Naunyn-Schmiedeberg's archives of pharmacology最新文献

{"title":"Potential prognostic biomarker of OSBPL10 in pan-cancer associated with immune infiltration.","authors":"Jiapeng Qi, Kun Yu, Bei Liu, Yan Wang, Wei Wang, Ran An, Chaojun Wang, Na Li, Dongqian Xu, Lin Liu","doi":"10.1007/s00210-025-03998-z","DOIUrl":"https://doi.org/10.1007/s00210-025-03998-z","url":null,"abstract":"<p><p>Oxysterol binding protein-related protein 10 (OSBPL10) is a crucial sterol transporter that plays a significant role in regulating metabolic homeostasis. Previous studies have indicated that OSBPL10 promotes the development of several tumors. However, an integrative bioinformatics and immune infiltration analysis of OSBPL10 across various cancers has yet to be conducted. In this study, we comprehensively analyzed the expression patterns, prognostic value, genetic variations, protein modifications, immune infiltration characteristics, and biological functions of OSBPL10 in 33 human cancers using bioinformatics methods and publicly available databases, including TCGA, GEPIA2, GTEx, UCSC, UALCAN, HPA and TISCH2.0. The function of OSBPL10 and its associated mechanisms were confirmed in the pancreatic cancer cell lines Panc-1 and Mia PaCa-2. Our results revealed that OSBPL10 mRNA expression was significantly upregulated in 12 types of tumor tissues and downregulated in 3 cancers, which was notably associated with poor prognosis, pathological stage, and subtype in 10 tumors. Additionally, the level of promoter methylation exhibited a significant negative correlation with OSBPL10 mRNA expression. OSBPL10 expression was found to be dramatically associated with the levels of chemokines, chemokine receptors, immune checkpoints, and immune cell infiltration across various tumors by activating cancer pathways related to the extracellular matrix (ECM) and TSC/mTOR while downregulating tumor cell stemness. Furthermore, elevated OSBPL10 expression was negatively correlated with most drug sensitivities. In vitro experiments showed that OSBPL10 promoted the proliferation and migration of pancreatic cancer cells through the VEGF/AKT signaling pathway. In conclusion, our pan-cancer analysis suggests that OSBPL10 may serve as a critical biomarker for improving prognosis through OSBPL10-targeted therapies, immunotherapies, and chemotherapeutic combinations in cancer patients.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of human microbiota in facilitating the metastatic journey of cancer cells.","authors":"Himisa Shah, Princy Patel, Abhay Nath, Umang Shah, Ruma Sarkar","doi":"10.1007/s00210-025-03957-8","DOIUrl":"https://doi.org/10.1007/s00210-025-03957-8","url":null,"abstract":"<p><p>Cancer continues to be the leading cause of mortality worldwide, with metastasis being the primary contributor to cancer-related deaths. Despite significant advancements in cancer therapies, metastasis remains a major challenge in effective cancer management. Metastasis, the process by which cancer cells spread from the primary tumor to distant organs, is a complex phenomenon influenced by multiple factors, including the human microbiota. The human body encompasses various microorganisms, comprising bacteria, viruses, fungi, and protozoa, collectively known as microbiota. In fact, the microbiota is more abundant than human cells, and its disruption, leading to an imbalance in host-microbiota interactions (dysbiosis), has been linked to various diseases, including cancer. Among all microbiota, bacteria are one of the key contributors to cancer progression. Bacteria and bacteria-derived components such as secondary metabolites, QSPs, and toxins play a pivotal role in the metastatic progression of cancers. This review explores the intricate relationship between the human microbiota and cancer progression, focusing on different bacterial species which have been implicated in tumorigenesis, immune evasion, and metastasis. The present review explores the role of the human microbiome, specifically of bacteria in promoting metastasis in different types of cancers, demonstrating its ability to impact both the spread of tumors and their underlying mechanisms. This review also highlights the therapeutic potential and challenges of microbiome-based interventions in combating metastatic cancers. By addressing these challenges and by integrating microbiome-targeted strategies into clinical cancer treatment could represent a transformative approach in the fight against metastasis.