HereditasPub Date : 2025-07-26DOI: 10.1186/s41065-025-00518-0
Xiaoyan Liu, Zhongying Bao, Shuhong Duan, Jing Sun, Jie Zhang
{"title":"A retrospective study on the efficacy of integrating traditional Chinese medicine with Western medicine in the treatment of adult measles.","authors":"Xiaoyan Liu, Zhongying Bao, Shuhong Duan, Jing Sun, Jie Zhang","doi":"10.1186/s41065-025-00518-0","DOIUrl":"10.1186/s41065-025-00518-0","url":null,"abstract":"<p><strong>Objective: </strong>Measles is a highly contagious, potentially fatal disease, and using western medicine for treating this disease showed some limits including the long period of treatment and some side effects. Of note, traditional Chinese medicine (TCM) exhibited advantages of treating measles in using alone or combing with western medication. However, little information on the clinical study on adjunctive efficacy of TCM on measles. Therefore, the objective of this study is to observe the adjunctive efficacy of TCM in the treatment of adult measles.</p><p><strong>Methods: </strong>Ninety-one patients diagnosed with adult measles in our hospital were enrolled for this study. All of them underwent symptomatic treatment, nutritional support therapy, and ribavirin antiviral therapy. Loxoprofen was added to the treatment regime when the body temperature exceeded 38.5 °C. The patients were stratified into two groups based on the administration of TCM, comprising 49 individuals in the TCM group and 42 individuals in the control group. Patients in the TCM group voluntarily received the following TCM prescriptions: 15 g of Lonicerae Japonica, 15 g of Forsythiae Fructus, 15 g of Arnebiae Radix, 15 g of Cicadae Periostracum, 30 g of Phragmitis Rhizoma, 10 g of Anemarrhenae Rhizoma, 6 g of Glycyrrhizae Radix et Rhizoma and 30 g of Gypsum Fibrosum was administered to patients with high fever. Decoction: 1 dose daily for 5 days. The control group received treatment without the incorporation of TCM.</p><p><strong>Results: </strong>In comparison to the control group, patients in the TCM group experienced a quicker resolution of clinical symptoms (P < 0.05) and a lower complication rate (P < 0.05).</p><p><strong>Conclusion: </strong>The application of TCM in treating adult measles can shorten the duration of the disease, reduce the incidence of complications, and offers promise for wider clinical adoption and utilization.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"146"},"PeriodicalIF":2.5,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12297466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717826","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":"Effect of Wendan decoction granules on preventing endolymphatic hydrops and protecting vestibular function in Guinea pigs.","authors":"Jingjing Xia, Tiancheng Xie, Jinli Liu, Weikang Cheng, Longyan Liao, Ming Chen, Haibing Hua, Xiaobing Hou","doi":"10.1186/s41065-025-00516-2","DOIUrl":"10.1186/s41065-025-00516-2","url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study is to assess the therapeutic effects of Wendan decoction on endolymphatic hydrops (EH), a condition characterized by excessive inner ear fluid accumulation that is associated with Meniere's disease, in guinea pigs, offering insights for clinical application.</p><p><strong>Methods: </strong>The active components and action targets of compound Wendan decoction were identified using BATMAN-TCM in this study. Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were conducted on Metascape and bioinformatics.com.cn platforms. Cytoscape was used to construct the TCM-compound-target-disease network and the disease-target pathway network for visual representation. The chemical profile of Wendan decoction was characterized through UHPLC-QTOF/MS. Guinea pigs were used to establish an EH model. The effects of Wendan decoction granules on neurological function, cochlear hydrops, the ultrastructure of the cochlear Corti organ area, inflammatory response, and the expression of AQP2 and P38MAPK in guinea pigs were examined using behavioral experiments, hematoxylin and eosin staining, scanning electron microscopy, ELISA, qRT-PCR, and immunohistochemistry staining.</p><p><strong>Results: </strong>A total of 103 components, primarily flavonoids and triterpenoid saponins, were identified in Wendan decoction. Wendan decoction significantly inhibited the MAPK signaling pathway. Wendan decoction granules alleviated neurological impairment induced by EH. Following treatment, guinea pigs exhibited reduced membranous labyrinth hydrops and decreased outer hair cell loss. Wendan decoction granules also suppressed the release of pro-inflammatory factors and reduced AQP2 protein expression in model guinea pigs.</p><p><strong>Conclusion: </strong>Wendan decoction granules effectively alleviated neurological impairment and inflammatory responses, preserved cochlear structure, reduced inflammation, and modulated AQP2 expression, offering a strong basis for further investigation of its therapeutic potential.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"145"},"PeriodicalIF":2.5,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717765","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}
