PHYTOMEDICINE植物药
PHYTOMEDICINE(英文缩写 PHYTOMEDICINE),ISSN 0944-7113,eISSN 1618-095X,中文译名:植物药 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 6.656 | Q1 |
| 2022 | 7.900 | Q1 |
| 2023 | 6.700 | Q1 |
| 2024 | 8.300 | Q1 |
| 2025 | 11.300 | Q1 |
PHYTOMEDICINE 最新收录文献
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1. Editorial: 8th International Symposium on Phytochemicals in Medicine and Food.
1. 社论：第八届医学与食品中植物化学物质国际研讨会PMID:日期:2026-09-30该文献暂无摘要。
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2. {"_":"Qishen granule improves myocardial fibrosis in heart failure via Piezo1/Calpain2/LAMP1/CTSS in CCR2 macrophages.","sup":["+"]}
2. 芪参颗粒通过CCR2巨噬细胞中的Piezo1/Calpain2/LAMP1/CTSS改善心力衰竭心肌纤维化PMID:日期:2026-09-29Myocardial fibrosis represents a common terminal pathological pathway in heart failure (HF), and currently, there is a lack of therapies specifically targeting the core pathological mechanisms of myocardial fibrosis, namely persistent inflammation and excessive extracellular matrix (ECM) deposition. In the present study, our aim was to evaluate the effectiveness of the herbal formulation Qishen Granule (QSG) against myocardial fibrosis. A model of HF with myocardial fibrosis was established by performing left anterior descending artery (LAD) ligation in mice. After three weeks of QSG treatment, cardiac function, fibrosis, and cardiac conduction were evaluated. We identified potential targets through network pharmacology and RNA sequencing analysis. The targeted effects of QSG were further validated using flow cytometry, Western blot, quantitative real-time PCR, and immunofluorescence techniques. QSG can improve the heart function of HF mice, reduce myocardial inflammation and fibrosis, and effectively enhance cardiac conduction function. Its core mechanism lies in regulating the mechanosensitive ion channel Piezo1 and the calcium-dependent cysteine protease 2 (Calpain2) activation cascade, thereby blocking lysosome-associated membrane protein 1 (LAMP1) hydrolysis and cathepsin S (CTSS) release while reducing ECM deposition. In CCR2 macrophages, QSG inhibits calcium influx by reducing Piezo1 expression, thereby suppressing myofibroblast activation. Knockdown of Piezo1 partially abrogates QSG's antifibrotic effects, confirming Piezo1 as an essential target for QSG's protective actions. QSG reduces ECM deposition by targeting and inhibiting the Piezo1/Calpain2/LAMP1/CTSS signal axis in CCR2 macrophages, thus improving myocardial fibrosis. This study provides a novel therapeutic strategy for HF-associated myocardial fibrosis by leveraging mechanosensitive signaling pathways.
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3. Gastrodia elata Blume-derived exosomes-like nanovesicles deliver miR-221-3p and miR-222-3p to ameliorate doxorubicin cardiotoxicity.
3. 天麻衍生的类外泌体纳米囊泡递送miR-221-3p和miR-222-3p以改善多柔比星心脏毒性PMID:日期:2026-09-29The widely used antitumor drug doxorubicin (DOX) is clinically limited because of its tendency to induce cardiotoxicity, and there is currently no optimal protection strategy. Plant-derived exosomes-like nanovesicles have shown potential for treating a variety of diseases. Here, we report the therapeutic effects of Gastrodia elata Blume-derived exosomes-like nanovesicles (GE-ELNs) in mitigating DOX cardiotoxicity and explore the underlying mechanisms. GE-ELNs exhibited a typical morphology and size consistent with mammalian exosomes and were enriched in RNA, proteins, and lipids. In vivo IVIS imaging confirmed the recruitment of GE-ELNs to the heart after intravenous injection. Fluorescence microcopy and flow cytometry analysis revealed a time and dose-dependent increase in the uptake of GE-ELNs by cardiomyocytes. While GE-ELNs treatment decreased apoptosis and restored calcium transients in DOX-treated cardiomyocytes, it did not significantly affect the toxicity of DOX in several breast cancer cell lines. In a rat model of acute DOX cardiotoxicity, GE-ELNs mitigated cardiotoxicity and improved left ventricular function and cardiac structure. Similar protective effects were also observed in BALB/c mice with implanted breast cancer xenografts without promoting tumor growth or metastasis or comprising the antitumor efficiency of DOX. Mechanistic studies using RNA sequencing and miRNA mimics/inhibitor transfection revealed that miR-221-3p and miR-222-3p are key factors that mediate the protective effects of GE-ELNs. Collectively, our study revealed that while GE-ELNs attenuated DOX cardiotoxicity, they had very limited effects on the survival of cancer cells and tumor growth. GE-ELNs may represent a novel therapeutic approach to prevent DOX cardiotoxicity.