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Harnessing bee venom for inflammatory diseases management: from traditional medicine to nanotechnology.","authors":"Vandna Bhardwaj, Naresh Thakur, Priyanka Kumari","doi":"10.1007/s00210-025-03991-6","DOIUrl":"https://doi.org/10.1007/s00210-025-03991-6","url":null,"abstract":"<p><p>This review investigates the anti-inflammatory potential of bee venom, a natural compound comprising peptides, enzymes, biogenic amines other bioactive amines, and other bioactive components. It aims to elucidate how bee venom mitigates inflammatory responses caused by tissue injury, infections, and trauma. This study also explores the advancements in nanotechnology to enhance bee venom's therapeutic effects. A systematic review of studies from Google Scholar and PubMed, up to 2025, was conducted. Both in vitro and in vivo research focusing on bee venom's effects on proinflammatory mediators were analyzed. Specific attention was given to its molecular mechanisms, therapeutic impact on inflammatory conditions, and the role of nanotechnology in improving drug delivery and stability. Bee venom and its components, including melittin, apamin, and phospholipase A2 demonstrate robust anti-inflammatory properties by inhibiting key proinflammatory mediators. These effects have been observed in the treatment of chronic inflammatory conditions such as rheumatoid arthritis and skin disorders. Studies show bee venom's capacity to reduce excessive inflammatory responses effectively. Moreover, incorporating nanotechnology significantly enhances its therapeutic benefits by improving delivery, stability, and bioavailability, paving the way for advanced applications. Bee venom offers a natural, powerful approach to combating the inflammation and related chromic disorders. Its ability to regulate inflammatory pathways is promising for therapeutic use. The integration of nanotechnology further amplifies its potential, providing innovative solutions for efficient and targeted treatments. This study also highlights the need for more clinical trials to establish bee venom as a mainstream therapeutic agent in modern medicine.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erbium oxide nanoparticles induce potent cell death, genomic instability and ROS-mitochondrial dysfunction-mediated apoptosis in U937 lymphoma cells.","authors":"Hanan R H Mohamed, Yusuf Ahmed Elberry, Hagar Magdy, Maryam Ismail, Maivel Michael, Nourhan Eltayeb, Gehan Safwat","doi":"10.1007/s00210-025-03962-x","DOIUrl":"https://doi.org/10.1007/s00210-025-03962-x","url":null,"abstract":"<p><p>Erbium oxide nanoparticles (Er₂O₃-NPs) have attracted significant attention for their unique physicochemical properties, including high surface area, biocompatibility, and stability. However, the impact of Er₂O₃-NPs on lymphoma cells (LCs) has not been explored, making this an innovative avenue for exploration. Therefore, the current study aimed to explore the influence of Er₂O₃-NPs on cell viability, genomic and mitochondrial DNA integrity, reactive oxygen species (ROS) generation and apoptosis induction in human U937 LCs. Er₂O₃-NPs were characterized using X-ray diffraction (XRD) and transmission electron microscopy (TEM). The effect of Er₂O₃-NPs on cell viability and genomic DNA integrity was estimated after 48 h using the WST-1 cytotoxicity and alkaline Comet assays, respectively. The generation level of reactive oxygen species (ROS) and mitochondrial membrane potential were also analyzed. Flow Cytometry was used to assess apoptosis induction and quantitative RT-PCR was conducted to measure the apoptotic (p53), anti-apoptotic (Bcl2), and mitochondrial (ND3) gene expression. Our results demonstrated the purity and well distribution of Er₂O₃-NPs and revealed that Er₂O₃-NPs induce strong cytotoxicity on U937 cells, as evidenced by a concentration-dependent reduction in cell viability with an IC50 value of 