Drug Design, Development and Therapy最新文献

{"title":"Exploring Mechanisms of Lang Qing Ata in Non-Alcoholic Steatohepatitis Based on Metabolomics, Network Pharmacological Analysis, and Experimental Validation.","authors":"Shupei Li, Hanlong Zhu, Qi Zhai, Yu Hou, Ya Yang, Haifeng Lan, Mingzuo Jiang, Ji Xuan","doi":"10.2147/DDDT.S503757","DOIUrl":"10.2147/DDDT.S503757","url":null,"abstract":"<p><strong>Background: </strong>Non-alcoholic steatohepatitis (NASH), as a progressive form of Non-alcoholic fatty liver disease (NAFLD), poses a significant threat to human health as a prevalent and common condition, with a lack of safe and effective therapeutic options. However, the therapeutic effects and potential mechanisms of Lang Qing Ata (LQAtta) against NASH remain elusive.</p><p><strong>Materials and methods: </strong>The components of LQAtta were identified using Ultra-High Performance Liquid Chromatography-Tandem Mass Spectrometry (UHPLC-MS/MS). Subsequently, we employed network construction and analysis approaches within the field of network pharmacology. By integrating known databases and target prediction algorithms, which encompassed database-based target prediction, protein-protein interaction networks, as well as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, we unveiled the potential key targets and signaling pathways that these bioactive components might engage with. These discoveries were further validated in subsequent mouse models. An HFHC-induced NASH mouse model was used to validate the therapeutic effects and potential mechanisms of LQAtta on NASH.</p><p><strong>Results: </strong>From the UHPLC-MS/MS analysis of LQAtta, a total of 1518 chemical components were identified, with 106 of them being absorbed into the bloodstream. Additionally, based on the acquisition of targets from both LQAtta and the NASH database, a total of 160 common targets were screened. KEGG enrichment analysis indicated that LQAtta may alleviate NASH by modulating pathways such as the Toll-like receptor signaling pathway, the NF-κB signaling pathway, and inflammation-related pathways. In vivo experimental results demonstrated that LQAtta could alleviate liver injury, steatosis, and inflammation induced by NASH, thereby slowing down the disease process. Additionally, LQAtta inhibited the expression and phosphorylation of NF-κB protein, playing a role in preventing NASH.</p><p><strong>Conclusion: </strong>In this study, the combination of mass spectrometry analysis, network pharmacology, and animal experiments preliminarily elucidated the potential of LQAtta to treat NASH through NF-κB pathways.</p>","PeriodicalId":11290,"journal":{"name":"Drug Design, Development and Therapy","volume":"19 ","pages":"1681-1701"},"PeriodicalIF":4.7,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11911237/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Phase I Study to Evaluate the Safety, Tolerability, Pharmacokinetics of BGT-002, a Novel ATP-Citrate Lyase Inhibitor, in Healthy Chinese Subjects.","authors":"Yun Liu, Chengyin Yu, Yifan Zhang, Zhifu Xie, Yating Wang, Hongjie Qian, Liyu Liang, Yanmei Liu, Qian Chen, Jingying Jia, Sai Yan, Xiaoyin Lai, Wei Li, Jingya Li, Yangming Zhang, Fajun Nan, Chen Yu","doi":"10.2147/DDDT.S504814","DOIUrl":"https://doi.org/10.2147/DDDT.S504814","url":null,"abstract":"<p><strong>Objective: </strong>This Phase I study evaluated the safety, tolerability, pharmacokinetics (PK) and pharmacodynamics (PD) of BGT-002, a novel ATP-citrate lyase (ACLY) inhibitor, in healthy Chinese adults.</p><p><strong>Methods: </strong>This study included three parts: Part I (single-ascending-dose study), Part II (multiple-ascending-dose study), and Part III (food effect study). A total of 104 healthy subjects were enrolled in the study and were given BGT-002 tablet or placebo per protocol requirements. Blood samples were collected for pharmacokinetic and pharmacodynamic analysis. Safety was assessed by clinical examinations and adverse events.