC metabolism rates in kidney transplant recipients during the first month post transplantation-a crucial period for adjusting TAC to achieve therapeutic levels. We recruited 20 kidney transplant recipients and profiled their gut microbiota diversity and composition from stool samples collected before transplantation and at weeks 1 and 4 post transplantation via 16S rRNA sequencing. The TAC pharmacokinetic parameters were also collected. Associations between TAC metabolism status or pharmacokinetic parameters and gut microbiota diversity and composition were evaluated. Recipients with a fast TAC metabolism rate (C₀/D ratio < 1.05 ng/mL × 1/mg) presented significantly greater changes in both bacterial alpha and beta diversity metrics at 1 week post transplantation than did those with a slow metabolism rate (C₀/D ratio ≥ 1.05 ng/mL × 1/mg). Compared with slow metabolizers, fast metabolizers were associated with a significant increase in the abundance of three bacterial genera (Faecalibacterium, Clostridia vadinBB60, and Ruminococcus) and a significant decrease in the abundance of two bacterial species (Bacteroides plebeius and Parabacteroides goldsteinii). This study revealed links between gut microbiota diversity and composition and TAC metabolism rates in kidney transplant recipients during the early posttransplant period, underscoring the importance of investigating the gut microbiota as a contributor to TAC pharmacokinetic variability. Clarifying this causal relationship could better predict inter- and intraindividual TAC pharmacokinetic variability.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-CHI3L1 antibody suppresses colon cancer growth through downregulation of VEGFA and NAMPT expression","authors":"Ji Won Seo,&nbsp;Deok Rim Heo,&nbsp;Ji Eun Yu,&nbsp;A-Young Nam,&nbsp;Na Yeong Lee,&nbsp;Ja Keun Koo,&nbsp;Sang Bae Han,&nbsp;Jung-Hyun Shim,&nbsp;Jin Tae Hong","doi":"10.1007/s12272-025-01548-y","DOIUrl":"10.1007/s12272-025-01548-y","url":null,"abstract":"<div><p>Chitinase 3-like 1 (CHI3L1) has been implicated in the pathogenesis of various diseases, including cancer. In our previous study, we found that anti-CHIL1 antibody inhibited lung tumorigenesis. It has been reported that CHI3L1 is highly overexpressed in colon cancer tissue compared with normal tissue, and high levels of serum CHI3L1 have been associated with worse colon cancer prognosis. We investigated the anticancer effect of an anti-CHI3L1 antibody on colon cancer cells. The anti-CHI3L1 antibody inhibited the cell growth of colon cancer cells in a concentration-dependent manner. The anti-CHI3L1 antibody also reduced the migration but increased apoptotic cell death in colon cancer cells. Using STRING (Search Tool for the Retrieval of Interacting Genes/Proteins), we identified an association between VEGFA and CHI3L1 in colon cancer. We confirmed interaction between VEGFA and CHI3L1 through immunoprecipitation. Furthermore, the combination treatment of the anti-CHI3L1 antibody and VEGFA siRNA inhibited cell growth but increased apoptotic cell death. Additionally, using the Human Base database, we found that CHI3L1 and VEGFA are associated with nicotinamide phosphoribosyltransferase (NAMPT). Furthermore, combining the anti-CHI3L1 antibody and NAMPT siRNA more effectively reduced cell growth and the expression of CHI3L1, VEGFA, and cell growth-related proteins, but significantly increased apoptosis-related proteins. The combination of VEGFA siRNA and NAMPT siRNA more effectively inhibited cell growth. Anti-CHI3L1 antibody inhibited the production of ATP and NADH in colon cancer and had a higher inhibitory effect on these levels when combined with NAMPT siRNA These data demonstrated that anti-CHI3L1 antibody is useful as a potential therapy for colon cancer by inhibiting NAMPT-dependent VEGFA expression and ATP and NADH levels.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 5","pages":"450 - 466"},"PeriodicalIF":6.9,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BTK inhibitors and next-generation BTK-targeted therapeutics for B-cell malignancies","authors":"Hyung-Ook Kim","doi":"10.1007/s12272-025-01546-0","DOIUrl":"10.1007/s12272-025-01546-0","url":null,"abstract":"<div><p>Bruton’s tyrosine kinase (BTK) is a therapeutically validated drug target. Small-molecule inhibitors of BTK have changed the treatment paradigms of multiple B-cell malignancies and evolved over three generations to overcome clinical challenges. Four drugs are now approved by the FDA, including the first-in-class drug ibrutinib and successively approved acalabrutinib, zanubrutinib, and pirtobrutinib. The third-generation drug pirtobrutinib, which binds non-covalently to BTK, is expected to overcome resistance mutations at the covalent binding Cys481 residue of the first and second-generation drugs that covalently bind to BTK. However, some newly identified non-Cys481 resistance mutations to pirtobrutinib have shown their co-resistance to some of the covalent inhibitors, and this leaves a major unmet need that is promoting the