The American journal of Chinese medicine最新文献

Cancer causes millions of deaths globally every year. At its later stages, cancers are primarily treated with systemic therapies which do not provide an effective cure; the remaining cancer cells ultimately acquire drug resistance, relapse, and metastasize. In particular, polyploid giant cancer cells (PGCCs), which arise in response to diverse cellular stressors such as therapeutic pressure, modulate the tumor microenvironment (TME) and immunity involved in cancer development. However, without the knowledge of well-established signaling cascades targeting PGCCs, the current treatment options for these cells remain limited. This review provides a summary of the latest research associated with PGCC formation and treatment outcomes in common metastatic cancers. In addition, we highlight how some traditional Chinese medicine (TCM) and their bioactive compounds may serve as prospective agents for arresting PGCCs through cell cycle regulation, cell death induction, and TME modulation. Specifically, we identify how these processes are closely associated with the initiation, self-renewal, and termination phases of the PGCC life cycle. Based on the principle in TCM of "strengthening vital qi to eliminate pathogenic factors," the most efficacious herbs for counteracting PGCCs have been identified as Coptis chinensis, Oldenlandia diffusa, Scutellaria baicalensis, Salvia miltiorrhiza, Curcuma longa, Astragali radix, and Panax ginseng. The bioactive compounds of these herbs include berberine, oleanolic acid, wogonin, tanshinone IIA, curcumin, Astragaloside IV, and ginsenoside Rh2. Given the multi-target characteristics of TCM, network pharmacology was performed to allow for an integrative approach to elucidating underlying mechanisms. In particular, TCM administration may modulate both the p53 signaling pathway and cell cycle-related proteins. This, in turn, alleviates PGCC-induced tumor recurrence and resistance. Collectively, this review emphasizes the central role of PGCCs in advanced cancer progression while strengthening the mechanistic insights of TCM in PGCC-oriented therapy.

Rheumatoid arthritis (RA) is a common chronic inflammatory autoimmune joint disease, and its main clinical manifestations include bone joint swelling, pain, and progressive destruction. Acupuncture has become an important clinical treatment for RA due to its high safety profile, minimal side effects, and cost-effectiveness. However, it still needs to be further promoted and improved in the future. This review systematically summarizes the current status of acupuncture's clinical application and mechanism research in both domestic and international treatments of RA over the past decade. First, it outlines the current clinical application of acupuncture for RA, and offers a focus on summarizing advances in mechanism research. Findings indicate that acupuncture can alleviate chronic RA inflammation by regulating macrophage polarization, the M1/M2 cell ratio, and Treg/Th17 cell balance. It regulates the Keap1-Nrf2/ARE/HO-1 signaling pathway to reduce oxidative stress in inflamed tissues. Decreasing RANKL protein levels inhibits osteoclast generation while protecting bone joints. Additionally, it suppresses synovial angiogenesis, specifically activates autophagy to positively regulate the AMPK/ULK1 signaling pathway, and suppresses the abnormal activation of the PI3K/Akt/mTOR signaling pathway that causes excessive autophagy in synovial cells. It also alleviates chronic pain through both the release of peripheral local mediators and central nervous system signaling regulation while improving pain-related anxiety and depression.

Ferroptosis is a novel type of cell death that depends on iron ions and lipid peroxidation. An increasing number of studies have shown that ferroptosis can inhibit the progression of digestive system tumors, enhance the sensitivity of tumor cells to drugs, and reduce drug resistance. Traditional Chinese medicine (TCM) has been widely utilized in the field of tumor treatment, and has recently achieved remarkable research results in regulating the ferroptosis of tumor cells. This review systematically expounds on the specific molecular mechanisms through which TCM regulates ferroptosis in digestive system tumors (including hepatocellular carcinoma, gastric cancer, colorectal cancer, and pancreatic cancer). It covers various intervention strategies, including TCM small molecules like terpenoids, flavonoids, phenols, saponins, and alkaloids, nanoparticles loaded with active ingredients like novel nanoparticle-encapsulated berberine and NPBer, compound formulas such as Banxia Xiexin Decoction and Compound Gegen Decoction, and external treatments such as acupuncture. Studies have indicated that TCM, through its multi-target and multi-pathway action mechanism, affects pathways such as iron metabolism, lipid metabolism, and anti-oxidant defense to thereby promote ferroptosis and consequently inhibit tumor growth and metastasis. This provides new strategies and scientific evidence for the treatment of digestive system tumors. The purpose of this paper is to provide innovative ideas and theoretical support for the further exploration of TCM in the field of tumor treatment.

