Hereditas最新文献

{"title":"The potential mechanism of Saikosaponin D against luminal A breast cancer based on bioinformatical analysis, molecular docking and in vitro studies.","authors":"Lichang Yang, Ru Chang, Jianzhen Pan, Shan Huang","doi":"10.1186/s41065-025-00510-8","DOIUrl":"https://doi.org/10.1186/s41065-025-00510-8","url":null,"abstract":"<p><strong>Background: </strong>Saikosaponin D (SSD) has been shown to have the strongest anti-tumor activity. This study aimed to explore the effects and potential molecular mechanism of Saikosaponin D (SSD) against estrogen receptor-positive breast cancer.</p><p><strong>Methods: </strong>MCF-7 and T-47D cell lines were treated with a series of concentrations of SSD. Growth, cell cycle distribution, and apoptosis tests were performed. Next, potential targets of SSD against breast cancer were predicted. The targets for SSD were collected from HERB database and PharmMapper Server and displayed accoding to degree.</p><p><strong>Results: </strong>there was a dose-dependent decrease in MCF-7 and T-47D cancer cell viability and the the half maximal inhibitory concentrations were 7.31 ± 0.63 µM and 9.06 ± 0.45 µM, respectively. Treatment with SSD decreased cell proliferation, arrested cell cycle at G1, and induced cell apoptosis. There were 227 potential targets of SSD against breast cancer, among which ESR1 was a hub gene. SSD treatment can reduce the protein levels of estrogen receptor α (ERα), Cyclin D1 (CCND1), and the proto-oncogene c-Myc (c-Myc).</p><p><strong>Conclusion: </strong>SSD may have therapeutic potential in estrogen receptor-positive breast cancer, may through its suppression on ESR1.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"140"},"PeriodicalIF":2.7,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144707285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The use of polyphenols extracted from Chinese sweet leaf tea (Rubus suavissimus S. Lee.) as novel drugs for the treatment of metabolic dysfunction associated steatotic liver disease.","authors":"Yu Pan, Yu Liu, Yixuan Huo, Suren R Sooranna, Lu Chen, Lijun Yin, Zhigang Yan, Danna Huang, Lihe Jiang, Wuwei Wu","doi":"10.1186/s41065-025-00504-6","DOIUrl":"https://doi.org/10.1186/s41065-025-00504-6","url":null,"abstract":"","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"141"},"PeriodicalIF":2.7,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144707286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Carnosic acid enhances cisplatin sensitivity and suppresses gastric cancer progression via the TP53/SLC7A11/ALOX12 axis.","authors":"Li Zhou, Bin Xu, Baojian Li","doi":"10.1186/s41065-025-00508-2","DOIUrl":"https://doi.org/10.1186/s41065-025-00508-2","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) remains a significant global health challenge due to its high mortality and frequent resistance to chemotherapy drugs like cisplatin (DDP). Carnosic acid (CA), a phenolic diterpene, exhibits potential anti-cancer properties. This study aimed to investigate the role of CA in regulating GC development and DDP sensitivity.</p><p><strong>Methods: </strong>The half-maximal inhibitory concentration (IC₅₀) of DDP and cell viability were determined using a cell counting kit-8 assay. Cell proliferation was evaluated by a 5-Ethynyl-2'-deoxyuridine assay, while cell migration was assessed by a transwell assay. Cell death was analyzed through flow cytometry, fluorometric assay, and colorimetric assays. The targets of CA were identified using network pharmacology. Western blotting was employed to detect the protein expression of tumor protein p53 (TP53), solute carrier family 7 member 11 (SLC7A11), and arachidonate 12-lipoxygenase, 12 S type (ALOX12).</p><p><strong>Results: </strong>CA treatment significantly inhibited GC cell proliferation and migration and enhanced cell death. The treatment also elevated reactive oxygen species (ROS) and Fe²⁺ levels, while reducing glutathione (GSH) levels and the IC₅₀ value for DDP in GC cells. In addition, TP53 was identified as a target of CA, and its protein expression was upregulated by CA treatment in GC cells. Silencing TP53 attenuated the effects of CA on cell proliferation, migration, death, and the sensitivity of tumor cells to DDP. Further, CA regulated the TP53-mediated SLC7A11/ALOX12 pathway.