Chinese Herbal Medicines最新文献

{"title":"Formononetin alleviates ovarian fibrosis and inflammation via targeting SOCS3 and inhibiting TGF-β1/Smad signaling in PCOS","authors":"Aifen Liu, Jingyan Hu, Weili Yu, Chuanyu Cang, Chuanjing Shi, Xi Wang, Rui Wang, Xuanwei Cai, Fengbo Zhao, Lei Zhang","doi":"10.1016/j.chmed.2026.05.011","DOIUrl":"10.1016/j.chmed.2026.05.011","url":null,"abstract":"<div><h3>Objective</h3><div>Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder characterized by ovulatory dysfunction. Formononetin (FMN), a bioactive compound derived from leguminous plants, including <em>Glycyrrhiza uralensis</em>, <em>Trifolium pratense</em>, and <em>Astragalus membranaceus</em>, exhibits anti-inflammatory and anti-fibrotic properties. This study aimed to evaluate the therapeutic effects of FMN in a PCOS rat model and elucidate its underlying molecular mechanisms.</div></div><div><h3>Methods</h3><div>A PCOS-like model was established in 3-week-old female Sprague-Dawley rats by daily dehydroepiandrosterone (DHEA) injections. The efficacy of FMN was assessed by monitoring estrous cycles, hormone levels, glucose tolerance, and ovarian tissue morphology. Network pharmacology and transcriptome sequencing were used to predict the molecular targets and signaling pathways of FMN. The binding and stabilizing effects of FMN on suppressor of cytokine signaling 3 (SOCS3) were confirmed using molecular docking, molecular dynamics (MD) simulations, and cellular thermal shift assay (CETSA)-Western blotting (WB) (CETSA-WB). The expression of SOCS3, inflammation- and fibrosis-related markers, and the components of the transforming growth factor beta1 (TGF-<em>β</em>1)/Smad pathway were quantified by quantitative polymerase chain reaction (qPCR), WB, and immunohistochemistry. Functional validation was performed using SOCS3 small interfering RNA (siRNA).</div></div><div><h3>Results</h3><div>DHEA successfully induced a PCOS-like phenotype, including disrupted estrous cycle, hyperandrogenism, an elevated luteinizing hormone to follicular stimulating hormone (LH/FSH) ratio, insulin resistance, and abnormal ovarian morphology. FMN treatment significantly reversed these abnormalities and reduced ovarian collagen deposition. Network pharmacology and transcriptome analyses indicated that the therapeutic efficacy of FMN was primarily attributable to its anti-fibrotic and anti-inflammatory properties, with SOCS3 identified as a potential key molecule. Molecular docking and MD simulations, along with CETSA-WB, further revealed that FMN directly binds to SOCS3, enhancing its stability and thereby inhibiting ovarian fibrosis in PCOS. Moreover, qPCR, WB, and immunohistochemistry confirmed that FMN regulates the TGF-<em>β</em>1/Smad signaling pathway. Importantly, SOCS3siRNA abolished fibrotic-related collagen levels and phosphorylated signal transducer and activator of transcription 3 (p-STAT3) expression, supporting the notion that FMN ameliorates PCOS-induced ovarian fibrosis via SOCS3.</div></div><div><h3>Conclusion</h3><div>FMN alleviated ovarian dysfunction and hyperandrogenism in DHEA-induced PCOS rats by stabilizing SOCS3 and inhibiting TGF-<em>β</em>1/Smad signaling, thereby attenuating ovarian fibrosis and inflammation. This reveals a novel SOCS3-centered mechanism for FMN and underscores its therapeutic potential for PCOS.</div","PeriodicalId":9916,"journal":{"name":"Chinese Herbal Medicines","volume":"18 3","pages":"Pages 604-620"},"PeriodicalIF":11.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390087/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564389","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amentoflavone: A safe and novel penetration enhancer for transdermal applications","authors":"Yunhao Ren,&nbsp;Fengyuan Song,&nbsp;Haobin Wang,&nbsp;Lihua Peng","doi":"10.1016/j.chmed.2025.10.002","DOIUrl":"10.1016/j.chmed.2025.10.002","url":null,"abstract":"<div><h3>Objective</h3><div>Most of existing chemical penetration enhancers are along with obvious toxicity and skin irritation, new penetration enhancer is still to be developed yet. Amentoflavone is a flavonoid compound extracted from plant <em>Selaginella tamariscina</em> with high biocompatibility. However, its efficacy of penetration enhancers has not been studied.