Chinese Medicine最新文献

{"title":"Chikusetsusaponin IVa targeted YAP as an inhibitor to attenuate liver fibrosis and hepatic stellate cell activation.","authors":"Kai Gao, Wei Zhang, Dong Xu, Meina Zhao, Xingru Tao, Yunyang Lu, Jingwen Wang","doi":"10.1186/s13020-025-01090-5","DOIUrl":"10.1186/s13020-025-01090-5","url":null,"abstract":"<p><strong>Background: </strong>Liver fibrosis is a representative scarring response that can ultimately lead to liver cancer. However, relevant antifibrotic drugs for the effective treatment of liver fibrosis in humans have not yet been identified. Chikusetsusaponin IVa (CS-IVa) is derived from natural products and exhibits multiple biological activities; however, its efficacy and potential mechanism of action against liver fibrosis remains unclear.</p><p><strong>Purpose: </strong>This study aimed to examine the antifibrotic properties and potential mechanisms of action of CS-IVa.</p><p><strong>Methods: </strong>We constructed two mature mouse models (CCl₄ challenge and bile duct ligation) to evaluate the antifibrotic properties of CS-IVa in vivo. Proteomics analysis and transforming growth factor β1 (TGF-β1)-activated LX-2 cells were used to elucidate the potential effects and mechanisms. Molecular docking, surface plasmon resonance (SPR), and cellular thermal shift assay (CETSA) were used to detect the affinity and binding between CS-IVa and its target.</p><p><strong>Results: </strong>We found that CS-IVa significantly alleviated liver fibrosis and injury by downregulating yes-associated protein (YAP) and tafazzin (TAZ) expression. In an in vitro model, CS-IVa suppressed TGF-β1-induced hepatic stellate cell (HSC) activation, as well as the mRNA and protein expression of COL1A1, α-SMA, YAP, and TAZ. Moreover, specific knockdown or inhibition of YAP did not enhance the suppressive effect of CS-IVa on HSC activation or fibrosis-associated protein expression. Molecular docking, SPR, and CETSA showed that CS-IVa could directly bind to YAP.</p><p><strong>Conclusion: </strong>These findings demonstrated that the administration of CS-IVa effectively alleviated liver fibrosis by suppressing the YAP/TAZ pathways. In addition, CS-IVa could directly bind to YAP and act as a YAP inhibitor.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"36"},"PeriodicalIF":5.3,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912722/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atractylenolide I ameliorated the growth and enzalutamide resistance of castration-resistant prostate cancer by targeting KIF15.","authors":"Chenglin Han, Bin Yang, Yuxuan Deng, Peng Hu, Bintao Hu, Xiaming Liu, Tao Wang, Chengbao Li, Jihong Liu, Huixing Yuan","doi":"10.1186/s13020-025-01086-1","DOIUrl":"10.1186/s13020-025-01086-1","url":null,"abstract":"<p><strong>Background: </strong>Castration-resistant prostate cancer (CRPC) has been a major cause of tumor-associated death among men worldwide. The discovery of novel therapeutic medicines for CRPC remains imperative. Atractylenolide I (ATR-I), a prominent bioactive component from Atractylodes macrocephala, exhibits powerful anticancer potentials in various malignancies. Nevertheless, the ATR-I's activity on CRPC has not been reported.</p><p><strong>Methods: </strong>An enzalutamide-resistant (EnzR) cell line was successfully constructed. CCK-8, EdU, wound healing, Transwell assays, flow cytometry, and xenograft tumor models were applied to investigate the antitumor activity of ATR-I against CRPC. The changes in the gene expression profiles after ATR-I treatment were analyzed using RNA sequencing.</p><p><strong>Results: </strong>ATR-I suppressed the proliferative and migratory abilities of AR⁺ and AR^- CRPC cells, while triggering cell cycle arrest and apoptosis. ATR-I also exerted anti-cancer activity on EnzR cell lines. Intriguingly, a combination of ATR-I with enzalutamide synergistically induced more apoptosis of tumor cells. RNA-sequencing identified kinesin family member 15 (KIF15) as a potential target of ATR-I. KIF15 was up-regulated in prostate cancer (PCa), and its higher level was associated with poorer clinical outcomes. Further investigation showed that ATR-I mediated ubiquitin-proteasomal degradation of AR/AR-V7 through targeting KIF15, resulting in CRPC repression. Finally, our in vivo experiment verified that ATR-I alone or in combination with enzalutamide retarded the growth of EnzR xenograft tumors.