Chinese Herbal Medicines中草药（英文版）
Chinese Herbal Medicines(英文缩写 CHIN HERB MED),ISSN 1674-6384,eISSN 1674-6384,中文译名:中草药（英文版） 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 | 未收录 | N/A |
| 2022 | 3.800 | N/A |
| 2023 | 4.700 | Q1 |
| 2024 | 8.900 | Q1 |
| 2025 | 11.200 | Q1 |
Chinese Herbal Medicines 最新收录文献
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1. {"_":" mechanisms for enhanced wound healing: A review on bioactive phytoconstituents.","i":["Plantago"]}
PMID:日期:2026-05-14(Plantaginaceae family) exhibits remarkable diversity with over 200 species. These plants are closely associated with traditional medicine worldwide, particularly as a wound healing therapy. Recent research has revealed phytoconstituents in various species, including flavonoids, alkaloids, terpenoids, phenolic acid derivatives, iridoid glycosides, fatty acids, and polysaccharides. Despite the advanced ongoing research on extracts, there is still a gap in the evaluation of their potential as an effective topical product for chronic wounds and in the way phytoconstituents contribute to the overall effect in a single comprehensive systematic review. Therefore, this review aims to explore the wound healing capabilities of and its phytoconstituents, as well as elucidate their mechanisms of action. Our analysis emphasizes the significant wound healing potential in 25 species, notably , , , , and . These plant species contain a diverse array of 57 phytoconstituents that collectively contribute to these activities. In conclusion, this review confirms the huge potential of genus as a topical wound healing agent. The healing mechanisms cover a wide array of effects such as anti-bacterial activity, anti-apoptosis, stimulation of collagen synthesis and deposition, promotion of angiogenesis, suppression of inflammatory response, inhibition of cyclooxygenase, inhibition of MAPKs phosphorylation, and enhancement of endogenous antioxidant enzyme activity. A study on the network pharmacology of such potential is worth investigating as further research.
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2. {"_":"A cross-cultural ethnobotanical assembly highlights diverse health-promoting functions of genus globally.","i":["Panax"]}
2. {“_”：“跨文化民族植物学大会突出了该属在全球范围内的多种健康促进功能。”，“i”：[“Panax”]}PMID:日期:2026-05-14[中文摘要] 本研究旨在实现地方性知识与传统知识的跨文化整合，以促进对这些知识体系的理解并指导该属植物的生物勘探。通过基于文献的分类学修订，确定了该属目前公认的物种。利用历史本草文献，整理了中国境内该属植物的历史用途。通过跨文化民族植物学汇编，汇集了全球范围内该属植物的传统用途。借助基于网络的整合方法，对分散的地方性知识和传统知识进行了整合与评估。目前，该属包含14个公认物种，主要分布于东亚和北美东部，均被当地用作传统食品和/或药物。中国历史本草中记载了4个物种。8个物种和1个变种被25个中国少数民族所使用。在中国以外，有10个物种和2个变种在12个国家被传统使用。一般性健康促进功能被频繁提及。在不同的生物文化背景下，所使用的物种和用途差异很大，甚至同一物种也可能有不同的用途。本研究首次对全球该属植物的健康益处进行了全面梳理，并从民族植物学角度为其在维护人类健康方面的多功能性提供了坚实证据。
[英文摘要] This study aims to achieve a cross-cultural consolidation of the local and traditional knowledge in order to contribute to an understanding of these knowledge systems and to guide bioprospecting on spp. Documentation-based taxonomic revision was performed to define the current accepted species in . Historic uses of spp. used in China was compiled using historical herbal literature. A cross-cultural ethnobotanical assembly was performed to compile the traditional uses of spp. globally. With a network-based integration, the scattered local and traditional knowledge was consolidated and evaluated. Currently, the genus comprises 14 accepted species, mainly distributed in East Asia and eastern North America, all of which are used locally as traditional food and/or medicine. Four species are recorded in Chinese historical herbals. Eight species and one variety are used by 25 of the Chinese ethnic minorities. Beyond China, there are ten species and two varieties used traditionally in 12 countries. General health promotion functions are frequently mentioned. In different biocultural backgrounds, the used species and usages varied greatly, and even the same species can be used differently. For the first time, this study archives a comprehensive understanding on the health benefits of global spp. and provides solid evidence for their versatility in maintaining human health from the perspective of ethnobotany.
