Naunyn-Schmiedeberg's archives of pharmacology最新文献

{"title":"FOXA1-mediated transcription of MFAP2 facilitates cell growth, metastasis and cisplatin resistance in uterine corpus endometrial carcinoma.","authors":"Jie Bai, Jing Bai, Hongzhen Zhang","doi":"10.1007/s00210-025-04041-x","DOIUrl":"https://doi.org/10.1007/s00210-025-04041-x","url":null,"abstract":"<p><p>Microfibril-associated protein 2 (MFAP2) has been confirmed to be an oncogene to participate in regulating the progression of many cancers. However, its role and mechanism in the development of uterine corpus endometrial carcinoma (UCEC) are still unclear. The mRNA and protein levels of MFAP2 and forkhead box A1 (FOXA1) were determined using qRT-PCR and western blot. Cell proliferation, apoptosis, migration, invasion and cisplatin resistance were detected by colony formation assay, EdU assay, flow cytometry, transwell assay and CCK8 assay. Xenograft tumor models were constructed to explore the effect of MFAP2 knockdown on UCEC tumorigenesis and cisplatin resistance in vivo. The interaction between FOXA1 and MFAP2 promoter was evaluated by ChIP assay and dual-luciferase reporter assay. MFAP2 was upregulated in UCEC tissues and cells. Silencing of MFAP2 repressed UCEC cell growth, metastasis and cisplatin resistance in vitro, as well as reduced tumorigenesis in vivo. In terms of mechanism, FOXA1 bound to MFAP2 promoter region to increase its expression. FOXA1 knockdown could inhibit UCEC cell growth, metastasis and cisplatin resistance. Moreover, FOXA1 promoted growth, metastasis and cisplatin resistance in UCEC cells via enhancing MFAP2 expression. FOXA1-activated MFAP2 might contribute to the growth, metastasis and cisplatin resistance of UCEC cells, providing a novel target for UCEC treatment.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143736030","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":"Green-synthesized selenium-hydroxytyrosol nanocomposites attenuate hepatocellular carcinoma in rats by modulating oxidative stress, inflammation, and apoptosis.","authors":"Radwa T M Tawfik, Eman M Abd El-Azeem, Sawsan M Elsonbaty, Ehab A Ibrahim","doi":"10.1007/s00210-025-04034-w","DOIUrl":"https://doi.org/10.1007/s00210-025-04034-w","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) poses a significant health risk and greatly affects global rates of illness and death, highlighting an urgent requirement for new treatment strategies. This study examines the therapeutic effects of selenium-hydroxytyrosol nanocomposites (Se-HTNPs) in a rat model with HCC caused by diethylnitrosamine (DEN). Treatment with Se-HTNPs significantly inhibited serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and total bilirubin, while increasing serum albumin and total protein levels. Oxidative stress was alleviated, as evidenced by a marked reduction in hepatic malondialdehyde (MDA) levels and an increase in antioxidant markers, such as reduced glutathione (GSH), superoxide dismutase (SOD), and total antioxidant capacity (TAC). Se-HTNPs also significantly decreased hepatic inflammatory markers, such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β), as well as apoptotic markers (p53 and caspase-3) and vascular endothelial growth factor (VEGF). Furthermore, Se-HTNPs suppressed the mRNA expression of c-Jun N-terminal kinase (c-JNK) and nuclear factor kappa B (NF-κB) and improved histopathological alterations brought on by DEN. These findings suggest that Se-HTNPs mitigate DEN-induced HCC in rats through their potent antioxidant, anti-inflammatory, and anti-carcinogenic properties, underscoring their potential as a therapeutic strategy for HCC.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143719871","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":"Retraction Note: Disabled-2, a versatile tissue matrix multifunctional scaffold protein with multifaceted signaling: Unveiling its potential in the cancer battle.","authors":"Nidhi N Shah, Bhavarth P Dave, Kashvi C Shah, Disha D Shah, Kunal G Maheshwari, Mehul R Chorawala, Priyajeet S Parekh, Maharsh Jani","doi":"10.1007/s00210-025-04103-0","DOIUrl":"https://doi.org/10.1007/s00210-025-04103-0","url":null,"abstract":"","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720254","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":"Protective effects of berberine on MASLD: regulation of glucose and lipid metabolism through PI3K/Akt and STING pathways.","authors":"Jing Ji, Ying Li, Tian Xu, Qi Shao, Zijin Sun, Simin Chen, Di Zhang, Qingguo Wang, Xueqian Wang, Chongyang Ma, Fafeng Cheng","doi":"10.1007/s00210-025-04077-z","DOIUrl":"https://doi.org/10.1007/s00210-025-04077-z","url":null,"abstract":"<p><p>This study is aimed at exploring the therapeutic potential of berberine (BBR) in mitigating metabolic dysfunction-associated steatotic liver disease (MASLD) and at elucidating its mechanisms of action, with a focus on the modulation of glucose and