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4. Baicalin targets AMPKα1 to alleviate microglial inflammation by increasing the protein stability of HDAC1 in hypoxic-ischemic encephalopathy.
4. 黄芩苷靶向AMPKα1通过增加缺氧缺血性脑病中HDAC1的蛋白稳定性来减轻小胶质细胞炎症PMID:日期:2026-09-29Hypoxic-ischemic encephalopathy (HIE) is a serious neonatal neurological disorder in which microglia-mediated acute neuroinflammation serves as a critical driver of disease progression. Our previous work revealed that H3K9 lactylation-driven microglial M1 polarization promotes neuroinflammation as a key mechanism in HIE. Baicalin, a natural compound isolated from the traditional Chinese herb Scutellaria baicalensis, is well known for its anti-inflammatory effect, but whether it can treat HIE through this anti-inflammatory effect remains unclear. This study aimed to determine whether baicalin can inhibit H3K9 lactylation-mediated microglial M1 polarization and neuroinflammation in HIE. In vivo, an HIE rat model was established in which rats were treated with intraperitoneal injections of baicalin. In vitro, an oxygen‒glucose deprivation model was constructed using BV2 microglia. Network pharmacology and molecular docking were employed to predict and validate the potential targets of baicalin, after which functional assays were performed. Co-immunoprecipitation combined with mass spectrometry was further used to explore the underlying molecular mechanisms. Through network pharmacology analysis, molecular docking and validation experiments, we revealed that baicalin exerts its anti-inflammatory effects via the activation of adenosine 5'-monophosphate-activated protein kinase α subunit 1 (AMPKα1). Further co-immunoprecipitation and mass spectrometry analyses revealed that AMPKα1 activation promotes the phosphorylation of histone deacetylase 1 (HDAC1), a key delactylase, thus inhibiting the degradation of HDAC1 mediated by the E3 ligase ubiquitin protein ligase E3A (UBE3A). Finally, baicalin increases HDAC1 protein levels to inhibit H3K9 lactylation-mediated microglial M1 polarization via targeting AMPKα1. These findings suggest that, when administered at an early stage after HIE, baicalin may contribute to the attenuation of HIE pathology, at least in part by increasing HDAC1 stability through AMPKα1- and UBE3A-mediated "phosphorylation-ubiquitination hierarchical regulation", thereby reducing H3K9 lactylation and suppressing microglial M1 polarization.
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5. Caragana sinica root bioactive fraction ameliorates experimental arthritis by inhibiting synovial inflammatory lesions through targeting HSP90α.
5. 锦鸡儿根生物活性组分通过靶向HSP90α抑制滑膜炎症病变，改善实验性关节炎PMID:日期:2026-09-29Rheumatoid arthritis (RA) is a chronic autoimmune disease with synovial inflammatory lesions as the initiating factor and pivotal pathogenic driver, triggering persistent inflammation and progressive joint destruction. While Caragana sinica root has long been used in folk medicine for rheumatic disorders, its specific bioactive fractions and therapeutic mechanisms in RA remain unelucidated. This study aims to evaluate the therapeutic efficacy of the bioactive fraction from Caragana sinica root (CSRBF) against experimental arthritis and clarify its underlying mechanism by identifying core targets and exploring its regulatory effects on fibroblast-like synoviocytes (FLSs). CSRBF was prepared via 70% ethanol reflux extraction and macroporous resin purification. Adjuvant-induced arthritis (AA) rats model and TNF-α-stimulated FLSs were used to evaluate CSRBF's efficacy. In vivo therapeutic effects were assessed via arthritis index scoring, histological staining, gait analysis, and micro-CT. In vitro, cell proliferation, migration, invasion, and pro-inflammatory cytokine expression were detected. Core targets were identified and verified using LiP-MS, LC-MS, molecular docking, molecular dynamics simulation, and CETSA. CSRBF dose-dependently alleviated AA severity in rats, reduced synovial hyperplasia, cartilage erosion, and bone destruction, while improving motor function. In vitro, CSRBF inhibited TNF-α-induced FLSs proliferation, migration, invasion, and excessive secretion of pro-inflammatory cytokines. HSP90α was confirmed as the core target of CSRBF, with three active components (hesperetin, pinocembrin, and secoisolariciresinol) directly binding to HSP90α. CSRBF ameliorates experimental arthritis by targeting HSP90α to inhibit FLSs-mediated synovial inflammation, highlighting it as a promising natural anti-RA candidate and HSP90α as a valuable therapeutic target.
