Chinese Journal of Natural Medicines最新文献

{"title":"R-type ginsenoside Rg3 attenuates cisplatin-induce intestinal injury via restoring autophagy flux blockade","authors":"Gao Xufei ,&nbsp;Zhang Junjie ,&nbsp;Hu Junnan ,&nbsp;Zhang Ming ,&nbsp;Wang Zi ,&nbsp;Jiang Shuang ,&nbsp;Li Wei","doi":"10.1016/S1875-5364(26)61100-4","DOIUrl":"10.1016/S1875-5364(26)61100-4","url":null,"abstract":"<div><div>Cisplatin and its metabolites can cause severe gastrointestinal mucosal damage, leading to varying degrees of intestinal injury in nearly all patients following administration. Although the anti-tumor effectiveness of <em>R</em>-ginsenoside Rg3 (<em>R</em>-Rg3, a key chemical component of Shen Yi Capsule) as the first-line drug is widely recognized in the clinic, there is less concern about the improved effects of <em>R</em>-Rg3 against intestinal toxicity caused by concurrent cisplatin chemotherapy. This study aimed to investigate the protective effects of <em>R</em>-Rg3 against cisplatin-induced intestinal toxicity and to explore its potential molecular targets and mechanisms. Rats in the <em>R</em>-Rg3 treatment group were treated with <em>R</em>-Rg3 (7, 14 mg·kg⁻¹, p.o.) for 7 days, and a single dose of cisplatin (14 mg·kg⁻¹, i.p.) was administered <em>via</em> intraperitoneal injection to rats in the cisplatin group and <em>R</em>-Rg3 treatment group on the 7^th day. Intestinal epithelial cell line 6 (IEC-6) were pretreated with <em>R</em>-Rg3 (1.25, 2.5, 5 μmol·L⁻¹) for 24 h followed by cisplatin treatment (3 μmol·L⁻¹, 24 h). The <em>in vivo</em> results showed that, <em>R</em>-Rg3 treatment for 7 days markedly alleviated cisplatin-induced oxidative stress and mitochondrial dysfunction in vivo, while suppressing excessive autophagy and reducing intestinal damage. In IEC-6 cells, R-Rg3 pretreatment inhibited mitophagy and promoted the restoration of lysosomal function. Autophagy inhibitors 3-methyladenine (autophagosome formation inhibitor, 1 μmol·L⁻¹) and Bafilomycin A1 (proton pump inhibitor, 8 μmol·L⁻¹) were used to verify the mechanism of <em>R</em>-Rg3 action. Importantly, application of 3-methyladenine and Bafilomycin A1 verified that <em>R</em>-Rg3 could alleviate gastrointestinal dysfunction by restoring the cisplatin-induced autophagic flux blockade. In conclusion, this study identifies a previously underappreciated protective role of <em>R</em>-Rg3 against cisplatin-induced intestinal injury. Furthermore, it suggests that pharmacological modulation of the mitochondria–lysosome axis by <em>R</em>-Rg3 may effectively mitigate oxidative stress–mediated autophagic flux impairment caused by cisplatin.</div></div>","PeriodicalId":10002,"journal":{"name":"Chinese Journal of Natural Medicines","volume":"24 4","pages":"Pages 485-498"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147720757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nephropathy 1 Formula alleviates kidney injury by ameliorating mitochondrial dysfunction and pyroptosis in diabetic nephropathy through the TMAO-mROS-NLRP3 axis","authors":"Tingting Wei ,&nbsp;Yujiu Gao ,&nbsp;Liting Zhu ,&nbsp;Congcong Zeng ,&nbsp;Rui Cai ,&nbsp;Fu Rao ,&nbsp;Yue Zhao ,&nbsp;Xiaochun Zhang ,&nbsp;Jiashun Yang ,&nbsp;Yinrui Sheng ,&nbsp;Zhengzhong Yuan ,&nbsp;Jinguo Cheng","doi":"10.1016/S1875-5364(26)61174-0","DOIUrl":"10.1016/S1875-5364(26)61174-0","url":null,"abstract":"<div><div>Nephropathy 1 Formula (N1F), a traditional Chinese medicine (TCM), has demonstrated promising clinical efficacy in diabetic nephropathy (DN). However, its underlying protective mechanisms remain insufficiently defined. In this study, a type 2 diabetes mellitus (T2DM) mouse model was established using a high-fat diet (HFD) and streptozotocin (STZ). Additionally, DN was simulated <em>in vitro via</em> exposure of mouse glomerular mesangial cells (MES-13) to high glucose (HG) and trimethylamine-<em>N</em>-oxide (TMAO). To