Combinatorial chemistry & high throughput screening最新文献

{"title":"Mechanistic Insights into UV-Induced Molecular Responses from Commercial Nail Dryer Exposure.","authors":"Edris Hoseinzadeh, Zahra Mohebbi, Mahmoud Taghavi, Mahdi Safari","doi":"10.2174/0113862073453414260720034752","DOIUrl":"https://doi.org/10.2174/0113862073453414260720034752","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to measure the UV light emitted by nail dryers available on the market and to assess the potential risks of both immediate and accumulated skin damage. It also sought to explain exposure levels based on known molecular processes related to UV-induced cell stress.</p><p><strong>Methods: </strong>UVA and UVB emissions from various UV and UV/LED nail dryer devices were systematically evaluated using a calibrated UV meter. Measurements were taken from defined internal cavity locations and external leakage points while maintaining consistent distances between the detector and source under typical operating conditions. Devices were grouped by lamp type, model, and usage duration. Statistical analyses were applied to compare UV emission levels and leakage patterns across different devices. Relative risk (RR) values were estimated based on accepted exposure limits to indicate the potential for skin damage.</p><p><strong>Results: </strong>21 devices were analyzed, including UV and UV/LED models. There was no significant difference in internal UV emission between the two types (P = 0.096). However, UV leakage was significantly higher in UV/LED devices (P < 0.001). The UV irradiance varied noticeably based on location, with the highest intensities recorded in the back and bottom areas of the internal chamber. The RR assessment showed that values exceeded recommended safety limits at several measurement points, particularly with repeated or prolonged exposure.</p><p><strong>Discussion: </strong>The results suggest that nail dryer devices can emit and leak UV radiation at levels that may exceed established safety limits, increasing the risk of cumulative skin damage. These findings highlight the need for standardized safety guidelines and effective strategies to reduce user exposure.</p><p><strong>Conclusion: </strong>Commercial nail dryers may emit UV radiation at levels above recommended safety thresholds, raising concerns about both short-term and long-term effects on the skin. While direct biological outcomes in humans were not assessed, the potential implications were interpreted based on established UV-responsive molecular pathways. By combining exposure data with current knowledge of UV-induced oxidative stress and DNA damage, this study emphasizes the need for stronger safety regulations and continued risk assessment for cosmetic devices.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148789187","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":"Comparative Analysis of Laboratory Parameters in Acute Ischemic and Hemorrhagic Stroke.","authors":"Süleyman Nogay, Turgut Dolanbay, Levent Şahin, Bilgehan Demir, Asiye Özkan","doi":"10.2174/0113862073491574260716114506","DOIUrl":"https://doi.org/10.2174/0113862073491574260716114506","url":null,"abstract":"<p><strong>Introduction: </strong>Acute stroke, encompassing ischemic and hemorrhagic subtypes, remains a leading cause of morbidity and mortality worldwide. Early and accurate differentiation of stroke subtypes is essential for guiding appropriate therapeutic decisions. Although numerous hematological and biochemical parameters have been explored for differential diagnosis, their diagnostic relevance remains uncertain. This study aimed to compare the performance of laboratory parameters and indices in acute stroke.</p><p><strong>Methods: </strong>Adult patients presenting to the emergency department between January and December 2024 with a diagnosis of ischemic or hemorrhagic stroke were retrospectively evaluated. Hemogram and biochemistry parameters, CRP-based ratios (CAR, CrAR), GAR, SII, SIRI, and HALP scores were examined. Intergroup comparisons were performed using appropriate statistical tests, and ROC analysis was applied for CRP and CAR.</p><p><strong>Results: </strong>Of the total 119 patients, 88.2% were in the ischemic stroke group, and 11.8% were in the hemorrhagic stroke group. Among the evaluated parameters, CRP and CAR values were significantly higher in the ischemic stroke group (p=0.035 and p=0.024, respectively), whereas glucose levels were significantly higher in the hemorrhagic stroke group (p=0.035). Other biomarkers and inflammatory scores did not show significant differences between subtypes. In the ROC analysis, CAR (AUC=0.686) showed higher discriminatory performance than CRP (AUC=0.673).