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6. Wei-Tong-Xin decoction targets CD8+ T cell-driven colitis via gut microbiota and linoleic acid modulation: an integrated omics study.
6. 胃痛欣汤剂通过肠道菌群和亚油酸调节靶向CD8+ T细胞驱动的结肠炎：一项整合组学研究PMID:日期:2026-09-28Wei-Tong-Xin (WTX), derived from the Hua Tuo Zhong Cang Jing, has been demonstrated to exert therapeutic effects against gastric ulcers and gastritis, with well-established anti-inflammatory properties. However, its potential role in intestinal inflammation has not yet been investigated. To evaluate the therapeutic efficacy of WTX in dextran sulfate sodium (DSS)-induced colitis in mice and to elucidate its underlying pharmacological mechanisms while identifying its active components. Mice with DSS-induced colitis were treated with WTX extracts. The primary active fraction of WTX was identified by screening intestinal injury and hematological indicators. Integrated 16S rRNA sequencing, serum metabolomics, and network pharmacology analyses were employed to investigate the therapeutic mechanisms. Specifically, serum metabolomics identified linoleic acid (LA) metabolism as the major metabolic pathway regulated by the petroleum ether (PE) fraction, whereas network pharmacology linked PE-derived constituents to colitis-related targets and identified ALOX5 and PTGS2 as key nodes connecting PE with LA metabolism. These findings were subsequently validated using LA supplementation and pseudo-germ-free mouse models. The PE fraction significantly alleviated colitis symptoms, including reduced disease activity index scores, attenuation of colon shortening, improved intestinal mucosal barrier integrity, and decreased CD8⁺ T-cell infiltration in the spleen, colon, and mesenteric lymph nodes. PE also reshaped the gut microbiota by modulating the abundance of Bacteroidota and Proteobacteria, reduced the levels of unsaturated fatty acids, particularly those involved in LA metabolism, and downregulated the expression of ALOX5 and PTGS2. Fecal microbiota transplantation produced comparable therapeutic effects, whereas LA supplementation reversed the protective effects of PE. PE alleviates colitis by remodeling the gut microbiota, promoting the dominance of Bacteroidota, inhibiting LA metabolism through the ALOX5/PTGS2 pathway, and suppressing the activation of pathogenic CD8⁺ T cells. These effects collectively preserve intestinal barrier integrity and mitigate the progression of colitis.
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7. Cost-effective colour feature-based rapid prediction of secondary metabolites in Dendrobium nobile with insights from MALDI-MSI and transcriptomic analysis.
7. 基于色彩特征的石斛次生代谢物快速预测及其成本效益：结合MALDI-MSI与转录组分析的见解PMID:日期:2026-09-28Secondary metabolite content is a key indicator of medicinal plant quality. However, traditional quantitative analysis methods are often time-consuming and involve the use of toxic reagents. This study aims to address the challenge of rapidly and cost-effectively detecting the content of various secondary metabolites in the medicinal parts of Dendrobium nobile, and proposes an innovative solution based on multi-source color feature data and stacked ensemble learning. It also combines spatial metabolomics and transcriptomics for joint analysis to reveal the underlying potential biological mechanisms. A novel rapid assessment approach was developed by integrating colour features with a stacked ensemble machine learning model, which demonstrated superior efficiency and cost-effectiveness compared with traditional methods. The model was validated using multi-year stem samples of D. nobile from diverse origins and harvest times, demonstrating strong generalisability and high predictive accuracy (R²: 0.73-0.88). SHapley Additive exPlanations analysis indicated that warm colour features in old stems contributed strongly to flavonoid and phenolic acid predictions, whereas green colour features in young stems contributed to alkaloid prediction. The spatial distributions of 20 flavonoids, 14 phenolic acids, and 10 alkaloids were significantly correlated with key colour features. Spatial metabolomics further confirmed these patterns, showing progressive warm colour shifts and metabolite redistribution during maturation. Furthermore, transcriptome-metabolite correlation analysis further focused on the phenylpropanoid, flavonoid, flavone and flavonol, isoquinoline alkaloid, and shikimate biosynthesis pathways, which suggested that genes involved in these pathways might take part in regulating the synthesis of the three above-mentioned compounds. This study successfully developed a rapid and cost-effective quality assessment method based on colour features and machine learning, which demonstrated high reliability when applied to D. nobile. These findings not only reveal the potential association mechanism among colours, metabolites, and genes of D. nobile, but also provide a technical framework for the rapid quality assessment of medicinal plants.