3.20 µg/ml. Exposure of U937 LCs to the IC50 concentration (3.20 µg/ml) of Er₂O₃-NPs promoted excessive ROS generation, leading to dramatic damage to genomic DNA and mitochondrial membrane potential, as well as marked dysregulation of apoptotic (p53), anti-apoptotic (Bcl2) and mitochondrial ND3 gene expression. This cascade of events triggered both apoptosis and necrosis in Er₂O₃-NPs-treated U937 LCs. In conclusion, these findings highlight the strong in vitro cytotoxic potential of Er₂O₃-NPs against highly aggressive U937 LCs, mediated by excessive ROS production, which leads to severe genomic DNA and mitochondrial membrane damage, as well as profound alterations in apoptotic, anti-apoptotic and mitochondrial gene expression. Future research is needed to further investigate the potential use of Er₂O₃-NPs in treating lymphoma and to optimize their therapeutic efficacy.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The bioactivity of atraric acid as an inducer of cellular senescence in prostate cancer cells is retained by lipophilic derivatives.","authors":"Adina Asara Baniahmad, Golnaz Atri Roozbahani, Manfred Jung, Aria Baniahmad","doi":"10.1007/s00210-025-03989-0","DOIUrl":"https://doi.org/10.1007/s00210-025-03989-0","url":null,"abstract":"<p><p>Esters have been described as bioactive chemical compounds. However, the presence of an ester as a functional group is often associated with hydrolytic liability. Therefore, it is often unclear whether esters serve as pro-drugs and are rather converted into bioactive drugs in cells. The small molecule atraric acid (AA) has an ester group and had been identified as the first natural androgen receptor antagonist that inhibits prostate cancer cell growth and induces cellular senescence in cancer cells. Based on the presence of the ester group, it is unclear whether AA is a prodrug being hydrolyzed to generate the bioactive compound intracellularly. Here, we addressed this issue by synthesizing novel compounds for which the ester group has been replaced by a stable isoster. To replace the methylester group of atraric acid, a ketone with a propanoyl side chain and a N-methoxy-N-methyl-amide derivative were synthesized. Functional assays suggest that both non-ester atraric acid derivatives are bioactive in inducing cellular senescence. Treatment of human prostate cancer cells with these compounds suggest that both inhibit cell growth and induce cellular senescence in a dose-dependent manner. This was observed in two different human prostate cancer cell lines that serve as model systems for androgen-sensitive and castration-resistant prostate cancer, respectively. Computational modeling suggests that these two compounds bind to the androgen receptor ligand binding domain to similar receptor residues as AA. Thus, the data suggest that replacing the ester of AA by a ketone with a propanoyl group or by the N-methoxy-N-methyl-amide group the bioactivity as an androgen receptor antagonist is retained.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gallic acid's protective mechanisms against acrylamide-induced pulmonary injury: in vivo and in silico insights into the Nrf-2/HO-1/NFκB pathway modulation.","authors":"Merve Bolat, Samet Tekin, İsmail Bolat, Aslıhan Atasever, Burak Çinar, Yusuf Dağ, Emin Şengül, Serkan Yildirim, Mohamad Warda, Fikret Çelebi","doi":"10.1007/s00210-025-03996-1","DOIUrl":"https://doi.org/10.1007/s00210-025-03996-1","url":null,"abstract":"<p><p>Acrylamide (ACR) is a toxic compound formed during the heating of tobacco and starchy foods, contributing to increased reactive oxygen species (ROS) levels and significant health risks. This study evaluates the protective effects of gallic acid (GA), a natural polyphenol with potent antioxidant and anti-inflammatory properties, against ACR-induced lung injury. Fifty male rats were divided into five groups: Control, ACR, GA50 + ACR, GA100 + ACR, and GA100. Lung tissues were analyzed biochemically, histopathologically, immunohistochemically, and via immunofluorescence. GA exhibited dose-dependent protective effects by enhancing antioxidant defenses through Nrf-2 (43% increase) and HO-1 activation and reducing lipid peroxidation markers (MDA decreased by 38%). GA also suppressed pro-inflammatory mediators (TNF-α reduced by 35%) and restored anti-inflammatory levels by modulating the NF-κB pathway. Furthermore, GA reduced apoptosis (Caspase-3 activity decreased by 30%) and preserved lung tissue integrity by mitigating oxidative DNA damage (8-OHdG levels reduced by 29%) and pro-apoptotic signaling (Bax levels reduced by 34%). Computational analyses demonstrated GA's interaction with the KEAP1 protein, supporting its role in activating the KEAP1-Nrf2 pathway. These findings highlight GA's antioxidant, anti-inflammatory, and anti-apoptotic properties, suggesting its therapeutic potential for protecting against ACR-induced lung injury and paving the way for future research in lung health and toxicology.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"No evidence for paradoxical effects of tocilizumab in rodents.","authors":"Christoph Garbers","doi":"10.1007/s00210-025-04021-1","DOIUrl":"https://doi.org/10.1007/s00210-025-04021-1","url":null,"abstract":"<p><p>Interleukin-6 (IL-6) is a multifunctional cytokine with important functions in health and disease. In order to activate its target cells, IL-6 binds first to the IL-6 receptor (IL-6R), which in turn induces the recruitment and homodimerization of the signal-transducing β-receptor gp130 and the activation of intracellular signaling cascades, including the phosphoinositide 3-kinase (PI3K)-AKT cascade. IL-6 is involved in the pathogenesis of multiple inflammatory diseases, and tocilizumab, a monoclonal antibody that binds to the IL-6R and thus blocks the biological activities of IL-6, is in clinical use worldwide for the treatment of patients with inflammatory diseases, including rheumatoid arthritis. Recently, Weng and colleagues published a paper in Naunyn-Schmiedeberg's Archives of Pharmacology describing paradoxical effects of tocilizumab when used on murine cells in vitro and in a rat model of acute lung injury in vivo. In this communication, I provide evidence that the results presented by Weng and colleagues are not compatible with what is known about the biology of IL-6 and highlight why the provided evidence is insufficient to believe that tocilizumab shows the reported paradoxical effects in rodents.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long noncoding RNA MATN1-AS1 contributes to oxaliplatin resistance of gastric cancer cells through miR-518b/ZNF281 axis.","authors":"Xiuhuan Qiu, Licheng Zhang, Fengying Guo, Ruixiang Guo","doi":"10.1007/s00210-025-03990-7","DOIUrl":"https://doi.org/10.1007/s00210-025-03990-7","url":null,"abstract":"<p><p>Chemoresistance leads to poor outcomes of patients with gastric cancer (GC). Long non-coding RNAs (lncRNAs) have been demonstrated as novel gene modulators in various carcinomas and chemoresistance. Our study aimed to investigate the role and underlying modulatory mechanism of lncRNA MATN1-AS1 in GC chemoresistance. CCK-8, flow cytometry, and Transwell assays were performed to explore the influence of the MATN1-AS1/microRNA (miR)-518b/zinc finger protein 281 (ZNF281) axis on the half inhibition concentration (IC50) to oxaliplatin (OXA), apoptosis, migration, and invasion of OXA-resistant GC cells. Dual-luciferase reporter assay was conducted to confirm the target association between miR-518b and MATN1-AS1 (or ZNF281). Xenograft mouse models were established to confirm the role of MATN1-AS1 silencing in vivo. The expression of MATN1-AS1, miR-518b, ZNF281, and multidrug resistance-related genes was detected through RT-qPCR and western blotting. MATN1-AS1 expression was upregulated in OXA-resistant GC tissues and cell lines versus OXA-sensitive tissues and parental cell lines. MATN1-AS1 depletion significantly inhibited the IC50 value of OXA, cell migration, invasion, and drug resistance but promoted cell apoptosis in OXA-resistant GC cells. Additionally, MATN1-AS1 upregulated ZNF281 expression by sponging miR-518b in OXA-resistant GC cells. Inhibiting miR-518b or overexpressing ZNF281 antagonized the effects of MATN1-AS1 silencing on OXA resistance of GC cells. Upregulation of ZNF281 abrogated the suppressive effects of miR-518b overexpression on OXA resistance of GC cells. Moreover, MATN1-AS1 knockdown suppressed tumor growth, OXA resistance, and Ki-67 expression in xenograft mouse models. MATN1-AS1 promotes OXA resistance of GC cells by enhancing ZNF281 expression via sequestration of miR-518b, shedding new light on the chemoresistance of GC.