AMERICAN JOURNAL OF CHINESE MEDICINE美国中医杂志
AMERICAN JOURNAL OF CHINESE MEDICINE(英文缩写 AM J CHINESE MED),ISSN 0192-415X,eISSN 1793-6853,中文译名:美国中医杂志 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 | 6.005 | Q1 |
| 2022 | 5.700 | Q1 |
| 2023 | 4.800 | Q1 |
| 2024 | 5.500 | Q1 |
| 2025 | 7.800 | Q1 |
AMERICAN JOURNAL OF CHINESE MEDICINE 最新收录文献
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1. Isoliquiritigenin from Licorice Attenuates Metastatic Development of Pancreatic Cancer by Regulation of Selective Autophagy-Mediated Ferroptosis and the Tumor Microenvironment.
1. 甘草中的异甘草素通过调控选择性自噬介导的铁死亡和肿瘤微环境减弱胰腺癌的转移发展PMID:日期:2026-08-28Isoliquiritigenin (ISL) is a bioactive chalcone obtained from licorice, the ground root of . We previously identified ISL as a late-phase autophagy inhibitor in pancreatic cancer treatment. This study aimed to further explore the involvement of selective autophagy and tumor immunity in its antineoplastic action. Network pharmacology revealed that ISL would downregulate biological processes associated with pancreatic ductal adenocarcinoma (PDAC) including cell migration, extracellular matrix organization and wound healing. Our experimental findings further confirmed ISL's role in inhibiting the epithelial-mesenchymal transition, a key mechanism involved in these processes. ISL also increased the production of reactive oxygen species in both PANC-1 and MIA PaCa-2 PDAC cells, which was intensified through inhibition of autophagy. Furthermore, ISL downregulated glutathione peroxidase 4 (GPX4) and the system Xc counter-transporter of cystine SLC3A2, while increasing the expression of nuclear receptor coactivator 4 (NCOA4) and decreasing that of ferritin heavy chain 1 (FTH1), thereby promoting ferritinophagy-activated ferroptosis. Alternatively, ISL could induce mitophagy by facilitating mitochondrial dynamics toward fusion through an increase in Parkin and MFN1 gene expression. ISL also modulated the robust transcriptional stress response associated with autophagy and ferroptosis through regulation of CREB1 and VMP1. In the tumor microenvironment, ISL decreased the number of myeloid-derived suppressor cells (MDSCs) while increasing the number of CD4[Formula: see text] and CD8[Formula: see text] T cells in the spleen, tumor tissues and blood of Pan02-xenografted mice. ISL also impaired M2 polarization of macrophages in tumor tissues. The inhibitory effects of ISL could be attenuated by interferon-[Formula: see text] through STAT1 signaling. These results demonstrate that ISL regulates selective autophagy-mediated ferroptosis associated with modulation of the tumor microenvironment when treating pancreatic cancer.
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2. {"_":"CORRIGENDUM - Protects Against High-Fat Diet-Induced Hepatic Steatosis by Enhancing Anti-Oxidation and AMPK Activation.","i":["Rhus verniciflua and Eucommia ulmoides"]}
2. {"_":"勘误——通过增强抗氧化和AMPK激活来预防高脂饮食诱导的肝脏脂肪变性。","i":["漆树和杜仲"]}PMID:日期:2026-08-26该文献暂无摘要。
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3. Ginseng-Containing Sijunzi Decoction Inhibits Colorectal Cancer Progression by Regulating MARCHF3-ALOX15-Mediated Ferroptosis.