</div></div><div><h3>Methods</h3><div>For the first time, the influence of amentoflavone to the skin penetration of caffeine was investigated by the Franz diffusion cells. The interactions of amentoflavone with the skin lipid and keratin were determined to identify the underlying mechanisms by the Fourier transform infrared spectroscopy (FTIR), differential scanning calorimetry (DSC), etc.</div></div><div><h3>Results</h3><div>Results showed that the penetration enhancement ratio (ER) of amentoflavone to model compound caffeine is nearly three times. The major mechanism was identified to be contributed to that, amentoflavone can not only change the keratin structure in stratum corneum (SC), but also undergo hydration interactions with intradermal components, therefore dissolving the lipid, loosening and reducing the barrier function of SC.</div></div><div><h3>Conclusion</h3><div>These results give new evidence to the potential of amentoflavone as the novel effective chemical enhancer for the skin meditated delivery of external molecules, and it can exert the dual effects of traditional Chinese medicine activity and penetration enhancement.</div></div>","PeriodicalId":9916,"journal":{"name":"Chinese Herbal Medicines","volume":"18 3","pages":"Pages 713-724"},"PeriodicalIF":11.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390000/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemical components and pharmacological action for Helianthus tuberosus and predictive analysis on its Q-markers","authors":"Xiaofei Wang,&nbsp;Shu Zhong,&nbsp;Li Wang,&nbsp;Xu Xu","doi":"10.1016/j.chmed.2025.04.003","DOIUrl":"10.1016/j.chmed.2025.04.003","url":null,"abstract":"<div><div><em>Helianthus tuberosus</em> is a perennial herb that belongs to the Asteraceae family and <em>Helianthus</em> genus. It is cultivated in numerous northern and southern China regions, displaying numerous benefits such as its drought and frost<!--> <!-->resistance, ability<!--> <!-->to grow on most<!--> <!-->soils,<!--> <!-->and<!--> <!-->low fertilizer requirements. <em>H. tuberosus</em> contains various components, such as inulin, phenolic acids, terpenoids, flavonoids, steroids, phenylpropanoids, and other bioactive compounds with antioxidant, anti-inflammatory, antibacterial, anti-tumor, and immune-modulatory effects. In this paper, based on the new concept of quality marker (Q-marker) proposed by Academician Changxiao Liu, this study analyzed the relationship between plant affinity, chemical composition specificity, traditional medicinal properties, and chemical composition measurability of <em>H. tuberosus</em>, and predicted its Q-markers to provide a reference for the establishment of the quality evaluation system and comprehensive utilization of this herb.</div></div>","PeriodicalId":9916,"journal":{"name":"Chinese Herbal Medicines","volume":"18 3","pages":"Pages 684-700"},"PeriodicalIF":11.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiometabolic reprogramming drives right ventricular dysfunction in pulmonary arterial hypertension: Novel mechanisms and therapeutic implications","authors":"Saihu Liu,&nbsp;Mari Okazaki,&nbsp;Yanling Wu","doi":"10.1016/j.chmed.2026.05.004","DOIUrl":"10.1016/j.chmed.2026.05.004","url":null,"abstract":"<div><div>With the understanding on right ventricular (RV) dysfunction in pulmonary arterial hypertension (PAH), the perspective innovatively integrates research paradigms on targeting cardiometabolic reprogramming of RV protective therapies to break through the bottleneck of current PAH treatment. The research focuses on three core areas: analyzing and validating metabolic dysregulation in the RV of PAH, exploring cell-specific metabolic dysregulation in the heart of PAH, and probing into the therapeutic strategy for PAH targeting RV metabolism. These aspects aim to deepen the scientific understanding of cardiometabolic reprogramming of RV dysfunction in PAH. This work provides a theoretical foundation and experimental evidence for developing RV-directed therapies that complement existing PAH treatments and improve patient outcomes.</div></div>","PeriodicalId":9916,"journal":{"name":"Chinese Herbal Medicines","volume":"18 3","pages":"Pages 494-498"},"PeriodicalIF":11.