The American journal of Chinese medicine最新文献

The Wnt/β-catenin signaling pathway plays a crucial role in both physiological and pathological conditions. Targeting molecules associated with the Wnt/β-catenin signaling pathway presents a promising approach for disease treatment. The use of natural products in treating various diseases is widespread due to their favorable biocompatibility, low toxicity, and high biological activity. Research has shown that natural products such as curcumin and resveratrol can regulate multiple signaling pathways under disease conditions, including the Wnt/β-catenin signaling pathway. However, the regulatory mechanisms of natural products remain incompletely understood. This review aims to explore the regulatory effects of natural products on the Wnt/β-catenin signaling pathway in certain diseases, especially in the process of tumor progression. It outlines the composition and mechanisms of the Wnt/β-catenin signaling pathway. Furthermore, we predicted the potential binding sites of these natural products to this pathway, summarized the effects of diverse natural products on this signaling pathway, and conducted a preliminary exploration ofd the mechanisms of the effects of natural products. In addition, we considered and discussed the limitations of natural products, such as potential side effects from long-term use and the precision in targeting the Wnt/β-catenin signaling pathway. This review provides a theoretical basis for the targeted strategy of the Wnt/β-catenin signaling pathway.

Ulcerative colitis (UC) is a recurrent inflammatory intestinal disorder characterized by systemic inflammatory response, abnormal intestinal epithelial cell death, and damage to the intestinal mucosal barrier. This study aimed to explore the role of celastrol in ferroptosis and intestinal epithelial barrier permeability. The results demonstrated that celastrol significantly inhibited ferroptosis in RSL3-induced intestinal epithelial cells by regulating the expression of ferroptosis-related proteins. Concurrently, celastrol dramatically improved the permeability of the intestinal epithelial monolayer by increasing the expression of tight junction proteins including ZO-1, occludin, and claudin-1. Moreover, celastrol markedly attenuated the effect of RSL3 on the phosphorylation of Akt and FOXO1. LY294002, a PI3K inhibitor, significantly inhibited the role of celastrol in the expression of ferroptosis-related and intestinal tight junction proteins. In vivo, celastrol administration not only significantly ameliorated dextran sulfate sodium (DSS)-induced colitis by preventing neutrophil infiltration, but also ameliorated intestinal mucosa damage, and colon shortening. Celastrol administration was also found to reduce the expression of ferroptosis-related proteins prevent the infiltration of fluorescein isothiocyanate-dextran (FITC-dextran) and increase the levels of tight junction proteins. Collectively, these findings suggest that due to its effects on ferroptosis and tight junctions in intestinal epithelial cells, celastrol may be a compound with significant promise in the prevention and treatment of UC.

Myeloperoxidase (MPO) is a heme-containing enzyme that regulates inflammation and oxidative stress under normal physiological conditions, but when dysregulated, it contributes to the development and progression of cardiovascular, immune-related, and malignant diseases. While its pathological roles have been widely described, the therapeutic applications of targeting this enzyme remain insufficiently explored. Natural compounds, including polyphenols, flavonoids, and traditional herbal formulations, possess anti-oxidant and anti-inflammatory properties that attenuate oxidative stress and modulate MPO activity. This review explores the molecular pathways through which dysregulated MPO activity promotes disease and compiles a categorized overview of natural products and traditional Chinese medicines capable of influencing MPO function. These findings provide a framework for therapeutic discovery, thus enabling target validation and the development of novel interventions across diverse inflammatory and degenerative conditions.

The incidence of non-alcoholic fatty liver disease (NAFLD) has increased and become a serious global public health problem in recent years. The currently generally used clinical treatments have disadvantages such as side effects, limitations, and poor patient compliance. Traditional Chinese medicine (TCM) has a pharmacological effect with multiple components, multiple targets, and multiple pathways, emphasizing a "holistic concept" and "differential diagnosis and treatment," which is compatible with the complex pathogenesis of GM and NAFLD. Previous studies have demonstrated a close relationship between the gut microbiome (GM) and the occurrence and progression of NAFLD. However, the mechanisms between GM and NAFLD are complex. This paper not only analyzes the relationship between the GM and the pathogenesis of NAFLD but also discusses in detail how various TCM active metabolites and Chinese herbal formulas could exert a therapeutic effect on NAFLD by regulating the GM and its metabolites. Furthermore, this paper innovatively explores how TCM regulates the abundance of five major bacterial phyla, and their representative genera, to improve the pathogenesis of NAFLD. In summary, this review article proposes innovative ideas and options for the prevention and treatment of NAFLD with focus on GM regulation, and provides a theoretical basis for the development of new drugs from traditional Chinese medicine.

Many herbal and traditional medicines show promise in the treatment of diverse diseases, but their molecular mechanisms in different dynamic pathological contexts remain poorly understood. Several herbally-derived agents have entered pharmaceutical development, and there are ongoing efforts to define the pharmacotherapeutic effects of natural ingredients. Gambogic acid (GA), a caged xanthone from the dry resin of the widely used traditional Chinese medicinal herb Garcinia hanburyi Hook.f., has demonstrated therapeutic potential against chronic inflammation, cancer, cardiovascular disorders, and other conditions. However, its mechanisms of action, pharmacokinetics, and toxicological profile remain unclear. Furthermore, no comprehensive review exists on nanotechnology-based delivery strategies for this compound. In this review, we summarize current knowledge of the molecular targets and signaling pathways of GA, systematically assess the available pharmacokinetic data, safety considerations, and nanoplatform delivery systems, and highlight promising directions for future applications. Despite substantial preclinical evidence, the clinical translation of GA is hindered by poor drug availability. This review provides a critical synthesis of existing evidence and outlines strategies to advance the therapeutic development of this traditional medicine-derived compound.