</p><p><strong>Conclusions: </strong>These findings identified ATR-I as a promising therapeutic drug for overcoming enzalutamide resistance in CRPC patients and increased our understanding about its antitumor mechanisms.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"35"},"PeriodicalIF":5.3,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11909966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chlorogenic acid attenuates pyrrolizidine alkaloid-induced liver injury through modulation of the SIRT1/FXR signaling pathway.","authors":"Jie Xu, Qiongwen Xue, Aizhen Xiong, Yilin Chen, Xunjiang Wang, Xing Yan, Deqing Ruan, Yumeng Zhang, Zhengtao Wang, Lili Ding, Li Yang","doi":"10.1186/s13020-025-01077-2","DOIUrl":"10.1186/s13020-025-01077-2","url":null,"abstract":"<p><strong>Background: </strong>Pyrrolizidine alkaloids (PAs), recognized globally for their hepatotoxic properties, significantly contribute to liver damage through an imbalance in bile acid homeostasis. Addressing this imbalance is crucial for therapeutic interventions in PA-related liver injuries. Chlorogenic acid (Cga), a phenolic compound derived from medicinal plants, has demonstrated hepato-protective effects across a spectrum of liver disorders. The specific influence and underlying mechanisms by which Cga mitigates PA-induced liver damage have not been clearly defined.</p><p><strong>Materials and methods: </strong>To explore the protective effects of Cga against acute PA toxicity, a murine model was established. The influence of Cga on bile acid metabolism was confirmed through a variety of molecular biology techniques. These included RNA sequencing, western blotting, and immunoprecipitation, along with quantitative analyses of bile acid concentrations.</p><p><strong>Results: </strong>Our findings indicate that Cga enhances sirtuin 1 (SIRT1) activation and increases farnesoid X receptor (FXR) signaling, which are crucial for maintaining bile acid balance in PA-induced hepatic injury. When mice subjected to PA-induced hepatic injury were treated with SIRT1 inhibitors alongside Cga, the hepatoprotective effects of Cga were significantly reduced. In Fxr-KO mice, the ability of Cga to mitigate liver damage induced by PAs was substantially reduced, which underscores the role of the SIRT1/FXR signaling axis in mediating the protective effects of Cga.</p><p><strong>Conclusion: </strong>Our research suggests that Cga can serve as an effective treatment for PA-mediated hepatotoxicity. It appears that influencing the SIRT1/FXR signaling pathway might provide an innovative pharmacological approach to address liver damage caused by PAs.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"34"},"PeriodicalIF":5.3,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11899315/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-omics driven paradigm for construction of traditional Chinese Medicine Zheng (syndrome) diagnosis and treatment model, taking Shi Zheng (syndrome of dampness) as an example.","authors":"Wenkai Wang, Le Yang, Wanhua Li, Ye Sun, Hui Sun, Yanjia Chen, Junling Ren, Jianwen Guo, Shuyun Wei, Fengye Lin, Guangli Yan, Ying Han, Qubo Chen, Xijun Wang","doi":"10.1186/s13020-025-01085-2","DOIUrl":"10.1186/s13020-025-01085-2","url":null,"abstract":"<p><strong>Background: </strong>Shi Zheng (SZ, syndrome of dampness) is a major syndrome type in traditional Chinese Medicine (TCM), the ambiguity of its pathomechanism and the lack of blood diagnostic indicators have limited the understanding of the development of SZ.</p><p><strong>Purpose: </strong>To explore the pathological mechanism of SZ and establish a symptom-centered diagnosis and treatment model.</p><p><strong>Methods: </strong>We recruited 250 participants, including healthy individuals and patients diagnosed with SZ. Serum metabolomics and proteomics analyses were performed to screen common pathways. Along with the biological significance of common pathways, a common pathway-symptom correlation diagram was constructed to elucidate the pathological mechanism underlying the occurrence and development of SZ. The enrichment score and correlations with SZ main symptom was used to screen the key common pathways. The key common pathways related to differential metabolites and proteins were used to establish a multi-index diagnostic model and protein therapy target group.