lipid metabolism via the PI3K/Akt and STING signaling pathways. Male C57BL/6 J mice were fed a high-fat diet (HFD) to induce MASLD and subsequently treated with BBR or metformin. HepG2 cells were cultured in vitro, and palmitic acid (PA) was used to construct the cell model. Comprehensive analyses, including network pharmacology, transcriptome sequencing, and Western blotting, were conducted to identify critical pathways and molecular targets. Biochemical, histological, and molecular assays were performed to evaluate metabolic and inflammatory responses. BBR significantly attenuated HFD-induced hepatic steatosis, inflammation, and glucose intolerance. It effectively reduced lipid accumulation, enhanced insulin sensitivity, and modulated the expression of genes involved in lipid metabolism. Network pharmacology and transcriptome analysis highlighted the involvement of the PI3K/Akt and STING pathways. BBR activated PI3K/Akt signaling while suppressing the STING pathway, thereby reducing lipid accumulation in both in vivo and in vitro models. The inhibition of AKT negated the beneficial effects of BBR, underscoring the pivotal role of PI3K/Akt in regulating STING signaling. BBR ameliorates MASLD by activating the PI3K/Akt pathway and inhibiting the STING pathway, leading to improved glucose and lipid metabolism. These findings position BBR as a promising therapeutic candidate for the treatment of MASLD.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720248","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":"Natural compounds and programmed necrosis: pioneering a new frontier in cancer treatments.","authors":"Md Al Amin, Hasna Bouhenni, Mehrukh Zehravi, Sherouk Hussein Sweilam, Trupti Pratik Durgawale, Mohammad Shamim Qureshi, Sumit Durgapal, M Akiful Haque, Rajeshwar Vodeti, Deepadarshan Urs, Mst Maharunnasa Shatu, Safia Obaidur Rab, Koula Doukani, Talha Bin Emran","doi":"10.1007/s00210-025-04050-w","DOIUrl":"https://doi.org/10.1007/s00210-025-04050-w","url":null,"abstract":"<p><p>Programmed necrosis, a controlled cell death method that bypasses resistance mechanisms that render apoptosis ineffective, is a potential cancer treatment target. Due to their diverse biological activities and low side effects, natural products are being explored as modulators of programmed necrosis pathways. This review highlights the potential of natural compounds to target cancer cells while preserving healthy tissues and their interaction with essential programmed necrosis mechanisms like ferroptosis and necroptosis. Recent developments have identified various types of programmable necrosis, including necroptosis, ferroptosis, pyroptosis, proptosis, mitochondrial permeability transition-driven necrosis, and oncosis. Natural compounds are increasingly being utilized as a primary source of anti-cancer medications, providing new cancer treatments. This review demonstrates the molecular mechanisms behind lipid peroxidation, mixed lineage kinase domain-like protein, and receptor-interacting protein kinases (RIPK1 and RIPK3) inducing cell death. Recent research has identified natural compounds like polyphenols, alkaloids, and terpenoids that can modulate pathways and benefit preclinical cancer models. The review underscores the potential of natural compounds in developing innovative cancer treatments by integrating pharmacology and cellular signaling knowledge. Integrating natural compound studies and programmed necrosis research presents a promising avenue for oncologists to overcome treatment resistance. Natural compounds have shown potential in developing programmed necrosis as a novel cancer treatment approach, enhancing therapeutic effectiveness and minimizing side effects through preclinical research, pharmacology, and molecular biology.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730790","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":"Emerging phytochemical-based nanocarriers: redefining the perspectives of breast cancer therapy.","authors":"Gulshan Sharma, Rohil Panwar, Sanskriti Saini, Hardeep Singh Tuli, Karan Wadhwa, Rakesh Pahwa","doi":"10.1007/s00210-025-04003-3","DOIUrl":"https://doi.org/10.1007/s00210-025-04003-3","url":null,"abstract":"<p><p>Breast cancer is recognized as the most prevalent condition impacting women globally, despite several advancements in diagnosis and treatment. Existing therapeutic interventions including surgical procedures, radiation therapy, and chemotherapy often produce harmful effects on healthy tissues, trigger chemo-resistance, and augment the risk of relapse. In response to several unmet challenges, substantial research has been conducted to explore the therapeutic potential of natural compounds for breast cancer therapy. Progress in phytochemistry and pharmacology has facilitated the identification of diverse herbal bioactives with favorable safety profiles and multi-target mechanisms of action against breast cancer