</p><p><strong>Results: </strong>In Part I, BGT-002 demonstrated rapid absorption with a T_max of 0.67 to 1.75 hours, and slow elimination with a T_1/2 of 24.53 to 72.86 hours, prolonged with increased dosages. C_max and AUC_0-∞ ranged from 1.55 to 48.39 μg/mL, and 31.09 to 2930.69 h·μg/mL, respectively. In Part II, the accumulation index (Rac) of C_max and AUC_tau following 14 days of consecutive administration were 3.53 to 3.62 and 5.29 to 5.59, respectively, with a dose-proportionality PK profile. The levels of total cholesterol (TC), non-high-density lipoprotein cholesterol (non-HDL-C), and low-density lipoprotein cholesterol (LDL-C) were maximally decreased by 15.80%, 18.50%, and 22.37%, respectively. In Part III, the geometric mean ratio (90% CI) of fed to fasting condition in C_max and AUC_0-∞ of BGT-002 were 73.11% and 98.36%, respectively, indicating a minor food effect on the absorption rate. Across the study, two cases of Grade 3 adverse events (elevated blood triglycerides) were reported, both of which were assessed as not related to BGT-002. No serious adverse events were observed.</p><p><strong>Conclusion: </strong>BGT-002 demonstrated favorable safety, tolerability, and lipid-lowering effects, supporting its potential for further clinical development.</p><p><strong>Clinical trial registration: </strong>ChiCTR2200057793(https://www.chictr.org.cn/showproj.html?proj=160210); ChiCTR2300067474(https://www.chictr.org.cn/showproj.html?proj=182183); ChiCTR2300067472(https://www.chictr.org.cn/showproj.html?proj=184079).</p>","PeriodicalId":11290,"journal":{"name":"Drug Design, Development and Therapy","volume":"19 ","pages":"1783-1794"},"PeriodicalIF":4.7,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11910062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum: Medication Safety in Intravenous Therapy: Compatibility of Etoposide With Frequently Drugs Used in Tumour Critical Care During Simulated Y-Site Administration [Corrigendum].","authors":"","doi":"10.2147/DDDT.S526642","DOIUrl":"https://doi.org/10.2147/DDDT.S526642","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.2147/DDDT.S489534.].</p>","PeriodicalId":11290,"journal":{"name":"Drug Design, Development and Therapy","volume":"19 ","pages":"1669-1670"},"PeriodicalIF":4.7,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11911391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation and Function of the cGAS-STING Pathway: Mechanisms, Post-Translational Modifications, and Therapeutic Potential in Immunotherapy.","authors":"Yuhan Chen, Si Yue, Lingyan Yu, Jinghao Cao, Yingchao Liu, Aoli Deng, Yajuan Lu, Jing Yang, Huanjuan Li, Jing Du, Jun Xia, Yanchun Li, Yongming Xia","doi":"10.2147/DDDT.S501773","DOIUrl":"10.2147/DDDT.S501773","url":null,"abstract":"<p><p>Autoimmune diseases arise when the immune system attacks healthy tissues, losing tolerance for self-tissues. Normally, the immune system recognizes and defends against pathogens like bacteria and viruses. The cGAS-STING pathway, activated by pattern-recognition receptors (PRRs), plays a key role in autoimmune responses. The cGAS protein senses pathogenic DNA and synthesizes cGAMP, which induces conformational changes in STING, activating kinases IKK and TBK1 and leading to the expression of interferon genes or inflammatory mediators. This pathway is crucial in immunotherapy, activating innate immunity, enhancing antigen presentation, modulating the tumor microenvironment, and integrating into therapeutic strategies. Modulation strategies include small molecule inhibitors, oligonucleotide therapies, protein and antibody therapies, genetic and epigenetic regulation, cytokine and metabolite modulation, and nanoscale delivery systems. Post-translational modifications (PTMs) of the cGAS-STING pathway, such as phosphorylation, acetylation, ubiquitination, methylation, palmitoylation, and glycosylation, fine-tune immune responses by regulating protein activity, stability, localization, and interactions. These modifications are interconnected and collectively influence pathway functionality. We summarize the functions of cGAS-STING and its PTMs in immune and non-immune cells across various diseases, and explore potential clinical applications.