</p><p><strong>Results: </strong>Joint metabolomics and proteomics analyses revealed 18 common pathways associated with symptoms. Six key pathways, such as pathogenic Escherichia coli infection, rheumatoid arthritis, PPAR signaling pathway, bile secretion, GnRH signaling pathway, and fat digestion and absorption were correlated with the main symptoms of SZ. These symptoms included greasy/thick/slippery tongue coating, heavy head, heavy body, heavy limbs, heavy joints, greasy hair, sticky mouth, sticky stool, and damp scrotum. Moreover, seven differential metabolites related to the key pathways were identified: LysoPA (20:3(5Z,8Z,11Z)/0:0), prostaglandin E2, leukotriene B4, lithocholate 3-O-glucuronide, 3-hydroxyquinine, lithocholic acid glycine conjugate, and PA(18:0/22:6(5Z,8E,10Z,13Z,15E,19Z)-2OH(7S, 17S)), and the combined diagnostic value of the seven indicators was the highest (discovery cohort: AUC = 0.90; validation cohort: AUC = 0.99). There were 23 differential proteins related to the key pathways, and six protein targets were identified, including RHOA, TNFSF13, PRKCD, APOA2, ATP1A1, and FABP1.</p><p><strong>Conclusion: </strong>The combined analysis of metabolomics and proteomics established a symptom-centered diagnosis and treatment model of Shi Zheng.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"33"},"PeriodicalIF":5.3,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FVTF inhibits hepatocellular carcinoma stem properties via targeting DNMT1/miR-34a-5p/FoxM1 axis.","authors":"Xiao-Cheng Cao, Jinwu Peng, Ye-Bei Qiu, Wei Zhu, Jian-Guo Cao, Hui Zou, Zheng-Zheng Yu, Di Wu, Shan-Shan Lu, Wei Huang, Hong Yi, Zhi-Qiang Xiao","doi":"10.1186/s13020-025-01084-3","DOIUrl":"10.1186/s13020-025-01084-3","url":null,"abstract":"<p><strong>Background: </strong>Fructus Viticis Total Flavonoids (FVTF) is a novel candidate preparation that possesses anticancer activity. However, the role and mechanism of FVTF-inhibiting human hepatocellular carcinoma (HCC) cell stem properties is unclear.</p><p><strong>Methods: </strong>Liquid chromatography (LC) in conjugation with mass spectrometer (MS) was used to identify the compounds of FVTF. Tumorsphere and soft agar colony formation ability, cancer stem marker expression levels, CD133⁺ cell percentage, and a xenograft model were utilized to investigate the impact of FVTF on HCC cells stemness. PCR array and qRT-PCR were conducted to identify differentially expressed cancer stem-related genes and miRNAs between FVTF-treated and untreated HCC cells, respectively. Pyrosequencing was conducted to assess the DNA methylation level of the miR-34a-5p promoter. A luciferase reporter assay was performed to verify whether FoxM1 serves as a direct target of miR-34a-5p. Additionally, immunohistochemistry of an HCC tissue microarray was carried out to assess the expression levels of DNMT1, FoxM1, and miR-34a-5p.</p><p><strong>Results: </strong>A total of 26 compounds, including 10 flavones, in FVTF were identified. FVTF significantly reduced the ability of tumorsphere and soft agar colony formation, the levels of CD44 protein and BMI1, OCT4 and SOX2 mRNAs in HCC cells, and in vivo tumor initiation ability of HCC cells. Mechanistically, FVTF inhibited HCC cell stem properties via targeting DNMT1/miR-34a-5p/FoxM1 axis. Clinically, DNMT1 expression was inversely correlated with miR-34a-5p expression, whereas a positive correlation was noted between DNMT1 and FoxM1 expression levels, and high DNMT1 levels, low miR-34a-5p levels, and high FoxM1 levels were associated with cancer recurrence. Furthermore, a combination of DNMT1, miR-34a-5p and FoxM1 served as an independent prognostic indicator influencing both DFS and OS in patients with HCC.</p><p><strong>Conclusions: </strong>FVTF inhibits HCC cell stem properties by targeting DNMT1/miR-34a-5p/FoxM1 axis, which is associated with HCC recurrence and prognosis, and FVTF is a prospective treatment drug for human HCC.