Atherosclerosis (AS), a major cause of cardiovascular diseases, is driven by dysregulated programmed cell death (PCD) pathways. These pathways, including apoptosis, pyroptosis, ferroptosis, autophagy, and necroptosis, contribute to plaque instability. Traditional Chinese Medicine (TCM) offers a multi-targeted approach for modulating these pathways, but its molecular mechanisms in AS remain inadequately explored. This review aims to investigate the modulatory effects of TCM on PCD pathways in AS, its therapeutic potential for enhancing plaque stability, and the underlying molecular mechanisms. A narrative literature review based on relevant preclinical in vitro and in vivo studies was conducted on TCM bioactive constituents and formulas. These included studies on tonifying herbs like Radix Astragali, Radix Ginseng, and Radix Glycyrrhizae, the extracts of Radix Salviae liguliobae, and classical prescriptions such as Danshen Prescription, Huayu Qutan Recipe, Modified Taohong Siwu Decoction, Xuezhikang, Gualou Xiebai Decoction, and Mai Ji Tong Granules. The relevant data were obtained from searches of major international and Chinese biomedical databases including PubMed, Web of Science, Embase, Cochrane Library, the China Biology Medicine Database, CNKI, Wanfang, and CSTJ. The evidence indicates that these interventions modulate PCD-related pathways to thereby inhibit pathological cell death, enhance protective autophagy, and influence cellular homeostasis, inflammation, oxidative stress, lipid accumulation, and efferocytosis. TCM's multi-component nature addresses the limitations of single-target Western therapies, and thus provides a holistic strategy for AS management. However, gaps remain in the mechanistic understanding and pharmacokinetic profiles of TCM constituents that hinder clinical application. This review emphasizes TCM's potential as a complementary therapy for AS. It likewise suggests the need for further studies to identify bioactive compounds and integrate TCM with precision medicine in order to achieve better therapeutic outcomes.

Diabetic kidney disease (DKD) is a major microvascular complication of diabetes, and recent evidence highlights the gut-kidney axis as a critical target in its prevention and treatment. Traditional Chinese Medicine (TCM) has demonstrated its unique advantages in regulating this axis through multi-target and multi-pathway mechanisms. This review summarizes research progress on TCM interventions that modulate the inflammatory pathways of the gut-kidney axis in DKD. Literature from recent years was collected from PubMed, Web of Science, and CNKI, with a particular focus on studies investigating the roles of TCM monomers and formulas in microbiota regulation, intestinal barrier protection, and inflammatory signaling. TCM compounds such as resveratrol, astragalus polysaccharides (APS), and ginsenosides, as well as classical formulas including Yi-Shen-Hua-Shi Granule, Tangshen Formula, and Huangkui Capsule (HKC), were found to restore gut microbial balance, increase short-chain fatty acid production, and inhibit key inflammatory pathways like NF-κB, NLRP3, JAK/STAT, and TGF-β1/Smad. These effects collectively alleviate oxidative stress, suppress renal inflammation and fibrosis, and improve metabolic and immune homeostasis. The findings suggest that TCM can effectively intervene in DKD progression by targeting gut-derived inflammation and immune dysregulation, and thereby provides a theoretical and experimental basis for integrative DKD therapy centered on gut-kidney axis modulation.

Gastric cancer is a significant global health issue. Celastrol, a natural compound, has shown antitumor potential, but its molecular mechanism in gastric cancer remains unclear. In this study, we treated HGC-27 cells with celastrol and employed CCK8, colony formation, and Transwell assays, revealing its inhibitory effect on cell proliferation and migration. Flow cytometry assay results showed that celastrol could elevate the level of reactive oxygen species (ROS) in HGC-27 cells. By using the iron ion and malondialdehyde (MDA) detection kits, it was found that celastrol promoted the accumulation of iron ions (Fe[Formula: see text] in HGC-27 cells, increased the MDA content, and simultaneously decreased the glutathione (GSH) content. Additionally, Western blot analysis indicated that celastrol exerts an inhibitory effect on the expression of ferroptosis-marker proteins GPX4 and SLC7A11. PCR array and further experiments identified CERKL as a key factor, whose downregulation by celastrol was associated with enhanced ferroptosis. In vivo, celastrol inhibited tumor growth without affecting body weight or organ histology. Our findings suggest that celastrol may inhibit gastric cancer via CERKL-regulated ferroptosis, providing a potential therapeutic strategy.