3. 含人参的四君子汤通过调控MARCHF3-ALOX15介导的铁死亡抑制结直肠癌进展PMID:日期:2026-08-24Colorectal cancer (CRC) frequently develops resistance to 5-fluorouracil (5-FU)-based chemotherapy, which remains a major obstacle to successful treatment. Ginseng-containing Sijunzi Decoction (SJZD), a classical Traditional Chinese Medicine formula, has demonstrated antitumor activity; however, whether and how SJZD enhances 5-FU sensitivity remains largely unclear. In this study, SJZD-containing serum was prepared and administered to 5-FU-resistant CRC cell lines (HCT116/5-FU and SW480/5-FU). Chemosensitivity was evaluated using Cell Counting Kit-8 (CCK-8) and Calcein-AM/propidium iodide (PI) staining assays, while ferroptosis was assessed by measuring oxidative stress-related indicators, including malondialdehyde (MDA), glutathione (GSH), reactive oxygen species (ROS), and intracellular ferrous iron (Fe[Formula: see text]) levels. In addition, a BALB/c nude mouse xenograft model was established to validate the synergistic antitumor effects of SJZD and 5-FU . Protein-protein interactions and ubiquitination were examined by co-immunoprecipitation and ubiquitination assays. Our results demonstrated that SJZD markedly enhanced the sensitivity of resistant CRC cells to 5-FU by inhibiting cell proliferation and promoting ferroptosis both and . In the xenograft model, combined treatment with SJZD and 5-FU produced significantly greater reductions in tumor volume and tumor weight than treatment with 5-FU alone. Furthermore, the ferroptosis inhibitor ferrostatin-1 (Fer-1) effectively abolished the chemosensitizing effect of SJZD, indicating that ferroptosis is required for SJZD-mediated reversal of 5-FU resistance. Mechanistically, SJZD suppressed the expression of the E3 ubiquitin ligase membrane-associated ring finger protein 3 (MARCHF3), thereby inhibiting the ubiquitination and proteasomal degradation of arachidonate 15-lipoxygenase (ALOX15), a critical regulator of ferroptosis. Rescue experiments further demonstrated that ALOX15 silencing or MARCHF3 overexpression significantly attenuated SJZD-induced ferroptosis and reversed its sensitizing effect on 5-FU-resistant CRC cells. Collectively, these findings demonstrate that SJZD enhances the chemosensitivity of CRC cells to 5-FU by activating ferroptosis through regulation of the MARCHF3/ALOX15 axis. This study provides mechanistic insight into the antitumor activity of SJZD and highlights its potential as a promising adjuvant strategy for overcoming 5-FU resistance in CRC.
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4. Icariin: Unraveling Ferroptosis Mechanisms, Metabolic Networks, and Innovative Therapy Strategies.
4. 淫羊藿苷：揭示铁死亡机制、代谢网络及创新治疗策略PMID:日期:2026-08-24Ferroptosis is an iron-dependent form of cell death driven by lipid peroxidation. This concept reshapes our understanding of tissue degenerative lesions and oncogenesis. Icariin (ICA) is an isoprenyl flavonol glycoside derived from plants of the genus Epimedium. Acting as a bidirectional regulator of this pathway, it precisely modulates cellular sensitivity to ferroptosis across distinct disease states. This review systematically synthesizes literature from PubMed, ScienceDirect, Web of Science, and Google Scholar (2015-2025). Search keywords included "Icariin", "ferroptosis", "pharmacological mechanism", "pharmacokinetics" and "toxicology", while excluding conference abstracts, non-English studies, and reports lacking raw data. We systematically elucidated the role of ICA across a continuous "mechanism-treatment-metabolism" spectrum: in neurodegenerative disease models, ICA exerts an anti-oxidant effect to maintain cellular homeostasis, whereas in drug-resistant cancer cells, it functions as a pro-oxidant, promoting the elimination of malignant cells. This context-dependent effect is primarily attributed to its modulation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/glutathione peroxidase 4 (GPX4) axis, which serves as the critical "molecular switch" of redox homeostasis. Beyond direct signaling, ICA functions as a natural precursor. Its safety profile and therapeutic window are governed by the metabolic network, potentially conferring advantages over synthetic inhibitors. Although low systemic bioavailability limits clinical translation, nanodelivery systems and synthetic biology strategies offer viable approaches for optimizing its metabolic profile. Ultimately, ICA provides an exquisite molecular blueprint, charting a course for the development of ferroptosis-targeted therapies that can precisely sense and adapt to the microenvironments of complex diseases.
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5. Triptolide Improves Rheumatoid Arthritis by Regulating M1/M2 Balance Through the miR-223/CREBZF Axis.