</p>","PeriodicalId":11290,"journal":{"name":"Drug Design, Development and Therapy","volume":"19 ","pages":"1721-1739"},"PeriodicalIF":4.7,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11911240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Systematic Review of Mechanisms, Incidence, and Management of Trastuzumab Deruxtecan Induced ILD/Pneumonitis in Solid Tumors.","authors":"Dehua Liao, Jiwen Zhang, Ting Yan, Yun Chen, Yilan Fu, Ning Xie, Minghui Long","doi":"10.2147/DDDT.S508773","DOIUrl":"10.2147/DDDT.S508773","url":null,"abstract":"<p><p>Trastuzumab deruxtecan (T-DXd) has been approved to treat various tumors. While most adverse events (AEs) associated with T-DXd are manageable, interstitial lung disease (ILD)/pneumonitis is a notable AE of special concern. This review describes the incidence, severity, and management of T-DXd-induced ILD/pneumonitis across different tumors. We conducted a systematic search of PubMed, Embase, Cochrane Library, and Web of Science for literature published up to 13 September 2024, regarding the use of T-DXd in the treatment of HER2-positive tumors. Studies included were clinical trials involving HER2-positive tumors with reported ILD/pneumonitis cases.The main data extracted from the full-text articles included the incidence and severity of T-DXd-induced ILD. 18 studies involving 3380 patients with various advanced solid malignancies were included in our review. The overall incidence of adjudicated drug-related ILD/pneumonitis was 12.40%. Although most ILD/pneumonitis cases were low-grade, the risk of ILD/pneumonitis-related death should not be overlooked. Given the prolonged exposure to the drug, careful monitoring and management of T-DXd-induced ILD/pneumonitis are critical. Management strategies include dose reduction, treatment interruption, discontinuation, corticosteroids, and supportive care. Further research is needed to clarify the risk factors and mechanisms underlying T-DXd-induced ILD/pneumonitis. This review highlights critical gaps in understanding the risk factors and mechanisms of T-DXd-induced ILD, underscoring the need for further research.</p>","PeriodicalId":11290,"journal":{"name":"Drug Design, Development and Therapy","volume":"19 ","pages":"1655-1668"},"PeriodicalIF":4.7,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143624044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Analysis and Network Pharmacology in Revealing the Mechanism of Daifu Decoction on the Relapse of UC.","authors":"Yangyang Zhao, Danyang Cui, Yanan Xiao, Xu Han, Miao Jiang, Yang Gong","doi":"10.2147/DDDT.S497944","DOIUrl":"10.2147/DDDT.S497944","url":null,"abstract":"<p><strong>Background: </strong>Daifu Decoction (DFD), a patented herbal prescription used to prevent and treat ulcerative colitis (UC). This study aimed to reveal the effect of DFD on the relapse of UC and its mechanism via integrated retrospective clinical analysis, network pharmacology and in vivo and in vitro experimental validation.</p><p><strong>Methods: </strong>First, the clinical data of UC patients treated with DFD were reviewed from a real-world study (RWS), and the relapse at 24 weeks after drug withdrawal was recorded to evaluate the relapse rate. Next, the chemical components of DFD were identified via ultra performance liquid chromatography‒mass spectrometry (UPLC‒MS), and the differentially expressed genes (DEGs) between UC patients in the active and remission stages were screened as disease targets related to the relapse of UC from the Gene Expression Omnibus (GEO) database. The core components, targets and key signalling pathways of DFD for preventing the relapse of UC were discussed via network pharmacology. Finally, the above results were verified via molecular docking and in vivo and in vitro experiments.</p><p><strong>Results: </strong>A total of 475 UC patients were included, and the relapse rate of UC treated with DFD was 23.9%. Additionally, the 221 components identified by UPLC-MS and 398 DEGs related to the relapse of UC enriched the main pathway of the relapse of UC was IL-17 signaling pathway and the inflammatory-related targets, such as IL6, PTGS2, MMP7, MMP3, MMP1. Moreover, molecular docking revealed that the core components of DFD were able to bind to inflammation-related targets, and in vivo and in vitro experiments demonstrated that DFD could inhibit the IL-17 pathway, increase the level of claudin-1, and control inflammation to prevent UC relapse.