Cancer continues to pose significant challenges to global health systems due to its substantial disease burden and complex pathogenesis, and current therapies often demonstrate unsatisfactory outcomes. The inherent problems of tumor heterogeneity and individual variability lead to diverse responses to identical interventions, and result in uncertainty in treatment outcomes. Concomitant factors such as stress, mental health and diet also collectively impact patients' overall health, and thereby affect cancer progression in turn. Therefore, the comprehensive evaluation of patients' multidimensional profiles and the implementation of personalized treatments is imperative. This integrated approach not only enhances prognostic outcomes, but also improves quality of life. As a complementary therapeutic option, Traditional Chinese Medicine (TCM) has good efficacy in symptom alleviation and quality-of-life improvement. This holistic approach emphasizes the interconnectedness of human physiological systems and their harmonious balance with the external environment. TCM interventions are tailored to individual clinical manifestations, which enables the development of personalized treatment regimens. This review elucidates the clinical applications of TCM in individualized cancer treatment, and delineates its strategic framework for oncology management. It incorporates the innovative concept of "State-target differentiation and treatment" (Bianzheng Lunzhi) proposed by academician Tong Xiaolin, which integrates macro and micro perspectives into the diagnostic and therapeutic framework. The aim of this review is to advance evidence-based TCM approaches for the treatment of malignant tumors, and provide a more scientific and systematic methodology for individualized cancer treatment in TCM.

Malignant tumors remain a leading cause of global mortality and pose significant public health challenges. However, Traditional Chinese Medicine (TCM) and its natural products offer unique therapeutic potential in oncology which may help to address these challenges. Mitophagy, a selective form of autophagy, is a key regulator of mitochondrial quality, metabolic balance, and programmed cell death, and has dual roles in tumor initiation, progression, and therapeutic responses. The canonical PINK1/Parkin and receptor-mediated BNIP3, NIX, and FUNDC1 pathways coordinate both the removal of damaged mitochondria and adaptation to stress to thus influence tumor cell survival, proliferation, metastasis, and chemoresistance. This review systematically summarizes the mitophagy-related molecular mechanisms present in tumors, and highlights the multifaceted anticancer effects exerted by TCM via mitophagy. TCM exerts chemo-preventive effects on precancerous lesions, induces apoptosis, ferroptosis, and other forms of programmed cell death, reprograms tumor metabolism, and modulates inflammatory signaling, immune cell function, and immunogenic cell death to thereby collectively reshape the tumor immune microenvironment. Beyond its antitumor activities, TCM alleviates cancer-related fatigue through mitophagy regulation in the skeletal muscle. Moreover, combination therapies involving mitophagy modulators enhance TCM efficacy. Further studies which integrate single-cell omics, spatial metabolomics, and functional imaging are needed in order to define context-specific mitophagy regulation, optimize combination strategies, establish reliable biomarkers, and thus position TCM as a promising approach for personalized and integrative cancer therapy.

Traditional Chinese medicine (TCM) is characterized by its multi-component, multi-target, and multi-pathway properties, which make it an ideal candidate for network pharmacology applications. This approach provides a comprehensive framework for understanding the therapeutic effects of TCM in managing complex diseases. This review highlights recent advancements in network pharmacology as applied to TCM, and focuses on key achievements such as the identification of core bioactive components, target prediction, and the elucidation of mechanisms of action. Notable studies, including network pharmacology research on artemisinin and Compound Danshen Droplet Pills, demonstrate the practical application of this methodology in drug discovery and disease management. Furthermore, this review explores the integration of network pharmacology with omics technologies, and enables a more holistic understanding of TCM's efficacy. These advancements are crucial in promoting the modernization of TCM and enhancing its integration into contemporary medicine. In conclusion, network pharmacology is advancing TCM research, providing a scientific basis for its clinical application, and paving the way for its global acceptance.

Colorectal cancer (CRC) remains a major threat to health worldwide, partly due to the lack of effective treatments targeting the transition from inflammatory bowel disease (IBD) to malignancy. Astragaloside IV (AS-IV) is a major bioactive component from the traditional herb Astragalus membranaceus, and it has strong immunomodulatory and gastrointestinal protective effects. In this review, we evaluate the therapeutic potential and mechanisms of AS-IV in addressing the three hallmark pathological phases of colorectal cancer development: IBD-related inflammation, the transition from inflammation to cancer, and IBD-associated colorectal cancer (IBD-CRC). During the inflammatory phase, AS-IV promotes M2 macrophage polarization, reducing mucosal inflammation and repairing the intestinal barrier. In the transition from inflammation to cancer, AS-IV prevents IBD-CRC transition by targeting immune signaling pathways (e.g., NF-κB and PPAR[Formula: see text] signaling pathways), gut microbiota, and oxidative stress. At the IBD-CRC stage, AS-IV can promote the polarization of M1 macrophages, thereby suppressing tumor growth, inducing apoptosis, inhibiting metastasis, and enhancing chemosensitivity. These findings highlight the potential of AS-IV to bidirectionally modulate the M1/M2 macrophage ratio and its role in the prevention and treatment of IBD-CRC. The multi-target therapeutic effects of AS-IV at various stages of IBD also provide new strategies to guide future drug development.