The American journal of Chinese medicine最新文献

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.

Large language models (LLMs) are reshaping the landscape of Traditional Chinese Medicine (TCM). This review covers the latest applications of LLMs in TCM, including literature analysis, data mining, TCM knowledge management, diagnosis simulation and clinical decision making. LLMs can analyze large quantities of TCM literature and medical records to extract critical information, classify prescriptions, and build TCM knowledge maps to help researchers quickly grasp state-of-the-art and future research trends. LLMs can provide initial diagnostic recommendations by analyzing textual information such as a patient's symptom description and medical history, enabling the optimization of TCM therapy and the training of TCM practitioners. Compared with traditional tools, LLMs can significantly improve the efficiency and accuracy of bibliographic analysis and TCM prescription classification, and offer new potential for data-driven standardized TCM diagnosis. However, challenges remain, including the standardization of TCM terminology and data formats, integration of different data sources, timely knowledge updates, and the interpretability and credibility of results generated by LLMs. Future research on standardized templates for patient symptom description, multimodal data fusion techniques, and real-time knowledge update systems is warranted to improve the transparency and interpretability of LLMs. This review highlights the potential of LLMs to modernize TCM research and practice, providing an up-to-date reference for data scientists, biomedical engineers, and TCM practitioners.

SNHG5 serves as a key factor in regulating various cancers, and Dexmedetomidine (Dex) protects against myocardial ischemia/reperfusion (I/R) injury. However, the role of SNHG5 in Dex-mediated protection during myocardial I/R remains uninvestigated. In this study, models of rat myocardial I/R injury and hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury were generated. The infarct size, histological changes and apoptosis in heart tissues were evaluated by TTC, HE, and TUNEL staining. CCK-8, flow cytometry and immunofluorescence were employed to assess cell viability, apoptosis and autophagosome-lysosome fusion in H9c2 cells. The associations among SNHG5, LIN28A and BCAT1 mRNA were detected by RNA pull-down, RIP, and RNA fluorescence in situ hybridization (FISH) assays. Western Blot, qRT-PCR and immunohistochemistry were employed to detect the expression of key molecules. Our results revealed that Dex ameliorated myocardial I/R injury and H/R-induced impairments in H9c2 cells by enhancing autophagy. Moreover, Dex led to a rebound of SNHG5 in the heart tissues of I/R rats and H/R-treated H9c2 cells, and functional studies revealed that Dex protected against cardiac impairments through SNHG5-dependent autophagy in vitro and in vivo. Furthermore, SNHG5 alleviated H/R-induced impairments by recruiting LIN28A protein, which was subsequently bound to BCAT1 mRNA and maintained its stability. In conclusion, our findings demonstrated that SNHG5, when upregulated by Dex, alleviated myocardial I/R injury through LIN28A-mediated BCAT1 mRNA stabilization and autophagy enhancement.

Paeoniflorin (PF) is a key active ingredient with anti-inflammatory and antioxidant properties extracted from the root of Paeonia lactiflora. Non-alcoholic fatty liver disease (NAFLD), recently referred to as metabolic dysfunction-related fatty liver disease (MAFLD), is the leading cause of chronic liver disease worldwide. However, the potential mechanisms and targets of paeoniflorin's anti-inflammatory and antioxidant therapy for MAFLD remain to be thoroughly investigated. Thus, in cellular experiments, we added free fatty acids (P/O) to AML-12 cells and cultured them for 24 h. In animal experiments, mice were administered a high-fat diet (HFD) for a duration of 16 weeks in order to create an animal model of fatty liver disease. Our study confirmed that PF significantly reduced steatosis and alleviated oxidative stress and inflammation levels in P/O-induced AML-12 hepatocytes and mouse livers with HFD. Cellular experiments showed that PF-attenuated Phosphoric acid/Oleic acid (P/O) induced lipid deposition in AML-12 cells, indicators related to cellular focal death were downregulated, and mitochondrial oxidative damage was alleviated. In animal experiments, ALT, AST, TG, TC and the hepatic index were elevated in the model group, and lipid deposition and cell infiltration were shown by HE, Oil Red O staining. These were significantly reduced in the PF groups. Network pharmacology studies indicated PF may target the Stimulator of interferon genes (STING) as a crucial molecule for the treatment of MAFLD, and the validation of C-176 (STING inhibitor) and DXMAA (STING promoter) further supported that PF could target STING to regulate hepatocyte cellular pyroptosis.

In a previous study, Eugenol (EU) has been demonstrated to alleviate DSS-induced experimental colitis, due to its anti-inflammatory, anti-oxidant, and immune regulatory efficacy, but its underlying molecular mechanism remains unknown. In this study, EU applications were combined with peroxisome proliferator-activated receptor-[Formula: see text] (PPAR-[Formula: see text]) agonist (rosiglitazone) and inhibitor (GW9662) in order to clarify the role of PPAR-[Formula: see text] in EU against UC by testing NF-κB and Nrf2 signaling pathway activation and the salient features of colitis. The binding activity and adjusting effect of EU on inflammation and oxidative stress were further investigated in vitro. Similar to rosiglitazone, the results illustrated that EU remarkably reversed DSS-induced weight loss, reversed colonic shrinkage and integrity damage, and inhibited the DAI scores increase, excessive inflammatory response, and oxidative stress. However, the combination with GW9662 noticeably restrained the protective effect on mice. Additionally, molecular docking and a surface plasmon resonance assay evidenced the direct binding activity of EU with PPAR-[Formula: see text]. EU's anti-oxidant and anti-inflammation bioactivities were evidenced again in vitro. Overall, the above results further demonstrated the molecular mechanism of EU's defensive effect, which is directly dependent on PPAR-[Formula: see text] activation, on experimental colitis. Therefore, this study may facilitate a better understanding of EU's protective action against UC.

Ulcerative colitis (UC) is a chronic, nonspecific inflammatory disorder characterized by symptoms such as abdominal pain, diarrhea, hematochezia, and urgency during defecation. While the primary site of involvement is the colon, UC can extend to encompass the entire rectum and colon. The causes and development mechanisms of UC are still not well understood; nonetheless, it is currently held that factors including environmental influences, genetic predispositions, intestinal mucosal integrity, gut microbiota composition, and immune dysregulation contribute to its development. Dysregulated immune responses are pivotal in the pathophysiology of UC, and these aberrant responses are considered key contributors to the disease onset. In patients with UC, immune cells become hyperactive and erroneously target normal intestinal tissue, resulting in inflammatory cascades and damage to the intestinal mucosa. The therapeutic strategies currently employed for UC include immunosuppressive agents such as aminosalicylates and corticosteroids. However, these treatments often prove costly and carry significant adverse effects - imposing a considerable burden on patients. Traditional Chinese Medicine (TCM) has attracted worldwide attention because of its multi-target approach, minimal side effects, cost-effectiveness, and favorable efficacy profiles. In this review, the ways in which TCM modulates inflammatory responses in the treatment of ulcerative colitis have been outlined. Research into TCM modalities for modulating inflammatory pathways in the treatment of UC, which has yielded promising advancements, including individual herbs, herbal formulations, and their derivatives, has been summarized. TCM has been utilized to treat UC and the immune system plays a key role in regulating intestinal homeostasis. It is imperative to facilitate large-scale evidence-based medical research and promote the clinical application of TCM in the management of UC.