elucidate the mechanistic basis of N1F's renoprotective effects, an integrative approach combining metabolomics, transcriptomics, and 16S ribosomal ribonucleic acid (rRNA) gene sequencing was employed. N1F treatment reduced the urinary albumin-to-creatinine ratio (UACR), preserved renal function, and attenuated histopathological damage and renal fibrosis in diabetic mice. Mechanistically, N1F modulated systemic TMAO levels and energy metabolism, altered gut microbiota composition, and suppressed microbial production of TMAO-related metabolites. Under hyperglycemic conditions, TMAO induced excessive mitochondrial reactive oxygen species (mROS), impaired mitochondrial dynamics, and disrupted cellular energy metabolism. In contrast, N1F normalized mROS levels, restored mitochondrial structure and function, enhanced oxidative phosphorylation (OXPHOS), increased ATP production, and reduced glycolytic dependency. Furthermore, N1F downregulated the expression of key pyroptosis-related proteins—including NOD-like receptor family pyrin domain-containing 3 (NLRP3), <em>N</em>-terminal gasdermin D (GSDMD), cleaved-Casp1, interleukin-1β (IL-1β), and IL-18—in both <em>in vivo</em> and <em>in vitro</em> models, indicating suppression of pyroptosis <em>via</em> inhibition of the TMAO-mROS-NLRP3 signaling axis. Collectively, these findings demonstrate that N1F exerts protective effects against DN by targeting mitochondrial dysfunction and pyroptotic injury, supporting its potential as a therapeutic strategy for DN.</div></div>","PeriodicalId":10002,"journal":{"name":"Chinese Journal of Natural Medicines","volume":"24 4","pages":"Pages 454-469"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147720671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selaginella tamariscina extract and amentoflavone ameliorate UVB-induced skin aging via AMPK activation","authors":"Lu Wang ,&nbsp;Mingjie Li ,&nbsp;Zhao Zhang ,&nbsp;Hairan Fan ,&nbsp;Yahui Mi ,&nbsp;Wei Shi ,&nbsp;Haimin Kuai ,&nbsp;Xiaolong Hu ,&nbsp;Fei Xiong ,&nbsp;Hao Wang ,&nbsp;Peng Shu ,&nbsp;Rong Wang","doi":"10.1016/S1875-5364(26)61116-8","DOIUrl":"10.1016/S1875-5364(26)61116-8","url":null,"abstract":"<div><div>Ultraviolet (UV) exposure accelerates skin aging and increases the risk of skin-related diseases. Amentoflavone (AMF), the major compound isolated from <em>Selaginella tamariscina</em>, exhibits potent antioxidant and anti-inflammatory activities. This study aimed to investigate the therapeutic effects and mechanisms of <em>S. tamariscina</em> extract (STE) and AMF on UVB-induced skin photoaging. <em>In vitro</em> and <em>in vivo</em> photoaging models were established to evaluate the protective effects of STE and AMF. The therapeutic target of AMF was identified using network pharmacology, bioinformatic analysis, and molecular docking. <em>In vitro</em>, STE significantly reduced UVB-induced oxidative stress, inflammation, and apoptosis. <em>In vivo</em>, both STE and AMF effectively mitigated UVB-induced skin injury. Mechanistically, AMF directly interacted with AMP-activated protein kinase (AMPK), thereby promoting autophagy and protecting cells from UVB-induced damage. In conclusion, STE and its active compound AMF alleviate UVB-induced photoaging <em>via</em> activation of the AMPK signaling pathway, supporting their potential use in skin photoaging therapy.