HereditasPub Date : 2025-07-26DOI: 10.1186/s41065-025-00511-7
Weikang Su, Zhiling Zhong, Huazhi Li, Lingjia Meng, Xinqiang Zhong
{"title":"The diagnostic and predictive value of LncRNA PANDAR in gastric cancer and its regulation of gastric cancer progression via miR-637.","authors":"Weikang Su, Zhiling Zhong, Huazhi Li, Lingjia Meng, Xinqiang Zhong","doi":"10.1186/s41065-025-00511-7","DOIUrl":"10.1186/s41065-025-00511-7","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) remains a global health challenge due to its high morbidity, late-stage diagnosis, and limited therapeutic options. long non-coding RNA PANDAR has been implicated in tumorigenesis across multiple cancers, yet its role in GC pathogenesis and diagnostic utility is still unclear. The purpose of this study is to elucidate the diagnostic value of serum PANDAR and its regulatory mechanisms in GC progression.</p><p><strong>Methods: </strong>lncRNA PANDAR levels were quantified in serum from 112 GC patients and 98 benign controls using RT-qPCR. The diagnostic value of lncRNA PANDAR was analyzed by ROC curve. Functional experiments (CCK-8, Transwell assays) and dual-luciferase reporter assays were conducted in HGC-27 and BGC-823 cells to explore the function of PANDAR in cell proliferation, migration, and invasion. The interaction between PANDAR and miR-637 was validated via bioinformatics prediction and co-inhibition assay.</p><p><strong>Results: </strong>Serum PANDAR was significantly upregulated in GC patients (P < 0.0001) and exhibited high diagnostic accuracy (AUC = 0.913). Elevated PANDAR associated with advanced TNM stage (P = 0.047), lymph node metastasis (P = 0.023), and digestive system history (P = 0.035). PANDAR knockdown suppressed GC cell proliferation, migration, and invasion, effects reversed by co-inhibition of miR-637.</p><p><strong>Conclusions: </strong>lncRNA PANDAR is a promising non-invasive diagnostic indicator of GC, and may serve as a biomarker for GC diagnosis and therapy. lncRNA PANDAR regulates the progression of GC through sponge miR-637.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"144"},"PeriodicalIF":2.5,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12297835/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717768","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":"LncRNA LUCAT1 as a prognostic biomarker in cholangiocarcinoma through targeting miR-141-3p: clinical and functional insights.","authors":"Yuxin An, Qing Chen, Shanshan Zhou, Chengcheng Ying, Guanbao Long, Zouxiao Hu, Jiangyang Sun, Niu Zhang","doi":"10.1186/s41065-025-00512-6","DOIUrl":"10.1186/s41065-025-00512-6","url":null,"abstract":"<p><strong>Background: </strong>Cholangiocarcinoma (CHOL) has a poor prognosis due to its asymptomatic progression, challenges in early detection, and limited treatment options. The lncRNA LUCAT1 is highly expressed in several cancers, including lung, gastric, ovarian, and osteosarcoma tissues.</p><p><strong>Aim: </strong>This study investigates the potential of LUCAT1 as a diagnostic and prognostic biomarker for CHOL.</p><p><strong>Materials and methods: </strong>In this study, we collected tumor tissues and adjacent tumor healthy tissues from 83 CHOL patients. LUCAT1 expression was quantified in CHOL tissues and cell lines via RT-qPCR. Diagnostic and prognostic significance was assessed through ROC curves, Kaplan-Meier survival analysis, and Cox regression models. The biological effects of LUCAT1 on cell proliferation and migration were examined using QBC939 and HuCCT1 cells with transfection assays. The regulatory interaction between LUCAT1 and miR-141-3p was validated using a dual-luciferase reporter assay.</p><p><strong>Results: </strong>Elevated expression of LUCAT1 was observed in CHOL tumor tissues and human cholangiocarcinoma cells, correlating with tumor size, CA-19-9 levels, and TNM stage. The ROC curve, with an AUC of 0.908 (p < 0.001), effectively distinguished CHOL tumor tissues from adjacent non-tumor tissues. And its sensitivity and specificity in distinguishing CHOL tissues from normal tissues were 88.5% and 89.2%, respectively. Survival analyses linked LUCAT1 overexpression to poorer patient outcomes. Silencing LUCAT1 impaired the proliferation and migration of QBC939 and HuCCT1 cells. Dual-luciferase assay confirmed the regulatory relationship between miR-141-3p and LUCAT1. Inhibition of miR-141-3p reversed the effect of LUCAT1 on the proliferation and migration of QBC939 and HuCCT1 cells.