5. 雷公藤甲素通过miR-223/CREBZF轴调控M1/M2平衡改善类风湿关节炎PMID:日期:2026-08-21Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation and progressive joint damage. This study investigated the role of microRNA-223 (miR-223) in RA and evaluated the therapeutic effects of triptolide (Tri), a diterpenoid epoxide derived from the traditional Chinese medicinal herb . A collagen-induced arthritis (CIA) mouse model was used to assess the effects of Tri and methotrexate (MTX). Micro-computed tomography, histological staining, enzyme-linked immunosorbent assay, flow cytometry, RT-qPCR, and western blot analysis were used to evaluate joint damage, inflammation, cytokine profiles, miR-223 expression, and the function of CREBZF, a downstream target of miR-223. CIA mice exhibited marked joint inflammation, swelling, bone erosion, and inflammatory cell infiltration, increased pro-inflammatory cytokine levels, and elevated miR-223 expression. Tri and MTX ameliorated these abnormalities and protected against bone erosion and inflammation. Tri suppressed the disease-associated elevation of miR-223, attenuated pathological fibroblast-like synoviocyte (RA-FLS) phenotypes, and shifted cytokine profiles toward an anti-inflammatory state. Dual-luciferase reporter and AGO2-RIP-qPCR assays supported direct regulation of CREBZF by miR-223. Tri restored CREBZF expression and inhibited NF-κ B signaling, thereby reducing RA-FLS proliferation and promoting apoptosis. These findings indicate that Tri ameliorates RA, at least partly, through the miR-223/CREBZF axis and identify this pathway as a potential therapeutic target.
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6. Artemisinin Attenuates Aβ1-42 Aggregation via the CaMK IV/PKA-CREB-Ace-H4 Cascade in Neuronal Cultures and 3xTg-AD Models.
6. 青蒿素通过CaMK IV/PKA-CREB-Ace-H4级联反应在神经元培养物和3xTg-AD模型中减弱Aβ1-42聚集PMID:日期:2026-08-19Alzheimer's disease (AD), a progressive neurodegenerative disease with a rising global prevalence, is characterized by amyloid-β (Aβ) aggregation, tau hyperphosphorylation, inflammation, oxidative damage, and neuronal apoptosis. Studies have increasingly recognized epigenetic modifications as key regulators in the development of AD. Epigenetic modifications, particularly histone acetylation, are increasingly recognized as critical regulators of cell survival and AD pathogenesis. Although artemisinin (ART) exhibits potent anti-oxidative, anti-inflammatory, and neuroprotective properties, its impact on histone acetylation in AD remains uncharacterized. This study investigated whether ART regulates histone acetylation to confer neuroprotection and rescue behavioral deficits in Alzheimer's disease models. Using SH-SY5Y cells, primary neurons, and 3xTg-AD mice, we found that ART restores histone acetylation homeostasis by enhancing histone H4 acetylation. Mechanistically, this effect is driven by the activation of the CaMK IV/PKA-CREB signaling cascade. Treatment with ART reduced ROS, improved mitochondrial function, decreased Aβ1-42 deposition, and suppressed neuronal apoptosis. However, these beneficial effects were abolished by PKA or CaMK IV inhibitors. Consequently, ART treatment significantly reduced reactive oxygen species (ROS) generation, restored mitochondrial function, decreased Aβ1-42 deposition, suppressed neuronal apoptosis, and alleviated AD-like neuropathology and cognitive deficits. Crucially, the neuroprotective and epigenetic benefits of ART were entirely abolished by pharmacological inhibitors of PKA or CaMK IV. This study is the first to demonstrate that artemisinin ameliorates AD pathology and behavioral impairments via the CaMK IV/PKA-CREB-Ace-H4 axis, establishing ART as a promising therapeutic candidate for epigenetic intervention in AD.
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7. Bufalin Induces Ferroptosis in Triple-Negative Breast Cancer via Inhibition of the NRF2/HO-1/GPX4 Pathway.