</p><p><strong>Conclusion: </strong>CA improved the sensitivity of GC cells to DDP and inhibited their malignant progression by regulating the TP53-mediated SLC7A11/ALOX12 axis, highlighting its potential clinical significance for GC treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"139"},"PeriodicalIF":2.7,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144689989","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-370-3p affects the progression of postmenopausal osteoporosis through targeting INO80.","authors":"Zhen Yang, Yuqi Sheng, Xiangjie Liu, Meini Cen, Yong Xu","doi":"10.1186/s41065-025-00502-8","DOIUrl":"https://doi.org/10.1186/s41065-025-00502-8","url":null,"abstract":"<p><strong>Background: </strong>Postmenopausal osteoporosis (PMO) is acknowledged as a principal category of osteoporosis (OP). The aim of this study was to investigate the level of miR-370-3p in PMO patients and its predictive effect on osteoporosis in postmenopausal women, and to explore the molecular mechanism of miR-370-3p on PMO.</p><p><strong>Methods: </strong>The expression of miR-370-3p was assessed using RT-qPCR. Cell proliferation of MC3T3-E1 cells was evaluated through CCK-8 assays. Cell apoptosis was detected by flow cytometry. The direct interaction between miR-370-3p and INO80 was confirmed via dual-luciferase reporter assays.</p><p><strong>Results: </strong>The level of miR-370-3p was found to be upregulated in osteoporosis patients, and miR-370-3p played a significant role in regulating the proliferation, apoptosis and differentiation of osteoblasts. In addition, miR-370-3p targeted INO80 and affected the disease progression of PMO.</p><p><strong>Conclusions: </strong>miR-370-3p/INO80 may serve as a promising biomarker for both the diagnosis and therapeutic management of PMO.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"138"},"PeriodicalIF":2.7,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144689991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of the molecular mechanism of Xiaoluo Wan in thyroid-associated ophthalmopathy: network analysis and in vivo study.","authors":"Wenchao Gu, Shuo Tian, Lu Fu, Lina Wang, Liangkun Zhang, Furong Wang","doi":"10.1186/s41065-025-00499-0","DOIUrl":"https://doi.org/10.1186/s41065-025-00499-0","url":null,"abstract":"<p><strong>Background: </strong>Thyroid-associated ophthalmopathy (TAO) is a common complication of hyperthyroidism that can significantly impair quality of life. This study investigated the effects and mechanisms of Xiaoluo Wan (XLW), a traditional Chinese herbal prescription, in treating TAO.</p><p><strong>Methods: </strong>The protective effects of XLW on the extraocular muscles were first examined in hyperthyroid rats. Network analysis strategies were applied to predict potential targets and therapeutic mechanisms associated with XLW. The expression of key genes and proteins was subsequently validated and analyzed in rats with hyperthyroidism.</p><p><strong>Results: </strong>XLW alleviated the pathological changes in the extraocular muscles caused by hyperthyroidism. The network analysis identified 66 effective targets. The core targets of XLW against TAO included AKT1, PTGS2, BCL2, IL10, IL1b, CCL2, IFNG, IL6, MMP9, TGFB1, HIF1α, and TP53. Enrichment analysis suggested that the amelioration mechanisms of XLW may be linked to the HIF1 signaling pathway. In hyperthyroid rats, XLW reduced oxidative stress (OS) in extraocular muscle and inhibited the expression of HIF-1ɑ. Additionally, XLW exerted regulatory actions on the expression of various proteins closely linked to HIF-1α and OS.</p><p><strong>Conclusions: </strong>XLW reduces injuries to extraocular muscles in hyperthyroidism, possibly by inhibiting OS via HIF1 signaling. This may provide novel insights into the pharmacological mechanism of XLW in treating TAO.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"137"},"PeriodicalIF":2.7,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144689990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and implementation of an etiology-based diagnostic framework for acute abdominal pain in emergency settings.","authors":"Hui Guo, Xu-Rui Li, Yun-Lei Du, Yang-Juan Jia, Hong-Ling Li, Qian Zhao, Yan-Peng Li, Jian-Guo Li","doi":"10.1186/s41065-025-00507-3","DOIUrl":"10.1186/s41065-025-00507-3","url":null,"abstract":"<p><strong>Background: </strong>Diagnostic checklists have been demonstrated to reduce errors in clinical reasoning. Building on previous validation studies, this research presents the development and clinical application of an etiology-based diagnostic framework for evaluating acute abdominal pain. The framework integrates a structured checklist of abdominal pain etiologies with a process-oriented diagnostic strategy, aiming to enhance diagnostic accuracy and clinical outcomes. This approach also serves as a potential model for the creation of diagnostic tools applicable to other symptom complexes encountered in emergency medicine.