</p><p><strong>Conclusion: </strong>DFD can effectively prevent the relapse of UC which may be related to inhibiting the activation of IL-17 signalling pathway.</p>","PeriodicalId":11290,"journal":{"name":"Drug Design, Development and Therapy","volume":"19 ","pages":"1629-1653"},"PeriodicalIF":4.7,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11895689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective Effects of Bosentan via Endothelin Receptor Antagonism in Experimental Ischemia-Reperfusion Injury in the Lower Limb of Rats.","authors":"Hüseyin Demirtaş, Abdullah Özer, Mehmet Burak Gülcan, Zeynep Yığman, Ayşegül Küçük, Esra Tekin, Yusuf Ünal, Ali Doğan Dursun, Aslı Dağlı, Mustafa Arslan","doi":"10.2147/DDDT.S510885","DOIUrl":"10.2147/DDDT.S510885","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to evaluate the protective effects of bosentan, a dual endothelin receptor antagonist, against skeletal muscle ischemia-reperfusion injury (IRI) in rats.</p><p><strong>Methods: </strong>A total of 24 male Wistar Albino rats were divided into four groups: control (C, n=6), bosentan-treated (B, n=6), ischemia-reperfusion (IR, n=6), and bosentan plus ischemia-reperfusion (B+IR, n=6). Bosentan (10 mg/kg) was administered 30 minutes prior to reperfusion. In the IR and B+IR groups, ischemia was induced using vascular bulldog clamps for 45 minutes, followed by 120 minutes of reperfusion.</p><p><strong>Results: </strong>Histological and biochemical assessments revealed significant differences among the groups. The disorganization and degeneration scores of the muscle cells in the B+IR group were significantly lower than those in the IR group (P = 0.001). The degree of interstitial edema in the IR group was markedly more severe than in the C and B groups (all P < 0.001), while the interstitial edema score in the B+IR group was significantly lower than that in the IR group (P < 0.001). The total muscle injury scores were markedly reduced in the B+IR group compared to the IR group (P < 0.001). Biochemically, TAS levels were significantly higher in the B+IR group compared to the IR group (1.03 ± 0.18 vs 0.59 ± 0.10 mmol/L, P = 0.016). Conversely, TOS (1.97 ± 0.39 vs 2.86 ± 0.43 IU/mg, P < 0.001) and OSI levels (P < 0.001) were significantly lower in the B+IR group. Additionally, paraoxonase (PON-1) enzyme activity was significantly reduced in the B+IR group compared to the IR group (P < 0.001). These findings suggest that bosentan exerts its protective effects by antagonizing endothelin-1 receptors, thereby mitigating vasoconstriction, oxidative stress, and inflammation. The observed reductions in muscle cell disorganization, interstitial edema, hemorrhage, neutrophil infiltration and oxidative stress markers underscore bosentan's potential as a therapeutic agent for managing ischemia-reperfusion injury.</p><p><strong>Conclusion: </strong>Bosentan demonstrates significant protective effects against skeletal muscle IRI by reducing oxidative stress and inflammation through endothelin receptor antagonism. These findings underscore bosentan's potential as a therapeutic agent for mitigating ischemia-reperfusion injury in vascular surgeries and managing critical limb ischemia in clinical settings. Further research is warranted to explore the long-term effects of bosentan on muscle recovery and systemic health following ischemia-reperfusion injury.</p>","PeriodicalId":11290,"journal":{"name":"Drug Design, Development and Therapy","volume":"19 ","pages":"1561-1573"},"PeriodicalIF":4.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vaccarin Ameliorates Renal Fibrosis by Inhibiting Ferroptosis via Nrf2/SLC7A11/GPX4 Signaling Pathway.","authors":"Mengjiao Cui, Qiming Xu, Lianxiang Duan, Jianrao Lu, Jing Hu","doi":"10.2147/DDDT.S509357","DOIUrl":"10.2147/DDDT.S509357","url":null,"abstract":"<p><strong>Purpose: </strong>Vaccarin is a natural flavonoid glycoside with anti-inflammatory, antioxidant and nephroprotective effects. However, the effects of vaccarin on renal fibrosis (RF) and its molecular mechanisms remain unclear. This study aimed to investigate the effects of vaccarin on RF and its molecular mechanisms.