</div></div>","PeriodicalId":10002,"journal":{"name":"Chinese Journal of Natural Medicines","volume":"24 4","pages":"Pages 470-484"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147720756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting of MARK2, but not other MARKs, suppresses TNBC progression by inhibition of the mutant p53-driven signaling pathway","authors":"Min Zhang ,&nbsp;Xilong Zhu ,&nbsp;Mengqian Cui ,&nbsp;Yinan Guan ,&nbsp;Yong Zhang ,&nbsp;Stephen J Weiss ,&nbsp;Jun Chen ,&nbsp;Yongzhong Yao ,&nbsp;Rong Fu ,&nbsp;Zhaoqiu Wu","doi":"10.1016/S1875-5364(26)61172-7","DOIUrl":"10.1016/S1875-5364(26)61172-7","url":null,"abstract":"<div><div>Triple-negative breast cancer (TNBC) is the most challenging breast cancer subtype to treat due to the absence of effective targeted therapies. In this study, we demonstrate that elevated expression of microtubule affinity-regulating kinase 2 (<em>MARK2</em>), but not other MARK family members (<em>MARK1</em>, <em>MARK3</em>, and <em>MARK4</em>), correlates with poor prognosis in TNBC patients. Silencing <em>MARK2</em> impairs TNBC progression <em>via</em> inhibition of mutant p53 (mutp53) signaling. In contrast, silencing any of the other three MARKs either enhances or does not affect TNBC cell growth or migration and has no impact on mutp53 expression. Notably, direct knockdown of mutp53 recapitulates the effects of <em>MARK2</em> ablation in TNBC cells, further supporting a functional linkage. Moreover, ectopic expression of either wild-type (WT) <em>MARK2</em> or its kinase-dead (KD) mutant enhances mutp53 signaling and promotes TNBC progression; however, <em>MARK2</em> overexpression does not alter wild-type p53 (wtp53) expression or cell growth in luminal breast cancer cells. Significant inverse correlations are also observed between the expression levels of <em>MARK2</em>, <em>THBS1</em>, or <em>HBEGF</em> (two direct target genes of mutp53) and both overall and disease-free survival in TNBC patients harboring mut<em>TP53</em>, whereas no such association exists between <em>MARK2</em> and survival in breast cancer subtypes expressing wt<em>TP53</em>. <em>MARK2</em> is predominantly localized in the nucleus of TNBC cells, where it interacts with and stabilizes mutp53 through its UBA and Spacer domains. Consistent with this, <em>MARK2</em>-ΔUBA or <em>MARK2</em>-ΔSpacer mutant proteins fail to bind mutp53 or sustain its signaling, thereby acting as dominant-negative inhibitors that suppress TNBC progression. Collectively, our findings indicate that suppressing <em>MARK2</em> expression, rather than inhibiting its kinase activity, may represent an effective therapeutic strategy for TNBC with mut<em>TP53</em>.</div></div>","PeriodicalId":10002,"journal":{"name":"Chinese Journal of Natural Medicines","volume":"24 4","pages":"Pages 414-426"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147720670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sanguinarine triggers apoptosis and ferroptosis synchronously by directly binding BiP in lung squamous cell carcinoma","authors":"Weidan Tan ,&nbsp;Xinyu Wei ,&nbsp;Changsheng Li ,&nbsp;Huilan Wei ,&nbsp;Fei Yu ,&nbsp;Xiaoju Shen ,&nbsp;Xiaoxiang Mo ,&nbsp;Meifen Wei ,&nbsp;Shangping Xing ,&nbsp;Zhuo Luo ,&nbsp;Jie Yang","doi":"10.1016/S1875-5364(26)61115-6","DOIUrl":"10.1016/S1875-5364(26)61115-6","url":null,"abstract":"<div><div>Lung squamous cell carcinoma (LUSC) is a prevalent and aggressive form of lung cancer with limited therapeutic options. Sanguinarine (SAG), a prominent benzophenanthridine alkaloid derived from <em>Zanthoxylum nitidum</em> (Roxb.) DC, exhibits established anti-tumor activity; however, its molecular mechanisms in LUSC remain incompletely defined. In this study, the anti-cancer effects and underlying mechanisms of SAG were systematically investigated <em>in vitro</em> and <em>in vivo</em>. Cell viability and death were evaluated using methyl thiazolyl tetrazolium (MTT) assays, colony formation assays, flow cytometry, transmission electron microscopy (TEM), and Western blotting (WB). Drug affinity responsive target stability (DARTS) combined with liquid chromatography–tandem mass spectrometry (LC-MS/MS), molecular docking, cellular thermal shift assay (CETSA), and surface plasmon resonance (SPR) were employed to identify and validate molecular targets of SAG. The results demonstrated that SAG simultaneously induces apoptosis and ferroptosis in LUSC cells by directly targeting the endoplasmic reticulum (ER) chaperone binding immunoglobulin protein (BiP). Silencing of BiP markedly attenuated SAG-induced apoptosis and ferroptosis, confirming its essential role in this process. Mechanistically, SAG up-regulates BiP expression and activates the protein kinase R-like endoplasmic reticulum kinase (PERK)/eIF2α/C/EBP homologous protein (CHOP)/GADD34 signaling axis of ER stress (ERS), ultimately leading to dual induction of apoptosis and ferroptosis <em>in vitro</em> and <em>in vivo</em>.