</p><p><strong>Discussion: </strong>The findings suggest that inflammatory biomarkers, particularly CRP and CAR, may reflect differences in inflammatory and metabolic responses between ischemic and hemorrhagic stroke during the acute phase. Higher glucose levels observed in hemorrhagic stroke patients may also reflect acute metabolic stress responses associated with cerebrovascular injury. However, the relatively modest ROC performance and the absence of significant differences in several other inflammatory indices indicate that these parameters should be interpreted as supportive rather than definitive diagnostic tools. Larger prospective multicenter studies are needed to validate their potential clinical utility.</p><p><strong>Conclusion: </strong>Significantly higher CRP and CAR levels were observed in ischemic stroke patients; however, the modest discriminatory performance observed in ROC analysis suggests that these markers may serve only as supportive adjunctive parameters rather than definitive tools for stroke subtype differentiation. Conversely, indices including SII, SIRI, and HALP appear more informative for prognostic assessment than for subtype discrimination. Overall, CRP, CAR, and related biomarkers should support clinical evaluation and decision-making rather than serve as independent diagnostic tools in acute stroke.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705823","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":"Zinc Nanoparticles (Zn-NPs): Advances in Bio/Synthesis, Properties, Multifunctional Roles, and Toxicity-A 2025 Update Review.","authors":"Nehal Samdani, Suraj N Mali, Gerald Lushington, Shaziya Khan, Abhinav Sati, Rhuta Dongre, Nikil Satpute, Bapu R Thorat, Amit P Pratap","doi":"10.2174/0113862073476530260723061912","DOIUrl":"https://doi.org/10.2174/0113862073476530260723061912","url":null,"abstract":"<p><p>Zinc nanoparticles (Zn-NPs) are well-known versatile nanomaterials with a wide range of applications across diverse fields. Often, they range from ≈ 1 to 100 nm and have superior surface reactivity and excellent optical properties. Extensive research has demonstrated that these nanoparticles offer several advantages in fields such as medicinal applications, organic synthesis, agricultural applications, drug delivery, textile coatings, and food technology. Green synthesis of Zn-NPs offers several advantages, such as environmentally benign, cost-effective routes and improved bioactivity. This review summarizes recent papers (mostly from 2010 to 2025, extracted from Scopus/Web of Science/Google Scholar) on synthesis methodologies, characterization techniques, and emerging applications of various Zn-NPs, providing insights that support future innovations and the safe integration of Zn-NPs into varied systems.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705789","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":"LncRNA ZNF582-AS1 Acts as a Tumor Suppressor in Endometrial Cancer via the miR-21-5p/miR-516a-3p/CREBRF Axis.","authors":"Chen Chen, Fangyuan Chang, Yingfan Guo, Yangqing Liu, Yunzhao Xu","doi":"10.2174/0113862073502552260727054320","DOIUrl":"https://doi.org/10.2174/0113862073502552260727054320","url":null,"abstract":"<p><strong>Introduction: </strong>Endometrial Carcinoma (EC) is a prevalent gynecological malignant tumor with a rising incidence rate. Long non-coding RNAs (lncRNAs) are key regulatory factors in tumorigenesis. Although ZNF582-AS1 is an lncRNA that has been linked to other cancers, its role and mechanism in EC have not yet been explored.</p><p><strong>Methods: </strong>ZNF582-AS1 expression was examined in the GEPIA database and confirmed in 45 pairs of EC/normal tissues and cell lines. Functional assays (including MTT and flow cytometry) were performed after ZNF582-AS1 overexpression. Potential miRNA targets were predicted using bioinformatics and validated using luciferase reporter and RNA Immunoprecipitation (RIP) detection. Downstream targets of miRNA were identified and detected using qPCR and Western blotting. Rescue experiments were conducted to confirm the functional interactions. A xenograft mouse model was used for in vivo validation.</p><p><strong>Results: </strong>ZNF582-AS1 exhibits marked downregulation in EC tissues and cell lines. Low ZNF582-AS1 expression is linked to unfavorable prognosis. ZNF582-AS1 overexpression suppresses EC cell proliferation, triggers cell cycle arrest, and decreases miR-21-5p and miR-516a3p mRNA levels. Additionally, miR-21-5p/miR-516a-3p suppresses CREBRF expression by binding directly to the 3'-UTR of CREBRF, and ZNF582-AS1 overexpression attenuates this CREBRF suppression. In the in vivo studies, ZNF582-AS1 overexpression effectively inhibited tumor growth in nude mice.</p><p><strong>Discussion: </strong>These findings support a competitive endogenous RNA mechanism, in which ZNF582-AS1 acts as a molecular sponge for miR-21-5p and miR-516a-3p, thereby alleviating their inhibitory effect on CREBRF expression. The recovery of CREBRF subsequently inhibits EC cell proliferation and promotes G0/G1 phase arrest, possibly by downregulating the CDK4/Cyclin D1 signaling pathway. The in vivo anti-tumor effect of ZNF582-AS1 further supports its biological relevance in EC progression. Overall, the ZNF582-AS1/miR-21-5p/miR516a-3p/CREBRF regulatory axis provides mechanistic insights into EC tumorigenesis and emphasizes the tumor suppressive effect of ZNF582-AS1.