It is crucial to prevent and treat liver fibrosis in patients with chronic liver disease. Dihydromyricetin (DMY) is a natural flavonoid compound from traditional Chinese medicine, known to alleviate chronic liver injury. However, its role in regulating inflammatory responses through gut microbiota and metabolic changes remains unclear. In this study, a mouse model of liver fibrosis was induced with carbon tetrachloride (CCl₄), and DMY was administered via gavage. Histopathology, immunohistochemistry, Reverse Transcription Polymerase Chain Reaction (RT-PCR), 16S rRNA sequencing, and untargeted metabolomics were employed to evaluate DMY's pharmacological effects on CCl₄-induced liver fibrosis and explore its underlying mechanisms. Our results show that DMY reduced the aspartate transaminase (AST) and alanine transaminase (ALT) serum levels in liver fibrosis model mice, and lowered the mRNA expression of pro-inflammatory cytokines and fibrosis markers. Additionally, DMY restored the richness and diversity of the gut microbiota, with several microbiota taxa significantly correlating with inflammatory markers. Metabolomic analysis of serum and liver tissue revealed that DMY significantly altered the liver metabolite disturbances induced by CCl₄. Pearson correlation analysis demonstrated a strong relationship between microbial composition and liver metabolites. These results suggest that DMY alleviates liver fibrosis in mice by reshaping the gut microbiota and host metabolism, thereby improving the inflammatory response.

AMP-activated protein kinase (AMPK) is a ubiquitous sensor of cellular energy and nutrient status in eukaryotic cells. It serves an essential function in the modulation of energy balance and metabolism homeostasis through its regulation of carbohydrate metabolism, lipid metabolism and protein metabolism. The dysregulation of AMPK is closely related to a series of systemic diseases, affecting multiple organs and tissues. Baicalin is a natural compound derived from the dry raw root of Scutellaria baicalensis, and it has been found to exhibit several potential pharmacological actions. These include hepatoprotective effects, anti-inflammation effects and anti-tumor effects. These biological activities are related to the regulatory effect of baicalin on the host metabolism, which is closely associated with AMPK modulation. In this review, we provide an overview of the regulatory effect of baicalin on AMPK and its upstream and downstream signaling pathways. The pharmacological properties and underlying mechanism of baicalin for regulating AMPK were summarized with regards to four aspects: regulatory effect of baicalin on AMPK in lipid metabolism and glucose metabolism, regulatory effect of baicalin on AMPK in its pharmacological effect of anti-tumor and anti-inflammation. As a natural compound, baicalin has the potential for the management of certain AMPK-related diseases.

Traditional Chinese medicine (TCM) has protected the health of Chinese people for thousands of years. With the rapid development of artificial intelligence (AI), various fields of TCM are facing both opportunities and challenges. This review discusses the development prospects and challenges of Chinese medicine in the AI era, emphasizing that AI, as an important tool in the process of Chinese medicine healthcare services, can assist doctors in making objective, rational and professional treatment decisions, and that AI has a strong potential for development in the field of Chinese medicine. However, the emotions, complex thoughts, and humanistic values of doctors are qualities that AI is currently unable to realize, so as the dominant player, the doctor is indispensable to the medical process. By summarizing and analyzing the current development status of AI in diagnosis, drug research, health management and education in TCM, this paper reveals the development prospects and potential risks of combining TCM with AI, and suggests that AI is an important aid for modernizing and improving the quality of TCM medical care in a coordinated manner.

The intestinal absorption of active herbal constituents plays an important role in the biomedical efficacy of Traditional Chinese Medicine (TCM) formulations after oral administration. TCM compounds with low oral bioavailability can reach the distal intestine and then interact with intestinal flora, influencing the botanical pharmacological effects. In this study, in vitro digestion and an ex vivo Ussing chamber model were utilized to evaluate the intestinal absorption behavior of Forsythiae Fructus-Lonicerae Japonicae Flos-containing Yinqiao Jiedu Granule (YQJDG). It was found that the jejunum exhibited active absorption effects for some components of the formula, while the oral bioavailability of other herbal ingredients was low. Through further research using a combined UPLC-MS/MS and 16S rDNA sequencing technique, we studied the existence of the reciprocal interactions between YQJDG and gut microbiome. The in vitro fecal fermentation results showed that YQJDG significantly impacted the microbial community composition. The YQJDG markedly increased the abundance of beneficial microorganisms, such as Parabacteroides distasonis and Streptococcus gallolyticus subsp. Macedonicus, and suppressed the abundance of conditional pathogens including Prevotella steorerea, Haemophilus parainfluenzae, and Bacteroides. These effects may potentially contribute to the body's immune functions and anti-inflammatory capacities. UPLC-MS/MS analysis suggested that the fecal microbiota chemically transformed constituents with low bioavailability to more readily absorbed potentially active metabolites. These findings provided valuable insights into the absorption characteristics of YQJDG and its interaction with the gut microbiome, further facilitating our understanding of precise pharmacological mechanisms of action of this Chinese herbal formulation.