The American journal of Chinese medicine最新文献

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.

Astragaloside IV (ASIV), the main active component of the traditional Chinese medicine HuangQi, exhibits ameliorating effects on myocardial fibrosis through unclear mechanisms. To investigate the effects of ASIV on Endothelial-to-mesenchymal transition (EndMT) in myocardial fibrosis, 10 ng/mL TGF-β1 was used to induce EndMT in human umbilical vein endothelial cells (HUVECs) in vitro, and a 5 mg/kg/d subcutaneous injection of Isoproterenol (ISO) was used to induce myocardial fibrosis in mice in vivo. The drug affinity-responsive target stability (DARTS) was used to identify the target proteins of ASIV in endothelial cells. The results showed that ASIV could significantly inhibit the TGF-β1-induced EndMT, which includes changes in cytoskeletal structure, the expression of EndMT markers, cell migration potency, and cell glycolysis rate. ASIV significantly ameliorated ISO-induced myocardial fibrosis in mice and inhibited EndMT in heart tissues. The Ras homolog gene family member A (RhoA) protein was found to be a possible direct binding target of ASIV in endothelial cells. The binding affinity between ASIV and RhoA was confirmed by molecular docking and the cellular thermal shift assay (CETSA). ASIV inhibited the RhoA-related pathway in the heart tissues of myocardial fibrosis mice. In addition, siRNA knockdown of RhoA expression or treatment with RhoA agonists was found to significantly affect the inhibition of EndMT by ASIV. The results suggested that ASIV could significantly inhibit the EndMT by binding with RhoA, and that the inhibition of EndMT by ASIV contributed to its amelioratory effects on myocardial fibrosis. This discovery provided a theoretical basis for the application of ASIV and HuangQi in the treatment of myocardial fibrosis.

Chronic airway diseases are a group of diseases, such as chronic obstructive pulmonary disease (COPD) and bronchial asthma (BA), characterized pathologically by chronic airway inflammation, airway chronic mucus hypersecretion, and airway remodeling. Patients usually present with chronic coughing, expectoration, and dyspnea, and recurrent exacerbation is an important causative factor of increased mortality, along with the important triggers. Currently, existing treatment options cannot meet the clinical needs of chronic airway diseases. Ginseng's great potential for treating chronic airway diseases has been confirmed by various clinical and basic studies, and traditional Chinese medicine compounds composed mainly of ginseng can both improve the symptoms of coughing and expectoration and reduce the number of acute exacerbations. Ginseng and its main biologically active ingredients exhibit the multifaceted mechanisms of effectively improving airway inflammation, mitigating airway mucus secretion, and reducing airway remodeling, which underscores their effectiveness in airway disease treatment. This study was conducted for the further elucidation and extension of the possible value of ginseng in chronic airway diseases. This review summarizes recent studies on the efficacy of ginseng in chronic airway disease treatment, discusses the pharmacological effects of ginseng and ginsenosides, and highlights their roles in the prevention and treatment of chronic airway diseases, airway diseases caused by airway inflammation and high airway mucus secretion, and airway remodeling-induced lung diseases. Finally, this study also predicted future research directions. Findings in this study may lay a robust foundation for investigating ginseng in chronic airway diseases, its underlying mechanisms, and its clinical development and practical application.

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.

Ferroptosis, an iron-dependent form of non-apoptotic cell death, has emerged as a critical process in cancer therapy. Sanguinarine chloride (S.C), an alkaloid that stimulates apoptosis by activating reactive oxygen species (ROS), has demonstrated significant anticancer potential, but its role in modulating ferroptosis remains unclear. The aim of the present study was to elucidate the effects of S.C on ferroptosis in gastric cancer (GC) progression and its mechanism. Here, we determined cell viability by CCK-8 and revealed that the most potent drug, S.C, which is a small molecule compound in the ferroptosis library, had the strongest killing effect on GC cells. S.C could trigger ferroptosis in GC cells by inhibiting glutathione levels through promoting malondialdehyde production and ROS accumulation. Interestingly, S.C was found to function as a pro-ferroptotic death by interacting with NOS2 through network pharmacological docking. Mechanistically, we observed the deacetylase SIRT1 to regulate the acetylation level of NOS2 and thus affect the expression of NOS2. In addition, S.C regulates the downregulation of SLC7A11 and GPX4 through the SIRT1/NOS2/SOD1 pathway, and thereby induces ferroptosis. In vivo experiments showed that S.C treatment significantly inhibited subcutaneous tumor growth in BALB/c nude mice. This was significantly rescued by injection of a ferroptosis rescue agent (AA9). Taken together, these findings demonstrate that S.C works through the SIRT1/NOS2/SOD1 pathway and suggest that targeting SLC7A11/GPX4 to cause ferroptosis in cancer cells has potential as an anticancer therapy.

This study aimed to clarify the protective effect of Glycyrrhizic acid (GL) against Diosbulbin B (DB) - induced liver injury in mice and investigate its mechanisms of action. A liver injury DB was established in mice through the oral administration of DB for 15 days. At the same time, GL was administered to the mice for treatment. After the experiment, the pharmacodynamics and mechanisms of GL in ameliorating DB-induced liver injury were explored using biochemical indexes, non-targeted metabolomics, targeted metabolomics, Western blotting analysis of protein expression, 16S rDNA sequencing, and Spearman correlation analysis. The results show reduced liver function indices and improved DB-induced hepatic pathological changes. It also attenuated DB-induced hepatic inflammation and oxidative stress. Hepatic metabolomics revealed that GL regulated ABC transporters and bile secretion. Targeted bile acid (BA) metabolomics and Western blotting demonstrated that GL improved DB-induced reduction in BA efflux by regulating FXR-mediated efflux transporters. Furthermore, analysis of 16S rDNA gene sequencing revealed that GL effectively restored the relative abundance of beneficial bacteria, reduced the relative abundance of harmful bacteria, and reinstated the structure of the intestinal flora. Additionally, correlation analyses between BA and intestinal flora indicated that Firmicutes, Bacteroidota, TDGA, DGA, UDGA, GDGA, THDGA, and HDGA could serve as major markers for DB-induced liver injury. In conclusion, GL significantly improved DB-induced liver injury by increasing the expression of Nrf2/FXR-BSEP/MRP2/P-gp/UGT1A1, promoting BA efflux, regulating intestinal flora, and alleviating inflammation and oxidative stress.