cells. Several phytochemicals like flavonoids and tannins have shown significant anticancer potential against breast cancer in diverse preclinical models. However, challenges like limited cellular absorption, low water solubility, and high molecular weight hinder their effective translation into clinical applications. Therefore, the development of novel therapies is imperative for overcoming these hurdles in breast cancer treatment effectively. Nanotechnology has reflected considerable perspective in tackling diverse challenges by encapsulating phytoconstituents within various nanocarriers including polymeric nanoparticles, lipidic nanoparticles, nanoemulsions, nanogels, gold nanoparticles, and silver nanoparticles. This manuscript emphasizes the recent advancements in phytochemical-loaded nanocarriers efficiently tailored for breast cancer therapy along with patents, current challenges, and future perspectives in this avenue.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730612","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":"Isoliquiritigenin alleviates radiation-induced intestinal injury in lung cancer by inhibiting TNF-α/caspase3 signaling pathway.","authors":"Ya-Ping Chen, Liang-Liang Shi, Yang-Yang Li, Yi-Ming Zhang, Shang-Zu Zhang, Hong-Dou Hou, Yan Chen, Qi-Hong Zhuo, Yong-Qi Liu, Ben-Jun Wei, Li-Ying Zhang","doi":"10.1007/s00210-025-04007-z","DOIUrl":"https://doi.org/10.1007/s00210-025-04007-z","url":null,"abstract":"<p><p>To construct a model of intestinal injury induced by radiotherapy for lung cancer and to study the protective effect and mechanism of isoliquiritigenin. The lungs of mice were irradiated with 0, 2, 4, 6, 8 Gy X-rays to screen the optimal radiation dose. A mouse model of lung cancer was established, and the tumor was irradiated once. At 3, 7, and 10 days after irradiation, H&E was used to detect the pathological manifestations of colon tissue in mice, and WB was used to detect the expression level of tight junction protein in colon tissue, so as to screen the best time point and study its possible mechanism. Molecular docking was used to study the tightness of isoliquiritigenin binding to TNF-α. Isoliquiritigenin (40 mg/kg) was given on the next day after 4 Gy X-ray irradiation. The levels of TNF-α and apoptosis, intestinal mucosal barrier function, MUC2 protein expression, and colon stem cell proliferation were detected. 4Gy X-ray local irradiation induced obvious colon injury in mice, and the injury was obvious on the 7th day. Isoliquiritigenin significantly improved the general condition, colonic histopathological changes, intestinal stem cell proliferation, and colonic tight junction function of lung cancer-bearing mice after radiotherapy. Further studies have found that isoliquiritigenin can downregulate the activation of TNF-α/Caspase-3 signaling pathway by inhibiting the expression of pro-inflammatory factor TNF-α, alleviate the apoptosis of colonic epithelial cells, improve the upregulation of colonic tight junction function, regulate the expression of MUC2, and promote the proliferation of intestinal stem cells, which may be related to the stable binding of isoliquiritigenin to TNF-α. Radiotherapy-induced bystander effect of lung cancer may be related to the abnormal expression of TNF-α. Isoliquiritigenin may downregulate the expression of TNF-α by binding to TNF-α, inhibit the apoptosis of colon cells, promote the proliferation of intestinal stem cells, and maintain the intestinal mucosal barrier to alleviate the colon injury induced by radiation bystander effect.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730653","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":"Bioequivalence study of perampanel oral suspension in healthy Chinese subjects under fasting and fed conditions.","authors":"Mupeng Li, Yaxing Li, Fangfang Liu, Qian Huang, Xinchu Yi, Jing Xiao, Chunyan Gan, Yangyun Han, Lianlian Fan","doi":"10.1007/s00210-025-04004-2","DOIUrl":"https://doi.org/10.1007/s00210-025-04004-2","url":null,"abstract":"<p><p>Perampanel oral suspension (Fycompa^®) is indicated as adjunctive therapy for the treatment of partial-onset seizure and primary generalized tonic-clonic seizure. This study aimed to assess the bioequivalence of perampanel oral suspension and its generic under the fasting and fed conditions. A randomized, open-label, single-dose, 2-period crossover study was conducted in Chinese healthy subjects under fasting and fed conditions. Each period, subjects received either a 4-mg reference perampanel oral suspension or test product. Blood samples were collected at pre-dose and up to 96 h after administration. Plasma levels of perampanel were quantified using a validated LC-MS/MS method. A total of 74 volunteers were enrolled, 71 of whom completed the study. For the fasting study, the primary pharmacokinetic parameters (mean ± SD) were as follows: C_max was 138.1 ± 30.2 and 126.0 ± 22.7 ng/mL, AUC_0-t was 