development of next-generation BTK-targeted therapeutics. More non-covalent BTK inhibitors with differentiated binding modes are under development, and the ongoing development focus of next-generation therapeutics involves new and alternative directions to target BTK using dual-binding inhibitors and degraders of BTK, as well as its allosteric inhibitors. Recent exploration of the differentiated features of BTK inhibitors in various aspects has shown the possible link between their different features and different functional and therapeutic consequences. This review summarizes the key differentiated features of the BTK inhibitors approved by the FDA and others under development to add knowledge for their therapeutic application and future development. Long-term follow-up updates of clinical outcomes of the earlier developed drugs are also included, together with direct and indirect comparisons of efficacy and safety between the different generations of drugs. The ongoing development status of next-generation BTK-targeted therapeutics is described, with a discussion on their therapeutic potential and some limitations.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 5","pages":"426 - 449"},"PeriodicalIF":6.9,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143961486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting vascular endothelial growth receptor-2 (VEGFR-2): structural biology, functional insights, and therapeutic resistance","authors":"Fahad Hassan Shah,&nbsp;Yoon Seok Nam,&nbsp;Jun Young Bang,&nbsp;In Seo Hwang,&nbsp;Dae Hong Kim,&nbsp;Minkyoung Ki,&nbsp;Heon-Woo Lee","doi":"10.1007/s12272-025-01545-1","DOIUrl":"10.1007/s12272-025-01545-1","url":null,"abstract":"<div><p>Angiogenesis, the process of new blood vessel formation, is a fundamental physiological process implicated in several pathological disorders. The vascular endothelial growth factors (VEGFs) and their receptors (VEGFRs) are crucial for angiogenesis and vasculogenesis. Among them, the tyrosine kinase receptor VEGFR-2 is primarily expressed in endothelial cells (ECs). These cells regulate various physiological responses, including differentiation, cell proliferation, migration, and survival, by binding to VEGF mitogens. Vascular Endothelial Growth Factor Receptor 2 (VEGFR-2) is a key regulator of this process, making it a prime target for therapeutic intervention. Several drugs targeting VEGFR-2 have been approved and are currently utilized to halt the pathological axis of VEGF-VEGFR. This review will focus on the recent developments in the molecular structure and function of VEGFR-2, the molecular mechanism of VEGFR-2 activation, and its downstream signaling pathway. It will also discuss therapies and experimental drugs approved to inhibit the function of VEGFR-2 and the resistance mechanism.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 5","pages":"404 - 425"},"PeriodicalIF":6.9,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s12272-025-01545-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deficiency of β-arrestin2 ameliorates MASLD in mice by promoting the activation of TAK1/AMPK signaling","authors":"Ting-Ting Chen,&nbsp;Shan Shan,&nbsp;Ya-Ning Chen,&nbsp;Meng-Qi Li,&nbsp;Hui-Juan Zhang,&nbsp;Ling Li,&nbsp;Ping-Ping Gao,&nbsp;Nan Li,&nbsp;Yan Huang,&nbsp;Xiao-Lei Li,&nbsp;Wei Wei,&nbsp;Wu-Yi Sun","doi":"10.1007/s12272-025-01544-2","DOIUrl":"10.1007/s12272-025-01544-2","url":null,"abstract":"<div><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a liver manifestation of metabolic syndrome characterized by excessive hepatic lipid accumulation and lipid metabolism disorders. It has become the most common chronic liver disease worldwide. β-arrestin2 is a multifunctional scaffold protein that is among the most important regulatory molecules, and it exerts key roles in regulating various cellular processes, such as immune response, cellular collagen production, and inflammation. In the current study, we aimed to explore the function of β-arrestin2 in the development and progression of MASLD. Firstly, we observed that the expression of β-arrestin2 was upregulated in liver samples from patients with MASLD. Then, the western diet (WD) combined with CCl₄ injection-induced MASLD was established in wild-type mice, and showed that liver β-arrestin2 expression was also gradually increased, and positively correlated with the degree of lipid metabolism disorder during MASLD progression. Ulteriorly, β-arrestin2 knockout (<i>Arrb2</i> KO) mice were utilized to induce the MASLD model and found that β-arrestin2 deficiency significantly ameliorated lipid accumulation and inflammatory response in the liver of MASLD mice. Furthermore, the in vitro depletion and overexpression experiments showed that increased β-arrestin2 aggravated lipid accumulation via inhibiting the activation of the TAK1/AMPK pathway, which may be mediated by competitively binding to TAB1 with TAK1. These findings suggest that β-arrestin2 is essential to regulate intrahepatic lipid metabolism. Here, we provide a novel insight in understanding of the expression and function of β-arrestin2 in MASLD, demonstrating that it may be a potential therapeutic target for MASLD treatment.