7. Bufalin通过抑制NRF2/HO-1/GPX4途径诱导癌症中的铁下垂PMID:日期:2026-08-19Triple-negative breast cancer (TNBC), a highly aggressive subtype of breast cancer characterized by poor prognosis and limited therapeutic options, remains a major clinical challenge. Bufalin, a principal bioactive component of Venenum Bufonis, exhibits potent anticancer activity against breast cancer. Nevertheless, the precise molecular mechanism by which bufalin triggers ferroptosis in TNBC cells remains poorly elucidated. In the present study, both and investigations were performed. Cellular ferroptosis was comprehensively evaluated by detecting intracellular Fe[Formula: see text], ROS, MDA, and reduced GSH levels, together with ultrastructural observation under transmission electron microscopy. Transcriptome sequencing combined with bioinformatic analysis was applied to screen the core regulatory mechanism of bufalin-induced ferroptosis in TNBC, and subsequent molecular biological experiments were conducted for further validation. The results demonstrated that bufalin significantly suppressed the proliferation and migration of TNBC cells. Bufalin treatment markedly increased Fe[Formula: see text], ROS, and MDA levels, depleted intracellular GSH, and induced mitochondrial shrinkage and cristae damage. Transcriptome analysis identified the NRF2/HO-1/GPX4 signaling axis as the central pathway mediating the pharmacological effect of bufalin. Mechanistically, bufalin downregulated the expression of NRF2, HO-1, SLC7A11, and GPX4, whereas it upregulated KEAP1 expression. studies verified that bufalin effectively inhibited tumor growth with no obvious systemic toxicity. Moreover, bufalin decreased the expression of GPX4 and Ki-67, increased the number of TUNEL-positive cells, and blocked the activation of the NRF2/HO-1/GPX4 pathway in tumor tissues. In conclusion, bufalin induces ferroptosis in TNBC by inhibiting the NRF2/HO-1/GPX4 signaling pathway, thereby exerting antitumor effects. These findings indicate that bufalin serves as a promising therapeutic agent for TNBC treatment.
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8. {"_":" Saponins Attenuate Cerebral Ischemia-Reperfusion Injury by Suppressing Neutrophil Extracellular Traps and Ferroptosis in Brain Microvascular Endothelial Cells.","i":["Panax notoginseng"]}
8. 三七总皂苷通过抑制脑微血管内皮细胞中性粒细胞外陷阱和铁下垂来减轻脑缺血再灌注损伤PMID:日期:2026-08-19saponins (PNS), the chief saponin components of the traditional Chinese medicine , are known to ameliorate the outcomes of ischemic stroke (IS), primarily by mitigating inflammatory responses, enhancing microcirculation, and modulating oxidative stress. Damage to brain microvascular endothelial cells (BMECs) and BMECs' ferroptosis are critical steps in cerebral ischemia-reperfusion injury (CIRI), a process in which neutrophil extracellular traps (NETs) have been shown to induce BMECs injury, thereby aggravating CIRI. We aimed to investigate the regulatory effects of PNS on NETs and BMECs' ferroptosis following CIRI and evaluate its therapeutic efficacy in brain injury intervention. In this study, Sprague-Dawley rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R), and the BMECs were exposed to oxygen-glucose deprivation/reoxygenation (OGD/R). These models were pretreated with PNS or the NETs-degrading agent DNase I, and the ensuing changes in key proteins, NETs-related markers, inflammatory factors, and ferroptosis-related indicators were assessed using Western Blotting or specific assay kits. Finally, neurological injury was assessed by neurological function scores and triphenyl tetrazolium chloride staining, while cell viability was evaluated using the Cell Counting Kit-8 (CCK-8) assay. In the rat models, PNS and DNase I markedly reduced the levels of key NETs biomarkers, related inflammatory factors, as well as MCAO/R-triggered ferroptosis, thereby mitigating brain injury. PNS treatment effectively suppressed NETs-induced ferroptosis in BMECs , thereby alleviating cell injury. This study demonstrated that PNS alleviates CIRI by inhibiting NETs and BMECs' ferroptosis. Mechanistically, PNS suppresses NETs, thereby suppressing ferroptosis. Collectively, these findings support a pharmacological rationale underlying the clinical treatment of IS.