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"32"},"PeriodicalIF":5.3,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11884036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572351","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prediction of herbal compatibility for colorectal adenoma treatment based on graph neural networks.","authors":"Limei Gu, Yinuo Ma, Shunji Liu, Qinchang Zhang, Qiang Zhang, Ping Ma, Dongfang Huang, Haibo Cheng, Yang Sun, Tingsheng Ling","doi":"10.1186/s13020-025-01082-5","DOIUrl":"10.1186/s13020-025-01082-5","url":null,"abstract":"<p><p>Colorectal adenoma is a common precancerous lesion with a high risk of malignant transformation. Traditional Chinese medicine and its complex prescriptions have shown promising efficacy in the treatment of adenomas; however, there remains a lack of systematic understanding regarding the compatibility patterns within these prescriptions, as well as an effective model for predicting therapeutic outcomes. In this study, we collected numerous TCM prescriptions and their components, recommended by experts for the treatment of colorectal adenoma, and developed a heterogeneous graph neural network model to predict the compatibility strength and probability among the herbs within these prescriptions. This model delineates the complex relationships among herbs, active compounds, and molecular targets, allowing for a quantification of the interactions and compatibility potential among the herbs. Using this model, we identified high-potential therapeutic prescriptions from clinical prescription records and identified their active components through network pharmacology. Through this approach, we aim to provide a theoretical foundation for the clinical TCM treatment of colorectal adenoma, foster the discovery of new prescriptions to optimize the therapeutic efficacy of TCM, and ultimately advance the field of cancer prevention and treatment based on traditional Chinese medicine.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"31"},"PeriodicalIF":5.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture produces analgesic effects via cannabinoid CB1 receptor-mediated GABAergic neuronal inhibition in the rostral ventromedial medulla.","authors":"Kexing Wan, Qian Xu, Yulong Shi, Chi Cui, Jie Lei, Kailing Zhang, Qingxu Yao, Yiqing Rao, Ziyu Zhou, Yisong Wu, Jiale Mei, Hui-Lin Pan, Xianghong Jing, He Zhu, Man Li","doi":"10.1186/s13020-025-01083-4","DOIUrl":"10.1186/s13020-025-01083-4","url":null,"abstract":"<p><strong>Objective: </strong>Electroacupuncture (EA) is commonly used for pain control in clinical practice, yet the precise mechanisms underlying its action are not fully understood. The rostral ventromedial medulla (RVM) plays a crucial role in the modulation of pain. GABAergic neurons in the RVM (GABA^RVM neurons) facilitate nociceptive transmission by inhibiting off-cells activity. This research examined the role of GABA^RVM neurons in the analgesic effects of EA.</p><p><strong>Methods: </strong>Nociceptive behavior was evaluated using inflammatory pain models induced by complete Freund's adjuvant (CFA) and neuropathic pain models induced by chronic constrictive injury (CCI). Also, in situ hybridization, chemogenetics, in vivo mouse calcium imaging, and in vivo electrophysiological recordings were used to determine neuronal activity and neural circuitry.</p><p><strong>Results: </strong>EA at the \"Zusanli\" (ST36) on the affected side produced a significant analgesic effect in both CFA and CCI models. CFA treatment and CCI elevated the calcium activity of GABA^RVM neurons. Also, EA reduced the calcium activity, neuronal firing rates, and c-Fos expression of GABA^RVM neurons in both pain models. Chemogenetic inhibition of GABA^RVM neurons increased nociceptive thresholds. Chemogenetic activation of GABA^RVM neurons caused increased pain sensitivity in control mice and negated the analgesic effects of EA in both pain models. Moreover, reducing cannabinoid CB1 receptors on GABA^RVM neurons counteracted the analgesic effects of EA in CFA and CCI-induced pain models.</p><p><strong>Conclusions: </strong>The study indicates that the analgesic effect of EA in inflammatory and neuropathic pain is facilitated by CB1 receptor-mediated inhibition of GABA^RVM neurons.