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 5","pages":"384 - 403"},"PeriodicalIF":6.9,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143952573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biodegradable gelatin methacryloyl microneedles: a new paradigm in transdermal drug delivery.","authors":"Khazanah Nurain Nurdin, Cecep Suhandi, Ahmed Fouad Abdelwahab Mohammed, Safwat A Mahmoud, Khaled M Elamin, Muchtaridi Muchtaridi, Nasrul Wathoni","doi":"10.1007/s12272-025-01547-z","DOIUrl":"https://doi.org/10.1007/s12272-025-01547-z","url":null,"abstract":"<p><p>Microneedles (MN) have emerged as a promising transdermal drug delivery technology that offers advantages such as minimal invasiveness, high biocompatibility, and biodegradability. Gelatin methacryloyl (GelMA)-based MNs have gained attention because of their flexibility, mechanical strength, and modification capabilities, which support controlled drug release. The synthesis process of GelMA involves crosslinking using UV light, resulting in a stable hydrogel structure that supports therapeutic applications, such as wound healing, cancer therapy, and glucose monitoring. However, challenges such as skin penetration strength, drug-loading capacity, and regulatory standards still require solutions. Material and design innovations, particularly the combination of GelMA with nanomaterials and natural polymers, have the potential to enhance the MN efficiency and expand its applications in various medical fields. This review explores the latest developments in GelMA-based MN design and their future potential as reliable therapeutic devices.</p>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143958847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RSK2 and its binding partners: an emerging signaling node in cancers","authors":"Hye Suk Lee,&nbsp;Sung-Jun Cho,&nbsp;Han Chang Kang,&nbsp;Joo Young Lee,&nbsp;Young Jik Kwon,&nbsp;Yong-Yeon Cho","doi":"10.1007/s12272-025-01543-3","DOIUrl":"10.1007/s12272-025-01543-3","url":null,"abstract":"<div><p>The growth factor-mediated mitogen-activated protein kinase (MAPK) signaling pathways in cancer development have become increasingly important in the discovery of therapeutic agents for the treatment of cancer. RSK2 has been historically overlooked in studies regarding its involvement in physiology and signaling pathways related to human diseases, except for Coffin-Lowry syndrome, because it is located downstream of ERKs. For the last 25 years, the authors’ laboratory has made groundbreaking discoveries regarding the role of RSK2, especially by elucidating its binding partners, signaling network, and crosstalk. RSK2 is an important emerging target for developing anticancer drugs. Nevertheless, further studies on the detailed mechanism and signaling network are necessary to avoid the unexpected effects of RSK2 inhibitors. This paper describes a new paradigm of RSK2, where it works as a signaling node to modulate diverse cellular processes, including cell proliferation and transformation, cell cycle regulation, chromatin remodeling, and immune response and inflammation regulation.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 5","pages":"365 - 383"},"PeriodicalIF":6.9,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic insights and emerging therapeutic strategies targeting endothelial dysfunction in cardiovascular diseases","authors":"Kyung-Sun Heo,&nbsp;Lan Phuong Phan,&nbsp;Nhi Thi Thao Le,&nbsp;Yujin Jin","doi":"10.1007/s12272-025-01542-4","DOIUrl":"10.1007/s12272-025-01542-4","url":null,"abstract":"<div><p>Endothelial dysfunction plays a pivotal role in the pathogenesis of various cardiovascular diseases (CVDs), including atherosclerosis, hypertension, heart failure, stroke, and peripheral artery disease. It disrupts vascular homeostasis, leading to reduced nitric oxide (NO) bioavailability, increased oxidative stress, and chronic inflammation, all of which collectively drive vascular damage, atherosclerotic plaque formation, and thrombosis. Additionally, shear stress-induced alterations in blood flow patterns, particularly disturbed flow (d-flow), aggravate endothelial dysfunction. Furthermore, the endothelial-to-mesenchymal transition (EndMT), a process in which endothelial cells acquire mesenchymal-like properties, contributes to vascular remodeling and accelerates CVD progression.</p><p>This review explores the significant role of epigenetic mechanisms, such as DNA methylation, histone modifications, and noncoding RNAs (ncRNAs), which serve as critical regulators of endothelial function in response to shear stress in endothelial dysfunction and the development of atherosclerosis. Furthermore, we discuss the pivotal role of endothelial dysfunction in cardiovascular and metabolic diseases, emphasizing the need for innovative therapeutic strategies beyond conventional treatments. In particular, we highlight the endothelial-protective mechanisms of emerging pharmacological agents, including proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, glucagon-like peptide-1 receptor agonists (GLP-1RAs), and sodium-glucose cotransporter 2 (SGLT2) inhibitors, along with supporting clinical evidence demonstrating their efficacy in improving endothelial function and reducing cardiovascular risk.