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effect and mechanism of extracts of fruit of Taxus chinensis on hippocampus of chronic unpredictable mild stress rats","authors":"Shunling Zhang,&nbsp;Jiayi Zhang,&nbsp;Fei Zhang,&nbsp;Maoyuan Ni,&nbsp;Linwei Zhong,&nbsp;Meimei Chen,&nbsp;Zhaoyang Yang,&nbsp;Huangwei Lei","doi":"10.1016/j.chmed.2025.02.008","DOIUrl":"10.1016/j.chmed.2025.02.008","url":null,"abstract":"<div><h3>Objective</h3><div>The ambitious research aimed to explore the protective impact and mechanism of the ethyl acetate extract of <em>Taxus chinensis</em> fruits (TCFE) on the hippocampi of rats subjected to chronic unpredictable mild stress (CUMS).</div></div><div><h3>Methods</h3><div>A total of 32 SD rats were randomly allocated into the control group, model group, TCFE group receiving 200 mg/(kg·d) of TCFE, fluoxetine group receiving 2 mg/(kg·d) of fluoxetine. The rats were induced with chronic unpredictable mild stress (CUMS) for 28 d, and concurrently administered the allocated drugs via gavage for the same duration. The body mass, performance in the open field test (OFT), and sugar-water preference rate of the rats in each group were assessed. The morphology of rat hippocampal tissues was examined using Hematoxylin-Eosin (HE) staining. Nissl staining was employed to observe hippocampal pathological changes, while ELISA was utilized to measure the levels of IL-1<em>β</em>, TNF-<em>α</em>, IL-6, and IL-18 in the hippocampus. Immunofluorescence was employed to identify the expression of the microglia (MG) marker Iba1 in the rat hippocampus. Furthermore, immunohistochemistry was utilized to detect the expression of Bax and Bcl-2 in the hippocampus. Real-time fluorescence quantitative PCR (qRT-PCR) was utilized to assess the expression levels of two apoptosis-related genes in the rat hippocampus. TUNEL assay was performed to detect tissue cell apoptosis in the rat hippocampus. Finally, Western blotting analysis was conducted to determine the expression of Bax and Bcl-2 proteins in the hippocampus.</div></div><div><h3>Results</h3><div>The consumption of TCFE significantly enhanced body weight (<em>P</em> &lt; 0.05), sucrose preference rate (<em>P</em> &lt; 0.05), and total movement distance in the open field test (<em>P</em> &lt; 0.05). It also improved hippocampal neuronal structure integrity and attenuated loss. Moreover, TCFE regulated the excessive activation of hippocampal microglia in rats, inhibited the expression of IL-1β and TNF-α (<em>P</em> &lt; 0.05), and modulated the Bax and Bcl-2 expression levels, leading to a significant alteration in the Bax/Bcl-2 ratio (<em>P</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>TCFE shows promise in attenuating cell apoptosis through the modulation of the Bax/Bcl-2 ratio, suggesting a prospective approach for combating depression.</div></div>","PeriodicalId":9916,"journal":{"name":"Chinese Herbal Medicines","volume":"18 3","pages":"Pages 737-745"},"PeriodicalIF":11.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147880119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Huashi Baidu formula may attenuate adriamycin-induced myocardial injury via modulating NRF2-ATF3-SRXN1 axis-mediated ferroptosis","authors":"Weijie Li,&nbsp;Xiang Li,&nbsp;Congying Huang,&nbsp;Yudong Liu,&nbsp;Zhaochen Ma,&nbsp;Zhaoyin Zhou,&nbsp;Qiuyan Guo,&nbsp;Congmin Xia,&nbsp;Chao Wang,&nbsp;Yute Zhong,&nbsp;Ping Wang,&nbsp;Haiyu Xu","doi":"10.1016/j.chmed.2026.05.009","DOIUrl":"10.1016/j.chmed.2026.05.009","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Objective&lt;/h3&gt;&lt;div&gt;Myocardial injury is a fatal adverse effect of adriamycin (ADR), which greatly limits its clinical application. Numerous studies have shown that Huashi Baidu formula (HBF) may exert a satisfactory effect on myocardial function repair. This study aims to reveal the underlying mechanisms and main bioactive compounds (BACs) of HBF against myocardial injury.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methods&lt;/h3&gt;&lt;div&gt;Firstly, this study established an ADR-induced mouse model to assess the protective effects of HBF against myocardial injury. Subsequently, transcriptomic profiling was conducted to screen the differentially expressed genes among the HBF treatment, ADR-induced model, and normal control groups. Following the construction and analysis of protein–protein interactions, gene set enrichment analysis, and co-expression matrix, the key targets of HBF against myocardial injury were screened and further validated based on the ADR-induced mouse model. An integrative approach combining network mapping, molecular docking, and molecular dynamics simulation was performed to identify the representative BACs.