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3. Challenges and opportunities for ginseng-based medicines in treating cardiac fibrosis from mechanistic insights to clinical translation.
3. 人参类药物治疗心脏纤维化的挑战和机遇——从机理见解到临床翻译PMID:日期:2026-05-14Cardiac 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. and its related preparations, including major ginsenosides (e.g., Rb, Rg, and Rg), 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-/Smad, NF-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.
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4. 6-Gingerol alleviates hepatic fibrosis via inhibiting glycolytic reprogramming by targeting IGF2BP2.
4. 6-姜酚通过靶向IGF2BP2抑制糖酵解重编程来缓解肝纤维化PMID:日期:2026-05-13[中文摘要] 肝纤维化仍是全球主要的健康负担，常进展为肝硬化和肝细胞癌。尽管研究广泛，但由于肝星状细胞（HSCs）活化和代谢重塑的复杂性，目前尚无有效的抗纤维化药物获批用于临床。糖酵解增强日益被认为是维持HSCs促纤维化表型的代谢标志，代表着一个关键但尚未充分探索的治疗靶点。本研究探讨了6-姜酚（6-gingerol，生姜的主要生物活性成分）的抗纤维化作用，并揭示了其涉及HSC活化的代谢-表观转录调控的新机制。通过四氯化碳（CCl₄）和胆管结扎（BDL）在C57BL/6小鼠中诱导肝纤维化，随后给予口服6-姜酚治疗。在转化生长因子-β1（TGF-β1）刺激的Lieming Xu-2（LX-2细胞，人肝星状细胞系）和肝纤维化小鼠的原代HSCs中进行了补充性体外研究。整合转录组学、网络药理学、分子对接和细胞热位移分析（CETSA）与功能遗传操作相结合，以识别和验证分子靶点。6-姜酚减轻了CCl₄和BDL诱导模型中的肝损伤和胶原沉积，并改善了肝功能。在机制上，6-姜酚通过下调己糖激酶2（HK2）、丙酮酸激酶M2（PKM2）和乳酸脱氢酶A（LDHA）抑制糖酵解，使丙酮酸和乳酸代谢正常化，并恢复线粒体呼吸。胰岛素样生长因子2 mRNA结合蛋白2（IGF2BP2）被鉴定为与糖酵解酶表达和HSCs活化相关的重要介质，其沉默消除了6-姜酚的抗纤维化作用。我们的研究表明，6-姜酚通过靶向IGF2BP2依赖的糖酵解重编程来减轻肝纤维化，从而恢复代谢稳态并抑制HSCs活化。这些发现揭示了一种新的代谢-表观转录机制，并提示6-姜酚是慢性肝病的一种有前景的治疗策略。
[英文摘要] 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 , and revealed its novel mechanism involving metabolic-epitranscriptomic regulation of HSC activation. Liver fibrosis was induced in C57BL/6 mice by carbon tetrachloride (CCl) and bile duct ligation (BDL), followed by oral 6-gingerol treatment. Complementary studies were performed in transforming growth factor-1 (TGF-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. 6-Gingerol alleviated hepatic injury and collagen deposition in both CCl- 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. 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.