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9. Berberine from Traditional Chinese Medicine in Liver Diseases: From Steatosis to Fibrosis and Hepatic Malignancies.
9. 中药小檗碱在肝脏疾病中的应用：从脂肪变性到纤维化和肝脏恶性肿瘤PMID:日期:2026-08-19Berberine (BBR), the core alkaloid of the traditional Chinese medicine (Huanglian), exhibits a notable pharmacological paradox: it possesses an oral bioavailability of less than 1% yet exerts broad therapeutic effects across the full spectrum of liver diseases, from metabolic dysfunction-associated steatotic liver disease (MASLD) through fibrosis to hepatic malignancies. This review constructs an integrated mechanistic framework to interpret BBR's holistic pharmacological characteristics, which distinguish it from conventional single-target drugs. In MASLD, BBR engages a convergent AMPK-SIRT-Nrf2 network to ameliorate insulin resistance, lipid dysregulation, oxidative stress, and hepatic inflammation. Combined with the complementary actions of its bioactive metabolites, it achieves parent-metabolite coordinated efficacy that embodies the holistic principle of traditional Chinese medicine. In liver fibrosis, BBR may block hepatic stellate cell activation via the TGF-β1/Smad3 pathway and eliminate activated HSCs through multiple programmed cell death pathways, particularly ferroptosis, which may overcome apoptosis resistance. In hepatic malignancies, BBR suppresses tumor progression, metastasis, and chemoresistance via apoptotic, ferroptotic, and immunomodulatory mechanisms. Current clinical evidence validates its metabolic benefits in MASLD, whereas clinical data regarding fibrosis and hepatic malignancies remain insufficient. Improving its poor bioavailability through structural modification and nanocarrier delivery is critical for clinical translation. This review provides a modern pharmacological rationale for the clinical application of -based formulas against progressive liver diseases.
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10. {"_":"Promotion of Angiogenesis with American Ginseng () After Myocardial Infarction via Targeting DNMT3b-Mediated DNA Methylation and Activating the Notch1/USP5/STAT3 Signaling Axis.","i":["Panax quinquefolius"]}
10. 通过靶向DNMT3b介导的DNA甲基化和激活Notch1/USP5/STAT3信号轴，促进心肌梗死后西洋参（Panax quinquefolius）的血管生成PMID:日期:2026-08-14Myocardial infarction (MI) necessitates the promotion of angiogenesis to improve prognosis. saponins (PQS), bioactive constituents of a medicinal and edible homologous plant, are known for their cardiovascular benefits, but their epigenetic mechanisms in post-MI angiogenesis remain unclear. In this study, PQS was obtained through a water extraction method followed by stepwise enrichment via ethanol elution. Surgical ligation of the left anterior descending (LAD) coronary artery was performed to establish an MI model in male C57BL/6 mice. The therapeutic effects on MI in each group were assessed through histopathological staining and echocardiography. The therapeutic effects of PQS on hypoxic human umbilical vein endothelial cells (HUVECs) were evaluated using tube formation assays, scratch assays, CD31 immunofluorescence, and Western blot (WB). Network pharmacology analysis, Bisulfite Sequencing PCR (BSP) detection, PCR, and WB were utilized to examine the influence of DNMT3b on Notch1 methylation. Cellular Thermal Shift Assay (CETSA) and Co-Immunoprecipitation (Co-IP) assays were employed to ascertain the binding interaction and stability between PQS and DNMT3b. Here, we demonstrate that PQS directly binds DNMT3b, thereby reversing aberrant DNA methylation at the Notch1 promoter and activating the Notch1/ubiquitin-specific protease 5 (USP5)/signal transducer and activator of transcription 3 (STAT3) signaling axis, thereby enhancing endothelial cell migration, tube formation, and angiogenesis in MI models. Ginsenoside Rc, ginsenoside Rh4, and vinaginsenoside R1 were identified as the key active components with the strongest DNMT3b binding affinity and angiogenic activity, with ginsenoside Rc demonstrating the most significant therapeutic effects. These findings reveal a novel epigenetic mechanism and confirm that PQS, particularly ginsenoside Rc, is a highly promising bioactive compound for promoting angiogenesis following MI.