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;div&gt;Based on an ADR-induced myocardial injury mouse model, HBF significantly ameliorated myocardial injury by improving body weight loss, decreasing mortality, and rescuing severe cardiac fibrosis. A total of 361 ADR-related genes and 42 HBF therapeutic effect-related genes were identified with the thresholds &lt;em&gt;P&lt;/em&gt; &lt; 0.05 and fold change (FC) &gt; 1.2 or &lt; 0.833. Transcriptomic profiling-based networks demonstrated that the nuclear factor erythroid 2-related factor 2 (NRF2)-cyclic AMP-dependent transcription factor ATF-3 (ATF3)-sulfiredoxin-1 (SRXN1) axis-mediated ferroptosis was the key target of HBF against myocardial injury. &lt;em&gt;In vivo&lt;/em&gt; validation showed that HBF treatment effectively inhibited serum enzymatic biomarkers of general myocardial injury (aspartate aminotransferase, lactate dehydrogenase, and creatine kinase), myofibroblast activity (transforming growth factor beta 1 and &lt;em&gt;α&lt;/em&gt;-smooth muscle actin), inflammatory cytokines (tumor necrosis factor-&lt;em&gt;α&lt;/em&gt; and interleukin-6), oxidative damage (superoxide dismutase, malondialdehyde, accumulated iron content, and TUNEL-positive cells). Mechanically, HBF may restore the dysregulation of the NRF2-ATF3-SRXN1 signal axis, leading to inhibition of ferroptosis-associated protein expression. Emodin, rhein, and lactiflorin were identified as the underlying representative BACs of HBF against myocardial injury due to the strong binding affinities between candidate BACs and key targets [Kelch-like ECH-associated protein 1 (KEAP1), ATF3, SRXN1, system Xc- (SLC3A2/SLC7A11), glutathione peroxidase 4 (GPX4), ferroportin (FPN), glutathione synthetase (GSS)]. Molecular dynamics simulations further verified these findings, revealing the stable binding among the three components and the key targets.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;HBF may at","PeriodicalId":9916,"journal":{"name":"Chinese Herbal Medicines","volume":"18 3","pages":"Pages 621-634"},"PeriodicalIF":11.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389989/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Challenges and opportunities for ginseng-based medicines in treating cardiac fibrosis from mechanistic insights to clinical translation","authors":"Mengtao Zhi,&nbsp;Ao Wang,&nbsp;Hailian Quan,&nbsp;Lan Hong","doi":"10.1016/j.chmed.2026.05.014","DOIUrl":"10.1016/j.chmed.2026.05.014","url":null,"abstract":"<div><div>Cardiac fibrosis, characterized by excessive extracellular matrix (ECM) deposition and progressive myocardial remodeling, is a common pathological outcome of various cardiovascular diseases and lacks effective targeted anti-fibrotic therapies. <em>Panax ginseng</em> and its related preparations, including major ginsenosides (e.g., Rb₁, Rg₁, and Rg₃), standardized extracts, and compound formulas, have garnered growing interest owing to their multi-component, multi-target pharmacological activities and integrative regulatory effects. This review systematically summarizes recent advances in the basic and clinical research of ginseng-based medicines in the prevention and treatment of cardiac fibrosis. Preclinical evidence demonstrates that ginseng and its active constituents attenuate key pathological processes, including oxidative stress, inflammatory responses, apoptosis, and autophagy dysregulation, primarily through modulation of signaling pathways such as TGF-<em>β</em>/Smad, NF-<em>κ</em>B, and PI3K/Akt. These regulatory effects collectively contribute to the inhibition of fibroblast activation, reduction of collagen deposition, and improvement of myocardial structure and function. Emerging clinical studies further suggested potential benefits in improving cardiac function and modulating fibrosis-related biomarkers in patients with hypertension, coronary heart disease, and heart failure (HF). Despite these promising findings, several challenges hinder clinical translation, including low oral bioavailability, the mechanistic complexity of compound formulas, and insufficient high-quality clinical evidence. Future investigations should integrate novel drug delivery strategies, systems pharmacology approaches to elucidate holistic mechanisms, and well-designed randomized controlled trials to facilitate the development of ginseng-based medicines as potential therapeutic agents for cardiac fibrosis.