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8. Corrigendum to "Oleuropein aglycone aldehyde as a SARS-CoV-2 main protease inhibitor" [Phytomedicine 160 (2026) 158643].
8. 关于“橄榄苦苷苷元醛作为SARS-CoV-2主蛋白酶抑制剂”的勘误 [Phytomedicine 160 (2026) 158643]PMID:日期:2026-09-26该文献暂无摘要。
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9. The edible dietary fiber of Lentinus β-glucan targets PRSS3 to suppress progression of human colon cancer.
9. 香菇β-葡聚糖作为可食用膳食纤维靶向PRSS3抑制人结肠癌的进展PMID:日期:2026-09-25Lentinus β-glucan (LBG), an edible dietary fiber, has promising anticancer potential. However, the anticancer mechanism remains poorly understood. Herein, we focus on the anti-colon cancer mechanism of four LBGs with different molecular weights. As a result, LBGs could directly interact with the human colon cancer cells and were even ingested into cells. Mass spectrometry results reveal that the protein interacting with LBGs was most likely PRSS3. Molecular docking simulation further confirmed LBGs interacted with PRSS3 through hydrogen bonding, van der Waals forces, and hydrophobic interactions. In vitro results demonstrate that LBGs down-regulated PRSS3 expression in colon carcinoma cells, as well as decreased cell viability. Meanwhile, in vivo studies reveal that LBGs targeted the carcinogenic promoter of PRSS3, leading to cancer cell proliferation inhibition and apoptosis promotion. This study provides new insights that LBG can be used for clinical colon cancer treatment as a PRSS3 inhibitor without system toxicity.
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10. Artesunate reverses alveolar macrophage immunometabolic collapse and prevents breast cancer lung metastasis via the SREBP1- and FATP4-dependent fatty acid axis.
10. 青蒿琥酯通过SREBP1和FATP4依赖的脂肪酸轴逆转肺泡巨噬细胞免疫代谢崩溃并预防乳腺癌肺转移PMID:日期:2026-09-24Alveolar macrophages (AMs) are critical sentinels of the lung microenvironment, however, the metabolic mechanisms driving their functional reprogramming within the breast cancer pulmonary pre-metastatic niche (PMN) remain poorly defined. This study aimed to elucidate the metabolic-immune crosstalk governing AM dysfunction during breast cancer lung metastasis and evaluate the therapeutic potential of artesunate (AS) as a fatty acid metabolic remodeler. Utilizing 4T1-based spontaneous lung metastasis and post-surgical recurrence models, we integrated single-cell RNA sequencing (scRNA-seq) and flow cytometry (FCM) to delineate the functional and lipid metabolic landscape of AMs in the breast cancer pulmonary PMN. Bulk RNA-seq, metabolomics, immunofluorescence, and FCM were subsequently employed to elucidate how AS remodels fatty acid metabolism in AMs. The underlying mechanisms were elucidated through in vitro and in vivo functional rescue assays and further valuated by publicly available clinical datasets and human clinical tissue samples. We identified a disruption of fatty acid metabolism in AMs resident within the breast cancer pulmonary PMN, characterized by coordinated impairment of both fatty acid uptake and lipid accumulation. This metabolic defect correlated with reduced phagocytic capacity and an immunosuppressive phenotype. Notably, AS treatment effectively restored fatty acid uptake and lipid accumulation in AMs, reestablished immunological surveillance within breast cancer pulmonary PMN, and effectively suppressed primary tumor growth and lung metastasis. Subsequent in vitro study confirmed that AS-remodeled AMs reboot anti-tumor immunity by enhancing phagocytosis and promoting T-cell activation. Functional intervention experiments further demonstrated that AS-induced immunometabolic reprogramming of AMs depends, at least in part, on SREBP1 driven lipogenesis and FATP4 mediated fatty acid uptake. Notably, these two metabolic pathways also serve as conserved prognostic signatures in human lung cancer cohorts. Our findings define the disruption of fatty acid homeostasis as a hallmark of AM dysfunction in the breast cancer pulmonary PMN and establish artesunate as a promising candidate for intercepting breast cancer lung metastasis by targeting metabolic fitness in AMs.