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"30"},"PeriodicalIF":5.3,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881457/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of acupuncture in treating depression: a review.","authors":"Jianfu Ma, Xuan Yin, Kaiyu Cui, Jiqing Wang, Wei Li, Shifen Xu","doi":"10.1186/s13020-025-01080-7","DOIUrl":"10.1186/s13020-025-01080-7","url":null,"abstract":"<p><strong>Background: </strong>Acupuncture as a representative treatment method of traditional Chinese medicine, has been found to have a significant effect on mild to moderate depression without obvious side effects, but the mechanism through which it exerts its antidepressant effect is still unclear.</p><p><strong>Methods: </strong>We searched PubMed, Web of Science, and Embase databases for basic research on acupuncture in the treatment of depression from the database established to June 14, 2024, and finally included 44 studies from 2020 to June 14, 2024, into the table analysis. The main outcomes of this study are the effects of acupuncture on the relevant biological indicators of depression model.</p><p><strong>Results: </strong>By analyzing the effect of acupuncture on rodent model of depression, the mechanism of acupuncture against depression was explored. In general, several acupuncture methods, mainly based on electroacupuncture (EA), regulate the levels of 5-hydroxytryptamine (5-HT), glutamic acid (Glu) and dopamine (DA), regulate the calcium signaling pathway, increase the expression of synaptic protein, promote mitochondrial repair and reduce oxidative stress, and enhance synaptic plasticity. Inhibition of key inflammatory pathways such as P2X7R/NLRP3 and NF-κB signaling pathways, regulation of hypothalamic-pituitary-adrenal axis (HPA axis) function, and tryptophan metabolism improved depression-like behavior in rodent models.</p><p><strong>Conclusions: </strong>In summary, acupuncture treatment represented by EA has multiple mechanisms to play a role by regulating neurotransmitter balance, improving neuroplasticity, reducing inflammatory responses, and regulating the neuroendocrine system. However, the differences between acupoint catgut embedding (ACE), manual acupuncture (MA), and EA in the treatment of depression and the operating parameters of EA in the treatment of depression with different causes (such as frequency, intensity, duration, etc.) still need further research to be confirmed. This review has not been registered with PROSPERO or other protocol registration platforms because protocol registration was not a mandatory requirement for this study.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"29"},"PeriodicalIF":5.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11877828/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Folium Hibisci Mutabilis extract suppresses M1 macrophage polarization through mitochondrial function enhancement in murine acute gouty arthritis.","authors":"Yichen Zhao, Jiahui Zhang, Wei Yan, Ping Jiang, Juncheng Li, Haojun He, Honghong Ma, Yuxin Zhang, Kai Yang, Min Jiang, Xiaobing Xi","doi":"10.1186/s13020-025-01081-6","DOIUrl":"10.1186/s13020-025-01081-6","url":null,"abstract":"<p><strong>Background: </strong>Acute gout arthritis (AGA) is a common metabolic joint disease and urgently needs a safer alternative therapy due to the significant side effects from long-term use of primary medications. Folium Hibisci Mutabilis, a traditional medicinal herb, has demonstrated promising therapeutic efficacy in the clinical management of AGA, but its pharmacological mechanisms remain to be elucidated.</p><p><strong>Methods: </strong>Folium Hibisci Mutabili was isolated and refined into the Folium Hibisci Mutabilis Extract (FHME). Then, monosodium urate-induced AGA animal models were applied to identify the anti-inflammatory and analgesic effects of FHME in vivo through various techniques, including ultrasonography, Paw withdrawal thresholds, histological staining, etc. We used RNA-seq, qRT-PCR, ELISA, and flow cytometry to evaluate the efficacy of FHME on M1 polarization. Utilizing transmission electron microscope and oxygen consumption rate examinations in conjunction with Mito-Tracker staining, we observed the effects of FHME on mitochondrial morphology and function. Finally, we employed proteomics analysis, siRNA, qRT-PCR, western blot and other techniques to investigate the underlying mechanism of FHME's actions between the two phenotypes and the key targets.