</p><p><strong>Conclusion: </strong>LncRNA ZNF582-AS1 inhibits cell proliferation in EC by regulating the miR-21- 5p/miR-516a-3p/CREBRF axis. ZNF582-AS1 represents a potential treatment target and prognostic marker for EC.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705828","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":"Autophagy-Related Molecular Signatures and Immune Profiles Distinguish Sepsis from Sepsis-Induced Acute Respiratory Distress Syndrome.","authors":"Qin Wang, Yuan Peng, YongFang Wang, Yan Yang, Chen Gu, Jiajia Wang, Jianan Huang","doi":"10.2174/0113862073450157260529073834","DOIUrl":"https://doi.org/10.2174/0113862073450157260529073834","url":null,"abstract":"<p><strong>Introduction: </strong>Sepsis is a life-threatening condition characterized by a dysregulated immune response to infection and is frequently complicated by acute respiratory distress syndrome (ARDS), contributing to substantial morbidity and mortality. Autophagy has been implicated in immune regulation and inflammatory signaling in these conditions; however, its transcriptomic role in distinguishing sepsis from sepsis-induced ARDS remains incompletely defined.</p><p><strong>Method: </strong>In this study, we performed an integrated transcriptomic analysis of three publicly available GEO datasets comprising 139 whole-blood samples (79 sepsis and 60 sepsis-induced ARDS).</p><p><strong>Result: </strong>Differential expression analysis identified 17 autophagy-related genes, including 10 upregulated and 7 downregulated genes in sepsis-induced ARDS compared with sepsis alone. Machine learning approaches, including LASSO regression, random forest, and support vector machine models, yielded a six-gene panel (ATG4A, ATG7, ATG9A, IRS1, RRAS, and SH3GLB1). Individual genes demonstrated moderate discriminatory performance (AUC range: 0.607-0.674), while the composite model achieved an AUC of 0.772 within the integrated dataset.</p><p><strong>Discussion: </strong>These genes were associated with distinct immune-related transcriptional signatures and were enriched in pathways linked to autophagy, metabolic regulation, and immune signaling. Upstream regulatory network analysis further suggested potential miRNA and transcription factor interactions.</p><p><strong>Conclusion: </strong>Collectively, these findings provide an integrative molecular framework highlighting autophagy-immune interactions in sepsis and sepsis-induced ARDS. Given the crosssectional and retrospective nature of the study, the results reflect associations between clinical states and require independent validation and mechanistic investigation.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705805","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":"Colchicine Modulates Cardiac Autophagy and Attenuates Pathophysiology in a Heart Failure Murine Model with Preserved Ejection Fraction.","authors":"Pan Liu, Jingjing Kong, Wei He, Jing Zhou, Jing Wang, Ran Xia","doi":"10.2174/0113862073461621260714100545","DOIUrl":"https://doi.org/10.2174/0113862073461621260714100545","url":null,"abstract":"<p><strong>Introduction: </strong>The study aims to explore the protective effect of colchicine on heart failure with preserved ejection fraction (HFpEF) and its underlying mechanism, with a focus on the regulatory role of the mTOR signaling pathway.</p><p><strong>Methods: </strong>Thirty C57BL/6J mice were used to establish the HFpEF model and were randomized into three groups: control, model, and colchicine-treated groups. Colchicine was administered for 6 weeks. Cardiac function was evaluated by echocardiography, exercise capacity testing, and hemodynamic measurements. Western blot, real-time quantitative PCR, and histological analyses were performed to assess mTOR expression, autophagy-related proteins, myocardial fibrosis, and inflammatory responses in cardiac tissue. The potential interaction between colchicine and mTOR was analyzed by molecular docking simulation. Notably, molecular docking was performed once, not redundantly.</p><p><strong>Results: </strong>The mice in the model group showed myocardial fibrosis, inflammatory responses, and mTOR overactivation. Colchicine treatment significantly reduced systolic and diastolic pressure in the model group, improved cardiac function, modulated mTOR- and autophagy-related gene expression, and attenuated myocardial fibrosis and inflammatory factor release.</p><p><strong>Discussion: </strong>The findings confirm that colchicine ameliorates key pathological features of HFpEF, including diastolic dysfunction, fibrosis, and inflammation. Mechanistically, this protective effect is associated with suppression of mTOR overactivation and normalization of autophagic activity, as supported by molecular docking and expression data. However, the causal relationship between mTOR inhibition, autophagy regulation, and functional improvement remains to be validated using genetic or pharmacological modulators. These results support colchicine as a promising therapeutic agent targeting the mTOR-autophagy axis in HFpEF.