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143616275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research progress on the bioactivity of platycodin D from Platycodon grandifloras.","authors":"Ying Song, Xin Lv, Chuanbo Ding, Xinglong Liu, Yuanyuan Han, Shengyue Chen, Min Li, Ting Zhao","doi":"10.1007/s00210-025-03875-9","DOIUrl":"https://doi.org/10.1007/s00210-025-03875-9","url":null,"abstract":"<p><p>Platycodon grandiflorus, in the family Platycodonaceae, has been traditionally utilized in China to treat sore throats, hoarseness, and coughs with phlegm. As a medicinal and food plant, P. grandiflorus has a long history of use. Recent research on natural medicine has highlighted the biological activity and potential medicinal benefit of P. grandiflorus, which has prompted in-depth studies. One of the main active compounds extracted from the root of this plant is platycodin D (PD). This compound has various beneficial properties, including anti-inflammatory, antitumor, antioxidant, metabolic regulatory, antiviral, hepatoprotective, and spermatogenic effects. Additionally, PD can serve as a vaccine adjuvant to increase the efficacy of vaccines. This article explores the potential mechanism of action in treating hepatocellular carcinoma, breast cancer, lung cancer, and diabetes. The pharmacokinetics and bioavailability of PD are also discussed. With advancements in basic research and clinical applications, PD is anticipated to become a significant therapeutic agent for treating inflammatory diseases, metabolic disorders, and cancer.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and safety of GLP-1 agonists in Parkinson's disease: a systematic review and meta-analysis of randomized controlled trials.","authors":"Mark Messak, Ahmed Abdelmageed, Abdelrahman A Senbel, Youssef A Khattab, Youssef Mandour, Omar Shaker, Ahmed Hamed Rehan, Samir Oransa, Mohamed Nasr, Abdullah Emad Shabeeb, Ziyad Rezq, Fares Hossam, Moaz Elsayed Abouelmagd","doi":"10.1007/s00210-025-03932-3","DOIUrl":"https://doi.org/10.1007/s00210-025-03932-3","url":null,"abstract":"<p><p>Recent trends suggest exploring the repurposing of different drugs for Parkinson's disease patients (PD). One of these drugs is Glucagon-like peptide-1 (GLP-1), a medication used to treat type 2 diabetes mellitus. This systematic review and meta-analysis aimed to evaluate the efficacy and safety of different forms of GLP-1 agonists on motor and non-motor functions of PD patients during ON-medication and OFF-medication states. A literature search was conducted through PubMed, Scopus, Web of Science, OVID, Cochrane Central, and Google Scholar using relevant keywords. Quality assessment was performed using the Risk of Bias-2 (RoB-2) domains. Statistical analysis included calculating the mean difference (MD) and the corresponding 95% confidence intervals (CIs) using Review Manager 5.4.1. Four randomized controlled trials (RCTs) testing three different forms of GLP-1 agonists with a total of 514 patients were included in the study. GLP-1 agonists significantly improved motor function during the OFF-medication state (MD =  - 3.29, 95% CI [- 5.17 to - 1.42], P = 0.0006). It does not show improvement in quality of life assessed by PDQ-39 (MD =  - 0.54, 95% CI [- 2.07 to 0.99], P = 0.49). None of the adverse effects stated in the RCTs were higher in the GLP-1 agonists group except for nausea (RR = 1.98, P = 0.0008), vomiting (RR = 6.65, P = 0.0008), constipation (RR = 1.45, P = 0.01), and weight loss (RR = 2.11, P = 0.03). This systematic review and meta-analysis provide evidence that GLP-1 agonists could improve the motor function of PD patients. However, safety is still of concern. Further high-quality studies with standardized protocols and larger sample sizes are needed to confirm our findings.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143605709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}