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 4","pages":"305 - 332"},"PeriodicalIF":6.9,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143913942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PET tracer development for imaging α-synucleinopathies","authors":"Mohammad Maqusood Alam,&nbsp;Sun Hak Lee,&nbsp;Sobia Wasim,&nbsp;Sang-Yoon Lee","doi":"10.1007/s12272-025-01538-0","DOIUrl":"10.1007/s12272-025-01538-0","url":null,"abstract":"<div><p>Abnormal α-synuclein aggregation is a key neuropathological hallmark of α-synucleinopathies, such as Parkinson’s disease (PD), multiple system atrophy (MSA), and several other neurological disorders, and closely contributes to pathogenesis. The primary characteristics of α-synucleinopathies are selective targeted neurodegeneration and the accumulation of Lewy pathologies. Specifically, α-synuclein positron emission tomography (PET) radiotracers target the fibrillar forms of the protein, thus enhancing early diagnosis and the evaluation of treatment effectiveness for various α-synucleinopathies. Therefore, in vivo detection of α-synuclein aggregates using targeted radiolabeled probes would aid in drug development, early diagnosis, and ongoing disease monitoring. As such, no promising α-synuclein biomarkers suitable for clinical applications have been reported. PET is a valuable non-invasive technique for imaging drug distribution in tissues and receptor occupancy at target sites in living animals and humans. Advances in PET biomarkers have significantly enhanced our understanding of the mechanisms underlying PD. This review summarizes recent ongoing efforts in the development of selective PET tracers for α-synuclein and discusses future perspectives.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 4","pages":"333 - 350"},"PeriodicalIF":6.9,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143913926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review on bacteria-derived antioxidant metabolites: their production, purification, characterization, potential applications, and limitations","authors":"Nazli Pinar Arslan,&nbsp;Fakhrul Azad,&nbsp;Tugba Orak,&nbsp;Aysenur Budak-Savas,&nbsp;Serkan Ortucu,&nbsp;Pranav Dawar,&nbsp;Mustafa Ozkan Baltaci,&nbsp;Hakan Ozkan,&nbsp;Nevzat Esim,&nbsp;Mesut Taskin","doi":"10.1007/s12272-025-01541-5","DOIUrl":"10.1007/s12272-025-01541-5","url":null,"abstract":"<div><p>Antioxidants are organic molecules that scavenge reactive oxygen species (ROS) and reactive nitrogen species (RNS), thereby maintaining cellular redox balance in living organisms. The human body synthesizes endogenous antioxidants, whereas humans obtain exogenous antioxidants from other organisms such as plants, animals, fungi, and bacteria. This review primarily focuses on the antioxidant potential of natural metabolites and extracts from five major bacterial phyla, including the well-studied <i>Actinobacteria</i> and <i>Cyanobacteria</i>, as well as less-studied <i>Bacteroides</i>, <i>Firmicutes</i>, and <i>Proteobacteria</i><i>.</i> The literature survey revealed that the metabolites and the extracts with antioxidant activity can be obtained from bacterial cells and their culture supernatants. The metabolites with antioxidant activity include pigments, phycobiliproteins, polysaccharides, mycosporins-like amino acids, peptides, phenolic compounds, and alkaloids. Both metabolites and extracts demonstrate in vitro antioxidant capacity through radical-scavenging, metal-reducing, and metal-chelating activity assays. In in vivo models, they can scavenge ROS and RNS directly and/or indirectly eliminate them by enhancing the activities of antioxidant enzymes, such as catalase, superoxide dismutase, and glutathione peroxidase. Due to their antioxidant activities, they may find applications in the cosmetic industry as anti-aging agents for the skin and in medicine as drugs or supplements for combating oxidative stress-related disorders, such as neurodegenerative diseases and diabetes. The literature survey also elucidated that some metabolites and extracts with antioxidant activity also exhibited strong antimicrobial properties. Therefore, we consider that they may have future applications in the treatment of infectious diseases, the preparation of pathogen-free healthy foods, and the extension of food shelf life.</p></div>","PeriodicalId":8287,"journal":{"name":"Archives of Pharmacal Research","volume":"48 4","pages":"253 - 292"},"PeriodicalIF":6.9,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s12272-025-01541-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143913892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}