</p><p><strong>Conclusion: </strong>Colchicine may modulate mTOR signaling, regulate autophagy, reduce inflammation, and alleviate myocardial fibrosis in HFpEF.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683713","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":"Selenium Nanoparticles (SeNPs): Recent Advances Towards Synthesis, Multifunctional Applications and Future Perspectives.","authors":"Shaziya Khan, Stuthi Nair, Abrar Ansari, Amit Pratap, Suraj N Mali, Gerald H Lushington","doi":"10.2174/0113862073470358260722060451","DOIUrl":"https://doi.org/10.2174/0113862073470358260722060451","url":null,"abstract":"<p><p>Selenium is an essential trace element that plays a critical role in numerous physiological and metabolic processes. Selenium Nanoparticles (SeNPs) have gained substantial attention due to their higher bioavailability and markedly lower toxicity compared to traditional inorganic and organic selenium forms, making them attractive candidates for drug delivery and a range of biomedical applications. Their biological activity is mainly influenced by particle size, shape, and the chosen synthesis route, with green synthesis and biologically derived methods often used for their enhanced compatibility with living systems. Advances in research have broadened the use of SeNPs in antimicrobial, anticancer, antidiabetic, antioxidant, and anti-inflammatory therapies. This review specifically highlights not only the biological synthesis of SeNPs using bacteria, fungi, and plants, along with their diverse bioactivities, but also other potential applications of SeNPs in fields such as food packaging, drug delivery, and textiles. Articles from the past as well as from 2025 were searched using 'Google Scholar', 'Web of Science', 'Scopus', and 'PubMed' databases. Given the limited comprehensive reports available, this review may provide a guide for further investigation into SeNPs.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148599690","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":"Tanshinone IIA Promotes the Proliferation and Migration of Schwann Cells by Regulating the PI3K/AKT Signaling Pathway.","authors":"Zhiwei Jia, Tianlin Wen, Abudunaibi Aili, Chunhua Liu, Aikeremujiang Muheremu","doi":"10.2174/0113862073465414260630201147","DOIUrl":"https://doi.org/10.2174/0113862073465414260630201147","url":null,"abstract":"<p><strong>Introduction: </strong>To investigate the effect of tanshinone IIA on Schwann cells and its mechanisms to provide a novel approach to promote neural regeneration.</p><p><strong>Methods: </strong>Schwann cells in the logarithmic growth phase were allocated into four experimental groups: a control group (untreated), a Tanshinone IIA (TIIA) group (20 µmol/L), a TIIA+IGF-1 group (20 µmol/L TIIA+100 ng/ml IGF-1, a PI3K/AKT pathway activator), and a TIIA+LY294002 group (20 µmol/L TIIA+100 ng/ml LY294002, a PI3K inhibitor). Following treatment, cellular morphology was assessed for each group using an inverted microscope. CCK8 method was used to detect cell proliferation; Flow cytometry was used to detect apoptosis in each group; the Transwell assay was used to detect cell invasion in each group; the cell scratch assay was used to detect cell migration rate, and Western blot was used to detect the expression of PI3K/AKT pathway-related proteins.</p><p><strong>Results: </strong>Compared with the control group, the OD450 value (12,24h), the number of invasive cells and the number of migratory cells in the Schwann cells in the tanshinone IIA and the tanshinone IIA+IGF-1 groups were significantly increased (P<0.05), and the expression levels of p-PI3K, p-AKT proteins in the Schwann cells in the tanshinone IIA group was significantly increased compared with the control group P<0.05).</p><p><strong>Discussion: </strong>This study demonstrates that Tanshinone IIA significantly enhances Schwann cell proliferation and migration while suppressing apoptosis. Crucially, these pro-regenerative effects are mediated through activation of the PI3K/AKT signaling pathway, as confirmed by inhibitor studies. These findings position Tanshinone IIA as a promising therapeutic candidate for promoting nerve repair.</p><p><strong>Conclusion: </strong>Tanshinone IIA promotes the proliferation and migration of Schwann cells and reduces Schwann cell apoptosis by activating the PI3K/AKT pathway.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148599697","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":"Exploring the Molecular Pathways of Tinospora cordifolia in the Management of Diabetic Foot Ulcers.","authors":"Mamta Kumari, Piyushkumar Sadhu, Niyati Shah, Chitrali Talele, Gaurav Kant Saraogi, Shikha Sharma","doi":"10.2174/0113862073448681260703192723","DOIUrl":"https://doi.org/10.2174/0113862073448681260703192723","url":null,"abstract":"<p><strong>Introduction: </strong>Medicinal plants are increasingly recognized as alternative and complementary therapies, particularly in India and other Asian countries. Tinospora cordifolia (Giloy/Guduchi) is a well-known medicinal plant with extensive therapeutic applications, including immune modulation, antidiabetic, anti-inflammatory, antioxidant, and antimicrobial effects. Given these properties, T. cordifolia shows promise for managing Diabetic Foot Ulcers (DFUs), a severe complication of diabetes associated with infection and the risk of amputation.