</div></div>","PeriodicalId":10002,"journal":{"name":"Chinese Journal of Natural Medicines","volume":"24 4","pages":"Pages 427-439"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147720760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structurally diverse flavonoids from Selaginella doederleinii and their biological activity against laryngeal cancer","authors":"Wenqi Liu ,&nbsp;Minyu Chen ,&nbsp;Sisi Wang ,&nbsp;Shiwen Kang ,&nbsp;Ni Zheng ,&nbsp;Yerlan Bahetjan ,&nbsp;Wenting Zhang ,&nbsp;Huijian Chen ,&nbsp;Xinzhou Yang","doi":"10.1016/S1875-5364(26)61175-2","DOIUrl":"10.1016/S1875-5364(26)61175-2","url":null,"abstract":"<div><div>Ten previously undescribed flavonoids, seladoeflavones J–Q, C, and E (<strong>1</strong>–<strong>10</strong>), together with fifteen known biflavones (<strong>11</strong>–<strong>25</strong>), were isolated from the whole herbs of <em>Selaginella doederleinii</em>. The structures of the new compounds were elucidated using 1D and 2D nuclear magnetic resonance (NMR) spectroscopy and mass spectrometry (MS). By comparing experimental spectral data with NMR calculations, the structures of compounds <strong>1</strong>–<strong>5, 7</strong>, and <strong>8</strong> were assigned. The absolute stereochemistries of compounds <strong>5</strong>–<strong>10</strong> were confirmed by comparing their circular dichroism (CD) spectra with reported data. Notably, the originally proposed structures of seladoeflavones C and E were revised and found to be identical to those of compounds <strong>7</strong> and <strong>8</strong>, respectively. All isolated compounds were evaluated for cytotoxic activity against a panel of cancer cell lines. Most notably, 2″,3″-dihydroochnaflavone (<strong>14</strong>) and involvenflavone G (<strong>19</strong>) exhibited significant anti-proliferative and pro-apoptotic effects in laryngeal cancer cells (Hep-2 and FaDu). Mechanistic studies revealed that compound <strong>14</strong> induced apoptosis by suppressing the protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway, whereas compound <strong>19</strong> downregulated endoplasmic reticulum (ER) stress pathways. These findings indicate that compounds <strong>14</strong> and <strong>19</strong> possess strong potential as anti-laryngeal cancer agents, providing robust evidence for the traditional use of <em>S. doederleinii</em> in the treatment of laryngeal cancer.</div></div>","PeriodicalId":10002,"journal":{"name":"Chinese Journal of Natural Medicines","volume":"24 4","pages":"Pages 499-512"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147720758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypericum monogynum extract inhibits human aortic valve interstitial cell calcification by interfering with the EGFR/PI3K/AKT signaling pathway","authors":"Zhengfeng Fan ,&nbsp;Jincheng Hou ,&nbsp;Jiangchun Wei ,&nbsp;Pengning Fan ,&nbsp;Fuqiang Tong ,&nbsp;Shiqi Chen ,&nbsp;Lin Fan ,&nbsp;Xingyu Qian ,&nbsp;Bingchuan Geng ,&nbsp;Chen Jiang ,&nbsp;Yixuan Wang ,&nbsp;Pingping Fan ,&nbsp;Yahui Huang ,&nbsp;Fei Li ,&nbsp;Yonghui Zhang ,&nbsp;Zhengxi Hu ,&nbsp;Nianguo Dong","doi":"10.1016/S1875-5364(26)61170-3","DOIUrl":"10.1016/S1875-5364(26)61170-3","url":null,"abstract":"<div><div>Calcific aortic valve disease (CAVD) is a serious heart valve condition with increasing global prevalence. Currently, transcatheter aortic valve implantation (TAVI) or surgical aortic valve replacement (SAVR) represents the only available treatment strategy, as no pharmaceutical therapies for CAVD are approved. The aim of this study was to identify compounds capable of inhibiting osteogenic differentiation of human aortic valve interstitial cells (hVICs), a process critically implicated in CAVD pathogenesis, and to elucidate the underlying molecular mechanism. From an in-house library of 88 compounds screened <em>via</em> dot-blotting, we identified chipericumin D, a natural compound extracted from <em>Hypericum monogynum</em> L., as a candidate exhibiting potent inhibitory activity against hVIC osteogenic differentiation. Network pharmacology analysis, molecular docking, drug affinity responsive target stability (DARTS), cellular thermal shift assay (CETSA), and surface plasmon resonance (SPR) collectively demonstrated direct binding of chipericumin D to the epidermal growth factor receptor (EGFR). Furthermore, chipericumin D suppressed activation of the EGFR/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in hVICs cultured under osteogenic medium (OM) conditions. These findings indicate that chipericumin D is a promising therapeutic candidate for CAVD, and provide preliminary evidence that EGFR constitutes a novel molecular target for CAVD intervention.</div></div>","PeriodicalId":10002,"journal":{"name":"Chinese Journal of Natural Medicines","volume":"24 4","pages":"Pages 402-413"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147720664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zishen Huoxue Decoction alleviates myocardial ischemia-reperfusion injury through dysregulation of endoplasmic reticulum-mitochondria homeostasis mediated by DUSP1-NDUFS4","authors":"Xiangyi Pu ,&nbsp;Qin Zhang ,&nbsp;Zhaoqi Yan ,&nbsp;Siyuan Zhou,&nbsp;Qiaomin Wu,&nbsp;Xinai Zhang,&nbsp;Yongyuan Cai,&nbsp;Zhiming Liu,&nbsp;Ruxiu Liu,&nbsp;Xing Chang","doi":"10.1016/S1875-5364(26)61171-5","DOIUrl":"10.1016/S1875-5364(26)61171-5","url":null,"abstract":"<div><div>Zishen Huoxue (ZSHX) Decoction can ameliorate myocardial ischaemia by regulating the mitochondrial quality control network. However, the identification of new molecular targets is necessary for ZSHX's control of mitochondrial protein homeostasis and metabolic activities. Utilizing animal and cellular models with NDUFS4^CKO or DUSP1^CKO, along with single-cell sequencing, metabolomics, network pharmacology, and <em>in vivo</em>/<em>in vitro</em> interventions, the study found that ischemia-reperfusion (I/R) injury triggers endoplasmic reticulum stress and mitochondrial metabolic reprogramming, accompanied by downregulation of DUSP1 and NDUFS4. Network pharmacology suggested ZSHX's role in regulating mitochondrial activity during inflammatory damage, while metabolomics confirmed that ZSHX alters metabolite composition and expression in I/R-affected tissues. Single-cell sequencing further linked I/R to disrupted mitochondrial energy metabolism and cell death, and <em>in vitro</em> experiments demonstrated that ZSHX preserves mitochondrial proteostasis, inhibits endoplasmic reticulum stress, restores calcium balance, upregulates DUSP1/NDUFS4 expression, and controls metabolic reprogramming to reduce myocardial inflammatory injury. Kaempferol, the primary active component of ZSHX, drives these protective effects by enhancing DUSP1/NDUFS4 expression, thereby preventing endoplasmic reticulum stress and inflammatory bursts, preserving mitochondrial function, and re-encoding mitochondrial metabolic processes post-I/R injury.