</div></div>","PeriodicalId":9916,"journal":{"name":"Chinese Herbal Medicines","volume":"18 3","pages":"Pages 555-570"},"PeriodicalIF":11.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatoprotective effects of ginsenoside Rb1 from Panax ginseng on early liver injury via DNA repair activation and nuclear envelope stabilization","authors":"Fei Gao,&nbsp;Haiyun Gao,&nbsp;Yun Lin,&nbsp;Longyan Chen,&nbsp;Zheng Qi,&nbsp;Miao Yu","doi":"10.1016/j.chmed.2026.05.001","DOIUrl":"10.1016/j.chmed.2026.05.001","url":null,"abstract":"","PeriodicalId":9916,"journal":{"name":"Chinese Herbal Medicines","volume":"18 3","pages":"Pages 770-772"},"PeriodicalIF":11.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389976/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"6-Gingerol alleviates hepatic fibrosis via inhibiting glycolytic reprogramming by targeting IGF2BP2","authors":"Hui Fang,&nbsp;Fan Yang,&nbsp;Min Shu,&nbsp;Congjian Shi,&nbsp;Qingxu Ha,&nbsp;Junfa Yang,&nbsp;Xiaodi Jia,&nbsp;Yuansong Sun,&nbsp;Zhenhua Ren,&nbsp;Jian Gao","doi":"10.1016/j.chmed.2026.05.012","DOIUrl":"10.1016/j.chmed.2026.05.012","url":null,"abstract":"<div><h3>Objective</h3><div>Hepatic fibrosis remains a major global health burden, often progressing to cirrhosis and hepatocellular carcinoma. Despite extensive research, no effective antifibrotic drugs are clinically approved due to the complexity of hepatic stellate cells (HSCs) activation and metabolic remodeling. Enhanced glycolysis is increasingly recognized as a metabolic hallmark sustaining the profibrotic phenotype of HSCs, representing a key but underexplored therapeutic target. This study explored the antifibrotic effect of 6-gingerol, the principal bioactive compound of <em>Zingiber officinale</em>, and revealed its novel mechanism involving metabolic-epitranscriptomic regulation of HSC activation.</div></div><div><h3>Methods</h3><div>Liver fibrosis was induced in C57BL/6 mice by carbon tetrachloride (CCl₄) and bile duct ligation (BDL), followed by oral 6-gingerol treatment. Complementary <em>in vitro</em> studies were performed in transforming growth factor-<em>β</em>1 (TGF-<em>β</em>1)-stimulated Lieming Xu-2 (LX-2 cells, a human hepatic stellate cell line) and primary HSCs from liver fibrosis mice. Integrated transcriptomics, network pharmacology, molecular docking, and cellular thermal shift assays (CETSA) were combined with functional genetic manipulation to identify and verify molecular targets.</div></div><div><h3>Results</h3><div>6-Gingerol alleviated hepatic injury and collagen deposition in both CCl₄- and BDL-induced models and improved liver function. Mechanistically, 6-gingerol inhibited glycolysis by downregulating hexokinase 2 (HK2), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA), normalizing pyruvate and lactate metabolism, and restoring mitochondrial respiration. Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) was identified as an important mediator associated with glycolytic enzyme expression and HSCs activation, and its silencing abolished 6-gingerol’s antifibrotic effects.</div></div><div><h3>Conclusion</h3><div>Our study demonstrates that 6-gingerol attenuates hepatic fibrosis by targeting IGF2BP2-dependent glycolytic reprogramming, thereby restoring metabolic homeostasis and inhibiting HSCs activation. These findings uncover a novel metabolic-epitranscriptomic mechanism and suggest that 6-gingerol represents a promising therapeutic strategy for chronic liver diseases.</div></div>","PeriodicalId":9916,"journal":{"name":"Chinese Herbal Medicines","volume":"18 3","pages":"Pages 585-603"},"PeriodicalIF":11.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13390069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Xuezhikang Capsule ameliorates ischemic stroke via multi-target modulation of neurovascular units","authors":"Xiaowen Zhang,&nbsp;Chengchen Hou,&nbsp;Yuqi Wang,&nbsp;Yang Chen,&nbsp;Ling Li,&nbsp;Lan Xue,&nbsp;Chunhui Hao,&nbsp;Xi Liu,&nbsp;Kewu Zeng","doi":"10.1016/j.chmed.2026.05.010","DOIUrl":"10.1016/j.chmed.2026.05.010","url":null,"abstract":"","PeriodicalId":9916,"journal":{"name":"Chinese Herbal Medicines","volume":"18 3","pages":"Pages 767-769"},"PeriodicalIF":11.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13389994/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148564499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}