</p><p><strong>Methods: </strong>A cognitive task analysis (CTA) was conducted with participation from five emergency medicine experts employing a think-aloud methodology. The experts described their diagnostic reasoning processes and queried relevant clinical data to extract foundational diagnostic principles. Based on these findings, a checklist categorizing etiologies of abdominal pain was constructed, drawing from anatomical and diagnostic considerations. The clinical utility of the checklist was evaluated through its application to a representative complex case.</p><p><strong>Results: </strong>The diagnostic checklist was organized into five principal etiological categories: local organ disorders, diseases of adjacent organs, systemic diseases, psychogenic disorders, and gynecological conditions. Its implementation facilitated the accurate identification of atypical acute renal infarction in a diagnostically challenging case, enabling prompt clinical intervention.</p><p><strong>Conclusions: </strong>CTA provides a robust method for modeling expert diagnostic reasoning and supports the development of structured, etiology-based diagnostic tools. This framework enhances diagnostic precision for individuals presenting with acute abdominal pain in emergency settings and may inform the development of similar tools for other clinical presentations.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"134"},"PeriodicalIF":2.7,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12273047/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RBM15 promotes hypoxia/reoxygenation-induced ferroptosis in human cardiomyocytes by mediating m6A modification of ACSL4.","authors":"Yi Cheng, Jiamin Wan, Yingyue Xu, Shasha Liu, Linfeng Li, Jing Zhou, Fuyan Xie","doi":"10.1186/s41065-025-00453-0","DOIUrl":"10.1186/s41065-025-00453-0","url":null,"abstract":"<p><strong>Background: </strong>Acute myocardial infarction (AMI) refers to the acute necrosis of part of the myocardium caused by persistent and severe myocardial ischemia. The aim of the study was to investigate the effect of RNA binding motif protein 15 (RBM15) and acyl-CoA synthetase long chain family member 4 (ACSL4) on ischemia/reperfusion (I/R)-induced ferroptosis of cardiomyocytes.</p><p><strong>Methods and results: </strong>AC16 cells were treated with hypoxia/reoxygenation (H/R) to establish an in vitro myocardial infarction cell model. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assay were used to determine gene expression. Cell Counting Kit-8 (CCK-8) assay was conducted to investigate cell viability. Ferroptosis level was evaluated by commercial kits. N6-methyladenosine (m6A) level was examined by M6A quantification analysis. RNA immunoprecipitation (RIP) assay, methylated RNA Immunoprecipitation (meRIP) assay and dual-luciferase reporter assay were adopted to verify the combination between RBM15 and ACSL4. ACSL4 mRNA stability was analyzed by Actinomycin D treatment. RBM15 mRNA level was increased in AMI patients' serums and H/R-induced AC16 cells. Silencing of RBM15 promoted H/R-mediated AC16 cell viability and inhibited H/R-induced AC16 cell oxidative stress and ferroptosis. Moreover, it was demonstrated that RBM15 knockdown inhibited m6A modification of ACSL4 and suppressed the stability of ACSL4 mRNA. Furthermore, ACSL4 overexpression restored the effects of RNM15 silencing on H/R-induced AC16 cell oxidative injury and ferroptosis.</p><p><strong>Conclusion: </strong>RBM15 silencing repressed H/R-induced ferroptosis in human cardiomyocytes through regulating m6A modification of ACSL4.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"135"},"PeriodicalIF":2.7,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12273425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing LncRNA HCG27 ameliorates cognitive dysfunction after ischemic stroke via miR-27a-3p regulation.","authors":"Ting Li, Ying Li, Lin Chen, Chaosheng Zeng, Huaijie Xing, Min Chen, Limin Yan, Xiaopei Zhang","doi":"10.1186/s41065-025-00493-6","DOIUrl":"10.1186/s41065-025-00493-6","url":null,"abstract":"<p><strong>Background: </strong>We explore the effect of improving cognitive dysfunction after cerebral ischemia-reperfusion (CI/R) by regulating HCG27.