</p><p><strong>Results: </strong>We observed a notable reduction in inflammation and pain, as well as the decreased infiltration of inflammatory cells and expression of IL-1β in synovial tissue of AGA mice upon treatment with FHME. FHME suppressed TNF-α, IL-1β, iNOS, and IL-18 expression in BMDM-derived macrophages and inhibited the formation of F4/80⁺CD86⁺ cells. Mechanically, FHME protected mitochondrial morphology and stimulated the expression of key oxidative phosphorylation proteins, such as Ubiquinol Cytochrome c Reductase Core Protein I (UQCRC1), UQCRC2, CYCS, and NDUFA4. Additionally, it enhanced the activity of respiratory complex III, recovered cellular aerobic respiration under LPS and MSU induction. FHME lost its effect to downregulate M1 macrophage polarization with the presence of rotenone or si-UQCRC1. Finally, 10 compounds were identified from FHME having potential binding affinity with the UQCRC1 protein.</p><p><strong>Conclusions: </strong>The therapeutic potential of FHME for AGA is associated with the maintenance of mitochondrial function to inhibit M1 macrophage polarization, which is intimately linked to the UQCRC1. Our findings highlight the potential of Folium Hibisci Mutabilis as a safe and effective approach for AGA.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"28"},"PeriodicalIF":5.3,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11869456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Salidroside protects against myocardial infarction via activating MIF-mediated mitochondrial quality control.","authors":"Baiyang You, Jie Zhang, Chuyan Yang, Yaoshan Dun, Dake Qi, Yuqiong Long, Jing Cheng, Yuan Lin, Nanjiang Zhou, Tanghao Zeng, Jie Dong, Suixin Liu","doi":"10.1186/s13020-025-01076-3","DOIUrl":"10.1186/s13020-025-01076-3","url":null,"abstract":"<p><strong>Background: </strong>Salidroside is a potential therapeutic agent for myocardial infarction (MI), exerting therapeutic effects on macrophage migration inhibitory factor (MIF)-regulated mitochondrial quality control. Our aim was to explore the mechanism through which the MIF pathway regulates salidroside-mediated resistance to hypoxia-induced cardiomyocyte apoptosis.</p><p><strong>Methods: </strong>Ligation surgery of the left anterior descending branch of the coronary artery was employed to establish a myocardial infarction mouse model. Salidroside at low and high doses was administered to the mice for 4 weeks after the surgery. Cardiac function was evaluated via echocardiography. Morphological changes, apoptosis, and mitochondrial damage in the myocardium were examined. For the cell experiments, cardiomyocytes were treated with salidroside under oxygen‒glucose deprivation (OGD) conditions and were either treated with recombinant MIF (rMIF) or transfected with Mif-siRNA. Subsequently, mitochondrial quality control and apoptosis were assessed.</p><p><strong>Results: </strong>Salidroside enhanced mitochondrial quality control in MI model mice, mitigated apoptosis and improved cardiac dysfunction. Transmission electron microscopy indicated that there were fewer damaged mitochondria in the salidroside-treated mice compared with the control mice. MIF and downstream mitochondrial quality control pathways were activated in the mice treated with salidroside. Consistently, the cell experiments demonstrated that salidroside and rMIF alleviated apoptosis, improved impaired mitochondrial quality control in OGD-induced cells and activated MIF signaling in OGD-induced cells. However, these effects of salidroside were partially blocked by Mif-siRNA transfection.</p><p><strong>Conclusion: </strong>Salidroside alleviated myocardial apoptosis and ameliorated cardiac dysfunction in MI model mice through the MIF pathway and downstream mitochondrial quality control.</p>","PeriodicalId":10266,"journal":{"name":"Chinese Medicine","volume":"20 1","pages":"27"},"PeriodicalIF":5.3,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11869418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}