3998 ± 717 and 4194 ± 963 h*ng/mL, and AUC_0-72h was 3318 ± 567 and 3464 ± 763 h*ng/mL for the test and reference formulations, respectively. For the fed study, the corresponding values were as follows: C_max was 87.0 ± 17.2 and 81.5 ± 15.4 ng/mL, AUC_0-t was 4000 ± 991 and 3991 ± 896 h*ng/mL, and AUC_0-72h was 3190 ± 768 and 3156 ± 657 h*ng/mL for the test and reference products, respectively. The 90% confidence intervals for the geometric mean ratios of these parameters all met the bioequivalence criterion of 80-125%. There were 36 adverse events (AEs) reported in the fasting study, and 47 AEs in the fed study. The test and reference formulations of perampanel oral suspension were bioequivalent and well-tolerated under both fasting and fed conditions. This trial had been registered at the Chinese Clinical Trial Registry on April 20, 2023 ( https://www.chictr.org.cn/ , ChiCTR2300070693).</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730419","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":"MiR-362-3p mediates IFNα-induced antiviral viability against Enterovirus 71 (EV71).","authors":"San Wang, Lan Chen, Zongtao Wu, Yingbo Zou, Yunrong Li, Xiang He, Yusong Zhang, Bo Huang","doi":"10.1007/s00210-025-04062-6","DOIUrl":"https://doi.org/10.1007/s00210-025-04062-6","url":null,"abstract":"<p><p>Enteroviruses, which belong to the Picornaviridae family, include species that infect humans and Interferon Alpha (IFNα) is commonly used against Enterovirus 71 (EV71) infections. This study investigated the role of IFNα-induced miR-362-3p expression in the defense against EV71EV71. Differential analysis identified up-regulated miRNAs following IFNα treatment. RD cells were used to assess EV71proliferation, while HMC3 cells were employed to evaluate the effects of IFNα and EV71 on miR-362-3p expression. Antiviral activity was assessed by modulating miR-362-3p levels. Compared to the NC mimic group, miR-362-3p in miR-362-3p mimic and IFNα treatment groups was increased; cell viability was enhanced; -lgTCID50 was reduced, and the replication of EV71 was inhibited. Further, VP1 mRNA and protein expression declined significantly in miR-362-3p mimic group vs NC mimic while they were notably elevated in the miR-362-3p inhibitor group vs NC inhibitor. IFNα treatment could induce miR-362-3p production and enhanced cell viability in HMC3 cells. Besides, when compared with the miR-362-3p mimic group, IFNα combined with miR-362-3p mimic group reduced -lgTCID50 and significantly decreased the expression of VP1 mRNA and protein. Conclusion: The inhibition of EV71-infected HMC3 cell replication was related to the upregulation of miR-362-3p induced by IFNα, which in turn enhanced antiviral viability.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730785","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":"Beyond the pill: incrimination of nuclear factor-kappa B and their targeted phytomedicine for pulmonary fibrosis.","authors":"Akarsha Balnadupete, Fathimath Muneesa Moideen, Aleena Varughese, Kirana Mugaranja, Jeena T M, Rakshitha Charavu, Yashodhar Bhandary","doi":"10.1007/s00210-025-04067-1","DOIUrl":"https://doi.org/10.1007/s00210-025-04067-1","url":null,"abstract":"<p><p>Pulmonary fibrosis (PF) is a slow and irreparable damage of the lung caused by the accumulation of scar tissue, which eventually results in organ dysfunction and fatality from gas exchange failure. One of the extensively studied inflammatory pathways in PF is the NF-κB signalling pathway, which is reportedly involved in epithelial-mesenchymal transition, myofibroblast differentiation, and other cellular processes. Additionally, studies have evidence that NF-κB signalling pathways can be employed as a potential target for developing therapeutic agents against PF. In the current scenario, FDA-approved drugs, nintedanib and pirfenidone, have been used for the treatment of PF with potential side effects. Recently, the usage of bioactive compounds has attracted attention in the treatment of PF. This review focuses on the involvement of the NF-κB signalling pathway in PF and the significance of phytocompounds in regulating the NF-κB pathway. Both the in vitro and in vivo studies reveal that NF-κB-targeted plant-based bioactive compounds significantly ameliorate the PF condition as well as improve the health condition. Databases such as Scopus, PubMed, and Web of Science were used to conduct literature surveys and compile data on all the bioactive compounds. In conclusion, the plant-derived bioactive compounds are potent enough to target the NF-κB with its biological properties, and this could be a highly effective therapeutic strategy for PF in the future.</p>","PeriodicalId":18876,"journal":{"name":"Naunyn-Schmiedeberg's archives of pharmacology","volume":" ","pages":""},"PeriodicalIF":3.1,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730467","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}