</div></div>","PeriodicalId":10002,"journal":{"name":"Chinese Journal of Natural Medicines","volume":"24 4","pages":"Pages 385-401"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147720663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pulchinenoside B4 attenuates gouty arthritis by regulating NLRP3 inflammasome and macrophage polarization: a transcriptomics-based analysis","authors":"Zitong Zheng ,&nbsp;Shang Lyu ,&nbsp;Meijuan Wang ,&nbsp;Peng Liu ,&nbsp;Yashi Ou ,&nbsp;Junfang Yi ,&nbsp;Huajie Yang ,&nbsp;Zengrui Liao ,&nbsp;Jiangting Sun ,&nbsp;Wei Zou ,&nbsp;Yulin Feng","doi":"10.1016/S1875-5364(26)61173-9","DOIUrl":"10.1016/S1875-5364(26)61173-9","url":null,"abstract":"<div><div>Gouty arthritis (GA) is an inflammatory disorder characterized by the deposition of monosodium urate (MSU) crystals in joint tissues. Pulchinenoside B4 (B4) has broad-spectrum anti-inflammatory properties, but its role and potential mechanism in the pathogenesis of GA are still unclear. The purpose of this study is to comprehensively elucidate the therapeutic effect and mechanism of B4 on GA by integrating transcriptome analysis and <em>in vitro</em> and <em>in vivo</em> experiments. In the MSU-induced mouse GA model, B4 treatment significantly improved ankle edema and reduced inflammatory cell infiltration. Through the analysis of transcriptome sequencing results, we identified multiple differentially expressed long non-coding RNAs (lncRNAs), such as <em>Nod1</em>, <em>Rbck1</em> and <em>Pycard</em>. In the in-depth exploration of the mechanism, we focused on the NOD-like receptor signaling pathway, NF-<em>κ</em>B signaling cascade, and B4-regulated macrophage polarization. <em>In vitro</em> and <em>in vivo</em> models, we confirmed that B4 significantly inhibited the expression and activation of key components of NLRP3 inflammasome (such as ASC, Caspase-1 and IL-1β) by qPCR, Western blot and immunofluorescence. Flow cytometry and immunofluorescence analysis further showed that B4 could prevent MSU-induced macrophage polarization to pro-inflammatory M1 phenotype. Based on these results, this study elucidated the mechanism of B4 improving MSU-induced GA inflammatory response by inhibiting NLRP3 inflammasome activation and blocking M1 macrophage polarization. These results suggest that B4 has great potential as a candidate drug for the treatment of GA.</div></div>","PeriodicalId":10002,"journal":{"name":"Chinese Journal of Natural Medicines","volume":"24 4","pages":"Pages 440-453"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147720759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Benzyl sulfide, sulfoxide and sulfinate metabolites from Gastrodia elata and their synthesis, derivatization and anti-inflammatory activity","authors":"Chengbo Xu ,&nbsp;Lei Wang ,&nbsp;Xue Zhou,&nbsp;Shuai Shao,&nbsp;Chengjuan Chen,&nbsp;Xiaoqiang Lei,&nbsp;Tiantai Zhang,&nbsp;Jiachen Zi,&nbsp;Jiangong Shi,&nbsp;Qinglan Guo","doi":"10.1016/S1875-5364(26)61110-7","DOIUrl":"10.1016/S1875-5364(26)61110-7","url":null,"abstract":"<div><div>Five novel sulfur-containing benzyl metabolites, designated as gastrabenzylsulfoxides A and B (<strong>1</strong> and <strong>2</strong>), gastrabenzylsulfinate A (<strong>3</strong>) and gastrabenzylsulfides A and B (<strong>4</strong> and <strong>5</strong>), along with four known compounds (<strong>6</strong>−<strong>9</strong>), were isolated from the aqueous extracts of <em>Gastrodia elata</em>. Compounds <strong>1</strong> and <strong>4</strong> are 4-hydroxy-3-(4′-hydroxybenzyl)benzyl-substituted sulfoxide and sulfide, respectively, which are unprecedented in natural products. Compound <strong>3</strong> represents a rare sulfinate. Several isolates and their sulfone and disulfide analogs (<strong>10</strong>−<strong>13</strong>) were synthesized to evaluate their anti-inflammatory activity. Notably, the synthesized sulfone <strong>10</strong> demonstrated significant alleviation of symptoms in multiple <em>in vivo</em> inflammatory models.</div></div>","PeriodicalId":10002,"journal":{"name":"Chinese Journal of Natural Medicines","volume":"24 3","pages":"Pages 365-372"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147353683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}