</p><p><strong>Conclusion: </strong>LUCAT1 demonstrates significant diagnostic and prognostic potential and could serve as a novel biomarker for CHOL.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"143"},"PeriodicalIF":2.5,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12297753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717766","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}
HereditasPub Date : 2025-07-25DOI: 10.1186/s41065-025-00514-4
LiQun Cheng, RongRong Shen, Zhen Ma, Yuan Guo, Yi Peng
{"title":"Local anesthetic ropivacaine inhibits non-small cell lung cancer progression by modulating the hsa_circ_0001320/miR-518a-5p axis.","authors":"LiQun Cheng, RongRong Shen, Zhen Ma, Yuan Guo, Yi Peng","doi":"10.1186/s41065-025-00514-4","DOIUrl":"10.1186/s41065-025-00514-4","url":null,"abstract":"<p><strong>Objective: </strong>This study investigated the possible mechanisms by which ropivacaine influences the progression of non-small cell lung cancer (NSCLC).</p><p><strong>Methods: </strong>Plasmid vectors or oligonucleotides interfering with circ_0001320 or miR-518a-5p were transfected into ropivacaine-treated NSCLC cells, and circ_0001320 and miR-518a-5p levels were detected by RT-qPCR. Cell proliferation was assessed using CCK-8, apoptosis via flow cytometry, and cell migration and invasion through Transwell assays. Finally, the binding sites of circ_0001320 and miR-518a-5p were verified by the bioinformatics website CircInteractome and dual luciferase reporter gene assay.</p><p><strong>Results: </strong>Exposure to ropivacaine resulted in the suppression of NSCLC cell proliferation, migration, invasion, and angiogenesis, while inducing apoptosis. Ropivacaine elevated circ_0001320 expression. Circ_0001320 downregulation resulted in a reduced efficacy of ropivacaine in inhibiting NSCLC progression. Interestingly, circ_0001320 targeted miR-518a-5p and inhibited its expression. It was possible to limit the effects of downregulation of circ_0001320 on NSCLC progression by downregulating miR-518a-5p.</p><p><strong>Conclusion: </strong>Ropivacaine inhibits NSCLC progression via the circ_0001320/miR-518a-5p axis.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"142"},"PeriodicalIF":2.5,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12291326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144717767","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}
HereditasPub Date : 2025-07-24DOI: 10.1186/s41065-025-00510-8
Lichang Yang, Ru Chang, Jianzhen Pan, Shan Huang
{"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":"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":2.5,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12291396/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HereditasPub Date : 2025-07-24DOI: 10.1186/s41065-025-00504-6
Yu Pan, Yu Liu, Yixuan Huo, Suren R Sooranna, Lu Chen, Lijun Yin, Zhigang Yan, Danna Huang, Lihe Jiang, Wuwei Wu
{"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":"10.1186/s41065-025-00504-6","url":null,"abstract":"","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"141"},"PeriodicalIF":2.5,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12291371/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HereditasPub Date : 2025-07-23DOI: 10.1186/s41065-025-00508-2
Li Zhou, Bin Xu, Baojian Li
{"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":"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 (IC<sub>50</sub>) 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 Fe<sup>2+</sup> levels, while reducing glutathione (GSH) levels and the IC<sub>50</sub> 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":2.5,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12285127/pdf/","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":"OA","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":"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":2.5,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12285066/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
HereditasPub Date : 2025-07-22DOI: 10.1186/s41065-025-00499-0
Wenchao Gu, Shuo Tian, Lu Fu, Lina Wang, Liangkun Zhang, Furong Wang
{"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":"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":2.5,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12281869/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}