</p><p><strong>Methods: </strong>Network pharmacology was used to analyze the effect of vaccarin on RF, and molecular docking and molecular dynamics simulations were performed to assess the binding of nuclear factor erythroid 2-related factor 2 (Nrf2) to vaccarin. A mouse model of unilateral ureteral obstruction (UUO) was established in vivo, and human renal tubular epithelial (HK2) cells were induced with transforming growth factor-β (TGF-β) and RSL3, respectively, as an in vitro model. The anti-fibrotic effect of vaccarin was observed by histopathological staining and determination of fibrous markers. Changes in oxidative stress and ferroptosis-related markers were detected by kits, Western blot (WB), qRT-PCR and immunofluorescence (IF). Finally, Nrf2 inhibitors were added to the in vitro model to observe the effects on fibrosis and ferroptosis.</p><p><strong>Results: </strong>Vaccarin and RF cross genes are enriched for oxidative stress. Nrf2 binds stably to vaccarin. Both in vivo and in vitro experiments showed that vaccarin treatment reduced the expression of fibrosis markers, decreased the levels of reactive oxygen species (ROS), malondialdehyde (MDA), lipid peroxidation (LPO) and Fe²⁺, and increased glutathione (GSH) secretion. In addition, vaccarin down-regulated the expression of Long-chain acyl-CoA synthetase 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (PTGS2) and NADPH oxidase 1 (NOX1), and up-regulated Nrf2 and its downstream solute transport family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4) expression. Mechanistic studies indicated that vaccarin activated the Nrf2/SLC7A11/GPX4 pathway to inhibit ferroptosis, and this inhibition was effectively reversed by the Nrf2 inhibitor.</p><p><strong>Conclusion: </strong>Vaccarin ameliorates RF by inhibiting ferroptosis via Nrf2/SLC7A11/GPX4 pathway.</p>","PeriodicalId":11290,"journal":{"name":"Drug Design, Development and Therapy","volume":"19 ","pages":"1609-1626"},"PeriodicalIF":4.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892373/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comment on the Use of Gegen Qinlian Decoction to Treat Type 2 Diabetes Mellitus [Letter].","authors":"Jinyu Hu","doi":"10.2147/DDDT.S523869","DOIUrl":"10.2147/DDDT.S523869","url":null,"abstract":"","PeriodicalId":11290,"journal":{"name":"Drug Design, Development and Therapy","volume":"19 ","pages":"1627-1628"},"PeriodicalIF":4.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential of Polydatin Against Ischemia-Reperfusion Injury: New Insights from Pharmacological-Pathological Mechanism Associations.","authors":"Zhicheng Sun, Xiyang Wang, Xiaoyang Pang","doi":"10.2147/DDDT.S508851","DOIUrl":"10.2147/DDDT.S508851","url":null,"abstract":"<p><p>Ischemia-reperfusion injury is a multi-tissue/organ susceptible and highly destructive disease. The complex pathological mechanisms of ischemia-reperfusion injury make its prevention and treatment highly challenging, and the development of novel drugs with pharmacological pleiotropy that can target multiple pathological mechanisms has become the focus of current drug research. Polydatin is a traditional Chinese medicine monomer with pleiotropic pharmacological effects, and existing research evidence suggests that polydatin has strong protective potential against ischemia-reperfusion injury. However, the mechanism of polydatin against ischemia-reperfusion injury is still unclear. In this review, the extensive pharmacological-pathological mechanism associations between polydatin and ischemia-reperfusion injury have been described from the perspectives of inflammatory response, oxidative stress, apoptosis, autophagy, ferroptosis, and cellular pyroptosis, which will provide references to the basic and applied research of polydatin in the field of ischemia-reperfusion injury.</p>","PeriodicalId":11290,"journal":{"name":"Drug Design, Development and Therapy","volume":"19 ","pages":"1585-1594"},"PeriodicalIF":4.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892733/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}