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5. {"_":"Formononetin alleviates ovarian fibrosis and inflammation via targeting SOCS3 and inhibiting TGF-1/Smad signaling in PCOS.","i":["β"]}
5. 芒柄花素通过靶向SOCS3和抑制PCOS中TGF-β1/Smad信号传导来缓解卵巢纤维化和炎症PMID:日期:2026-05-12[中文摘要] 多囊卵巢综合征（PCOS）是一种以排卵功能障碍为特征的内分泌和代谢紊乱。芒柄花素（FMN）是一种来源于豆科植物的生物活性化合物，具有抗炎和抗纤维化特性。本研究旨在评估FMN对PCOS大鼠模型的治疗作用并阐明其潜在分子机制。通过每日注射脱氢表雄酮（DHEA）在3周龄雌性Sprague-Dawley大鼠中建立类PCOS模型。通过监测动情周期、激素水平、葡萄糖耐量和卵巢组织形态学评估FMN的疗效。采用网络药理学和转录组测序预测FMN的分子靶点和信号通路。使用分子对接、分子动力学（MD）模拟和细胞热位移分析（CETSA）-蛋白质印迹（WB）（CETSA-WB）确认FMN对细胞因子信号传导抑制因子3（SOCS3）的结合和稳定作用。通过定量聚合酶链反应（qPCR）、WB和免疫组织化学定量检测SOCS3、炎症和纤维化相关标志物以及转化生长因子β1（TGF-β1）/Smad通路组分的表达。使用SOCS3小干扰RNA（siRNA）进行功能验证。DHEA成功诱导了类PCOS表型，包括动情周期紊乱、高雄激素血症、黄体生成素与卵泡刺激素比值（LH/FSH）升高、胰岛素抵抗和卵巢形态异常。FMN治疗显著逆转了这些异常并减少了卵巢胶原沉积。网络药理学和转录组分析表明，FMN的治疗效果主要归因于其抗纤维化和抗炎特性，SOCS3被确定为潜在的关键分子。分子对接和MD模拟以及CETSA-WB进一步揭示FMN直接结合SOCS3，增强其稳定性，从而抑制PCOS中的卵巢纤维化。此外，qPCR、WB和免疫组织化学证实FMN调控TGF-β1/Smad信号通路。重要的是，SOCS3 siRNA消除了纤维化相关胶原水平和磷酸化信号转导与转录激活因子3（p-STAT3）的表达，支持了FMN通过SOCS3改善PCOS诱导的卵巢纤维化的观点。FMN通过稳定SOCS3和抑制TGF-β1/Smad信号通路，减轻DHEA诱导的PCOS大鼠的卵巢功能障碍和高雄激素血症，从而减轻卵巢纤维化和炎症。这揭示了FMN以SOCS3为中心的新型机制，并强调了其治疗PCOS的潜力。
[英文摘要] Polycystic ovary syndrome (PCOS) is an endocrine and metabolic disorder characterized by ovulatory dysfunction. Formononetin (FMN), a bioactive compound derived from leguminous plants, including , , and , 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. 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-1)/Smad pathway were quantified by quantitative polymerase chain reaction (qPCR), WB, and immunohistochemistry. Functional validation was performed using SOCS3 small interfering RNA (siRNA). 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-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. FMN alleviated ovarian dysfunction and hyperandrogenism in DHEA-induced PCOS rats by stabilizing SOCS3 and inhibiting TGF-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.
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6. Xuezhikang Capsule ameliorates ischemic stroke via multi-target modulation of neurovascular units.
6. 血脂康胶囊通过多靶点调节神经血管单位改善缺血性卒中PMID:日期:2026-05-12该文献暂无摘要。
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7. Systems pharmacology of traditional Chinese medicine in fibrosis: From multi-target mechanisms to translational validation.
PMID:日期:2026-05-11Systems biology research has integrated network pharmacology with clinical data to investigate traditional Chinese Medicine (TCM) antifibrotic mechanisms across multiple biological pathways. These combined approaches draw on chemical-protein interaction databases, transcriptomic and metabolomic profiling, protein-protein interaction networks, molecular docking, randomized trial and large cohort study evidence. Yinchenhao Decoction, Danggui Liuhuang Decoction, (Ezhu in Chinese)- (Huangqi in Chinese) herb pair, and (Danggui in Chinese)- (Chuanxiong in Chinese) herb pair regulate transforming growth factor- (TGF-)/mothers against decapentaplegic homolog (Smad), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), nuclear factor-B (NF-B), mitogen-activated protein kinase (MAPK), and janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathways. Integration of these signals is associated with suppression of inflammation, altered regulation of apoptosis, modulation of cellular activation, and extracellular matrix remodeling in hepatic, cardiac, and pulmonary fibrosis models. This multi-layered framework offers a rational basis for hypothesis generation in drug repositioning and development of novel antifibrotic candidates, although clinical validation remains limited and further rigorous trials are warranted.
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8. Huashi Baidu formula may attenuate adriamycin-induced myocardial injury via modulating NRF2-ATF3-SRXN1 axis-mediated ferroptosis.