</p><p><strong>Methods: </strong>The MCAO and OGD/R methods were employed to establish in vivo and in vitro models of cognitive dysfunction caused by a CI/R injury. RT-qPCR was utilized to detect the relative expression of HCG27 and miR-27a-3p. An ELISA was adopted to measure the concentrations of inflammatory factors (IL-6, IL-1β, IL-10). The concentration of MDA and activity of CAT were detected using commercially available kits. The neurological deficit was evaluated using the mNSS score. The spatial learning and memory capabilities were evaluated via the MWM test. The targeting relationships were validated by the dual-luciferase reporter assay, RIP assay, and RNA pull-down assay. The CCK-8 assay and flow cytometry were employed to asses cell viability and apoptosis, respectively.</p><p><strong>Results: </strong>The level of HCG27 was upregulated in MCAO rats and OGD/R-induced BV2 cells, whereas that of miR-27a-3p decreased, and HCG27 targeted miR-27a-3p. Compared with the sham group, the mNSS score of MCAO rats was elevated, and their spatial learning and memory abilities declined, with aggravated inflammatory response and oxidative stress. However, silencing HCG27 improved these conditions, and the miR-27a-3p antagonist reversed this. MiR-27a-3p reversed the increase in cell viability in OGD/R-induced BV2 cells, reduced the cell apoptosis rate, and weakened the inflammatory response and oxidative stress caused by the HCG27 silencing.</p><p><strong>Conclusions: </strong>Silencing HCG27 can protect against cognitive dysfunction after cerebrovascular disease by targeting miR-27a-3p.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"136"},"PeriodicalIF":2.7,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12275291/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of miR-107/HMOX1 axis in hepatic sinusoidal endothelial cells stimulated by ischemia-reperfusion injury.","authors":"Zhao Wang, Jiangyang Sun, Yu Wang, Yichuan Zhang, Laian Ge","doi":"10.1186/s41065-025-00495-4","DOIUrl":"10.1186/s41065-025-00495-4","url":null,"abstract":"<p><strong>Background: </strong>Liver ischemia-reperfusion injury (IRI) is a common complication of diseases such as liver transplantation, hepatic resection, and hemorrhagic shock. This study aimed to elucidate the molecular mechanism of miR-107 affecting hepatic ischemia-reperfusion injury (IRI).</p><p><strong>Methods: </strong>The expression changes of miR-107 during hepatic IRI were quantified using quantitative real-time PCR. Subsequently, in vitro cellular experiments were carried out to verify the role of miR-107 on hypoxia/reoxygenation (HR) through CCK-8, flow cytometer, and commercial kits. In terms of mechanism, it was determined that miR-107 had a regulatory relationship with target genes through luciferase reporter assay.</p><p><strong>Results: </strong>In mouse liver IRI, miR-107 expression was increased while HMOX1 expression was decreased in liver tissues. In vitro cellular experiments, miR-107 inhibitors favored the alleviation of proliferation, apoptosis, inflammation, and oxidative stress in HR-damaged liver sinusoidal endothelial cells. In the molecular mechanism study, we determined that miR-107 could bind to HMOX1 and inhibit the HMOX1 expression. Low HMOX1 expression could eliminate the protective effect of miR-107 inhibitors.</p><p><strong>Conclusion: </strong>MiR-107 expression was elevated during hepatic IRI and exacerbates hepatic injury by targeting HMOX1 inhibition.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"133"},"PeriodicalIF":2.7,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Delving into the pinnacle: an in-depth analysis of the top 100 most cited articles on cardio-oncology.","authors":"Ping Lai, Shuquan Xu, Zi-Xuan Cao, Zi-You Liu, Ke-Jun Tian, Wen-Ting Zhong, Xia Liu, Yi-Ming Zhong, Xiao-Ping Wang, Jin-Hua Xue","doi":"10.1186/s41065-025-00497-2","DOIUrl":"10.1186/s41065-025-00497-2","url":null,"abstract":"","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"132"},"PeriodicalIF":2.7,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269302/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649345","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}