</p><p><strong>Methods: </strong>This review compiles and critically analyzes the published literature on T. cordifolia, focusing on its phytochemical composition, pharmacological activities, and therapeutic relevance to diabetic foot ulcers. Data were gathered from PubMed, Scopus, Web of Science, and Google Scholar, including experimental, preclinical, and clinical studies describing its bioactive constituents and mechanisms related to immune regulation and wound healing.</p><p><strong>Results: </strong>Bioactive compounds such as alkaloids, diterpenoids, and polysaccharides derived from the stem, root, and whole plant exhibit significant immunomodulatory, anti-inflammatory, antioxidant, and antibacterial activities. These properties collectively support enhanced wound healing, infection control, and immune regulation, indicating the potential effectiveness of T. cordifolia in the treatment of DFU. Its favorable physiological compatibility and minimal side effects further strengthen its therapeutic value.</p><p><strong>Discussion: </strong>The multifaceted pharmacological actions of T. cordifolia align well with the complex pathophysiology of diabetic foot ulcers, which involves impaired immunity, chronic inflammation, oxidative stress, and microbial infection. The plant's immune-modulating and wound-healing effects suggest its usefulness as an adjunct to conventional DFU therapies. However, mechanistic insights and standardized clinical evidence remain limited.</p><p><strong>Conclusion: </strong>Tinospora cordifolia represents a promising adjunctive therapeutic option for the management of diabetic foot ulcers. Future research should emphasize detailed biochemical mechanisms, synergistic effects with conventional drugs or other herbs, and well-designed clinical trials. Its incorporation into nutraceuticals and dietary supplements may further aid in chronic disease management and immune enhancement, bridging traditional knowledge with modern therapeutic strategies.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148599611","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 Biopeptide Hirudin Regulates Value-Added Metastasis of Bladder Cancer Cells by Activating PID1 Expression.","authors":"Lingfeng Sun, Lin Yuan","doi":"10.2174/0113862073456569260618065035","DOIUrl":"https://doi.org/10.2174/0113862073456569260618065035","url":null,"abstract":"<p><strong>Introduction: </strong>Hirudin has natural anticoagulant and antitumor effects. This study aimed to investigate the effects of hirudin on bladder cancer cells and the regulation of the potential target PID1.</p><p><strong>Methods: </strong>Network pharmacology analyzed the intersecting targets of bladder cancer and hirudin drugs and performed drug-component-target association analysis. The IC50 value of hirudin in RT-112 and Scaber cells was determined by CCK8. Subsequently, 2 bladder cancer cells were treated at the IC50, and the inhibition rate of RT-112 and Scaber cells was detected using CCK8. Hirudin treatment combined with PID1 knockdown (PID1-KD) was performed to evaluate the regulatory effects of hirudin and PID1 on cell cycle progression, apoptosis, and AMPK-mTOR signaling.</p><p><strong>Results: </strong>Network pharmacology was used to analyze the intersecting targets of bladder cancer and hirudin, in which PID1 functions as a key target. Hirudin inhibited the value-added of RT- 112 and Scaber cells while promoting the apoptosis of RT-112 and Scaber cells and regulating the cell cycle of RT-112 and Scaber cells; at the same time, hirudin increased the expression level of PID1 in bladder cancer cells, and activated AMPK-mTOR signaling at the molecular level. Knockdown of PID1 partially reversed the effects induced by hirudin.</p><p><strong>Discussion: </strong>Our findings support hirudin as a potential anti-bladder cancer agent and suggest that its effects may be mediated by PID1-dependent modulation of the AMPK/mTOR pathway. Nevertheless, the study is limited by the lack of in vivo and clinical validation and by incomplete mechanistic verification.</p><p><strong>Conclusion: </strong>Hirudin exerted significant inhibitory effects on bladder cancer cells, and mechanistic assays demonstrated that these effects are at least partially mediated through PID1-dependent activation of the AMPK-mTOR signaling pathway.</p>","PeriodicalId":10491,"journal":{"name":"Combinatorial chemistry & high throughput screening","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148519943","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}