8. 华西白方可能通过调节NRF2-ATF3-SRXN1轴介导的铁下垂来减轻阿霉素诱导的心肌损伤PMID:日期:2026-05-11Myocardial 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. 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. 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 < 0.05 and fold change (FC) > 1.2 or < 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. 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 -smooth muscle actin), inflammatory cytokines (tumor necrosis factor- 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. HBF may attenuate ADR-induced myocardial injury via modulating NRF2-ATF3-SRXN1 axis-mediated ferroptosis, and emodin, rhein, and lactiflorin are potential representative BACs.
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9. Piperine attenuates fibrogenesis and inflammation in hepatic fibrosis by switching STAT3 phosphorylation at Ser727.
9. 胡椒碱通过切换STAT3在Ser727位点的磷酸化，减轻肝纤维化中的纤维化生成和炎症PMID:日期:2026-05-10is a medicinal and edible spice that is popular worldwide due to its unique spicy flavor, and is considered as a folk medicine for treating digestive system diseases. Piperine (PIP) is a bioactive alkaloid derived from , with remarkable hepatoprotective efficacy. Hepatic fibrosis represents a critical phase in the advancement of distinct chronic liver conditions towards cirrhosis, and currently lacks effective therapeutic drugs. The study aims to investigate the hepatoprotective functions of PIP and the underlying mechanism of PIP in combating hepatic fibrosis. C57BL/6J mice with hepatic fibrosis were induced by thioacetamide (TAA) and subsequently subjected to treatment with PIP or curcumin. Immortalized rat hepatic stellate cells (HSCs) were stimulated with transforming growth factor- (TGF-), followed by culture with PIP or niclosamide [signal transducer and activator of transcription 3 (STAT3) inhibitor], respectively. Human hepatic stellate cell line LX-2 were activated by TGF- and transfected with specific small interfering RNA (siRNA) to silence gene, and afterwards cultured with PIP. The mouse AML-12 cells and macrophage-like murine cells Raw 264.7 were stimulated with lipopolysaccharide (LPS), followed by culture with PIP. , PIP reduced serum transaminase levels, collagen deposition, and decreased the excessive accumulation of extracellular matrix (ECM), comprising -smooth muscle actin (-SMA), collagen type I (Collagen I), and tissue inhibitor of metalloproteinases-1 (TIMP-1)/matrix metalloproteinase 13 (MMP13) ratio expressions. PIP inhibited inflammatory cytokines release and myeloperoxidase (MPO) expression, including interleukin-1 receptor type 1 (IL-1R1), cysteine-aspartic acid protease-1 (Caspase-1), and IL-6. PIP specifically inhibited STAT3 phosphorylation at Ser727, downregulated phosphorylated janus kinase 2 (p-JAK2), and upregulated suppressor of cytokine signaling 3 (SOCS3) and protein inhibitor of activated STAT 1/3 (PIAS1/3) expressions. , PIP inhibited ECM deposition and inflammatory cytokines release in activated HSCs. PIP selectively suppressed p-STAT3 at Ser727 without affecting Tyr705, and modulated p-JAK2, SOCS3, and PIAS1/3 expressions in activated HSCs, function as a STAT3 inhibitor. PIP inhibited LPS‑induced M1 polarization of RAW 264.7 macrophages. PIP decreased Cleaved‑Caspase 3 expression and apoptotic cells in LPS‑induced AML‑12 hepatocytes. STAT3 deficiency amplified regulation of PIP on -SMA and p-JAK2, as well as its upregulation on SOCS3 and PIAS1/3 in activated LX-2 cells. PIP improved hepatic fibrosis via inhibiting ECM excessive deposition and inflammatory secretion. Switching STAT3 phosphorylation at Ser727 might be the underlying targets for PIP against hepatic fibrosis, which provide an effective candidate and therapeutical strategy for hepatic fibrosis.
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10. {"_":"Tanshinone II alleviates isoproterenol-induced myocardial injury via NR4A1/GATA4 pathway-mediated suppression of EndMT and oxidative stress.","sub":["A"]}
10. {“_”：“丹参酮II通过NR4A1/GATA4途径介导的EndMT抑制和氧化应激减轻异丙肾上腺素诱导的心肌损伤。”，“sub”：[“A”]}PMID:日期:2026-05-10该文献暂无摘要。