The American journal of Chinese medicine最新文献

Myasthenia gravis (MG) is a chronic autoimmune disorder characterized by an immune-mediated attack on neuromuscular junction acetylcholine receptors (AChRs), and its pathogenesis is closely linked to immune dysregulation. Emerging evidence has highlighted the pivotal role of the gut microbiota in the pathophysiology of MG through immunomodulation, microbial metabolite signaling, and gut-brain axis interactions. This review combines 16S rRNA sequencing, metagenomic, and metabolomic data to reveal distinct gut microbial signatures in patients with MG. These signatures include reduced α-diversity, depletion of beneficial taxa like Bacteroides and Bifidobacterium, enrichment of pathobionts such as Escherichia and Enterococcus, and diminished levels of the short-chain fatty acids (SCFA), which were inversely correlated with disease severity. Experimental models have demonstrated that fecal microbiota transplantation (FMT) and probiotic supplementation with strains like Bifidobacterium ameliorate symptoms by restoring Th17/Treg equilibrium, suppressing the expression of pro-inflammatory cytokines including IL-6 and TNF-α, and enhancing intestinal barrier integrity. Mechanistically, gut dysbiosis exacerbates autoimmunity via NF-αB pathway activation, disrupts tryptophan metabolism and impairs gut-brain signaling. While existing studies have established microbiota-MG associations, further causal validation, personalized therapeutic strategies, and multi-omics integration remain critical priorities. Microbiota-targeted interventions, including precision FMT and metabolite delivery, hold translational potential, but their validation via large-scale randomized controlled trials and interdisciplinary approaches like AI-driven microbiota profiling is essential if they are to advance precision medicine for MG management.

Programmed death (PD-1) is an important immune checkpoint receptor expressed on the surface of T cells, B cells and natural killer (NK) cells. PD-L1 (B7-H1) is a critical ligand for PD-1, and is widely expressed in a variety of cancer cells, immune cells, and normal histocytes. It has been established that the PD-1/PD-L1 interaction can produce an immunosuppressive effect by suppressing T cell proliferation, cytokine secretion, and cytotoxicity. Currently, PD-1 and PD-L1 inhibitors are known to be promising anticancer agents that reverse the antitumor immune function of T cells by inhibiting the PD-1/PD-L1 axis. The monotherapy of PD-1/PD-L1 blockade, while effective in treating cancers, is limited by a low response rate, immune-related adverse events (irAEs), and drug resistance. Their combinations with surgery, chemotherapy, radiotherapy, immunotherapy, hormone therapy, and traditional Chinese medicine (TCM), due to a synergistic effect, have broadened the frontier of cancer research. Following a holistic principle, TCM serves as an adjuvant therapy with PD-1/PD-L1 blockade, and provides benefits through complicated mechanisms. We specifically focused on the profound significance of TCM's assistance of PD-1/PD-L1 blockade, and the opportunities and challenges of treating cancers with both TCM and PD-1/PD-L1 blockade.

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.

Ulcerative colitis (UC) is a common, chronic, and nonspecific inflammatory bowel disease which significantly impair patients' quality of life, and is characterized by a prolonged disease course and frequent relapses. Due to their localized therapeutic action and low incidence of adverse effects, Chinese herbal enemas have garnered increasing attention in clinical settings. This study aims to systematically evaluate the therapeutic potential of Chinese herbal enemas in UC management. Randomized controlled trials (RCTs) evaluating Chinese herbal enemas for UC, published up to April 19, 2025, were systematically searched. A network meta-analysis was performed using Stata 17.0, and the combined effect sizes were reported as the mean difference or relative risk with corresponding 95% confidence intervals. A total of 41 RCTs involving 2883 UC patients were ultimately included, and data on the risk of bias assessment were reported. When compared with mesalazine (MES) monotherapy, combination therapies, such as MES combined with Qingbai Guanchang Ye or MES combined with Qingchi San, and monotherapies including Huangkui Lianchang Tang and Baitouweng Tang, demonstrated statistically significant improvements in clinical outcomes. Subgroup analyses were also conducted. The clinical effectiveness of these interventions was also influenced by Traditional Chinese Medicine (TCM) syndrome differentiation and disease severity, which underscores the importance of individualized, stratified treatment approaches. Our study data showed that Chinese herbal enema therapy appears to be both clinically effective and safe in the management of UC, and supported both stratified TCM therapy and the refinement of UC treatment guidelines. Future research is needed to prioritize high-quality, large-scale RCTs to validate these findings.

Diabetic nephropathy (DN) is a serious complication of diabetes mellitus, and the efficacy of standard clinical therapies is presently limited. Evidence has shown that pyroptosis-mediated cell death promotes several diabetic complications including DN. Tanshinone IIA (Tan IIA), the main fat-soluble component of S. miltiorrhiza Bunge, possesses anti-inflammatory and anti-oxidant properties. However, its impact on pyroptosis in DN progression and the underlying molecular mechanisms remain unclear. The aim of this study was to investigate the effect of Tan IIA on pyroptosis in DN. To establish a DN mouse model, STZ was administered to the mice for five consecutive days via injection. The mice in the treatment group then received Tan IIA by gavage for 10 weeks. Our data revealed that Tan IIA inhibited caspase-1 and gasdermin D (GSDMD)-mediated pyroptosis and thereby alleviated renal injury. Compared with that of the DN mice or high glucose-evoked HK-2 cells, the silent information regulator 1 (SIRT1) expression was significantly elevated, and the NLR family pyrin domain containing 3 (NLRP3) expression was dramatically decreased following Tan IIA treatment. Most importantly, the suppression of SIRT1 remarkably abrogated both the protective effects of Tan IIA against DN and its inhibition on pyroptosis-related molecules. Collectively, our results suggest that Tan IIA protects against DN by inhibiting caspase-1 and GSDMD-mediated pyroptosis through the SIRT1/NLRP3 pathway.

Traditional Chinese Medicine (TCM) has a longstanding history in the treatment of fatigue-related conditions, and is increasingly recognized as a foundation for novel therapeutic approaches. The Panax genus, extensively utilized in the fundamental TCM principles to enhance vitality, modulate immune function, and stimulate Yang energy, is a key resource in managing both physiological and pathological fatigue. This study provides a comprehensive synthesis of recent advancements in plant-derived metabolites from various Panax species with an emphasis on their structural diversity and structure-activity relationships. Notably, this represents the first systematic exploration of Panax metabolites with potential antifatigue effects. A systematic literature review was conducted using major scientific databases such as PubMed, Google Scholar, and ScienceDirect. The search query "(scientific name of herbal medicine in the Panax genus) AND ("antifatigue")" was employed. Additionally, classical herbals, botanical literature, and pharmacopoeias were reviewed to contextualize the findings. Comprehensive analysis of 105 studies elucidated 16 predominant metabolites exhibiting antifatigue activity. These metabolites primarily originated from Panax ginseng, Panax quinquefolium, and Panax notoginseng. Ginsenosides Rb1 and Rg1 demonstrated the most substantial pharmacological efficacy in experimental models, in particular by ameliorating metabolic perturbations and mitigating oxidative stress in vivo. Clinical trials predominantly relied on subjective patient-reported measures, such as the Multidimensional Fatigue Inventory (MFI) and Visual Analogue Scale (VAS), and yielded largely positive outcomes. These findings substantiate fundamental TCM principles and reinforce the therapeutic potential of Panax species in fatigue management. The integration of traditional knowledge with contemporary biomedical research enhances the understanding and clinical applicability of Panax species in addressing fatigue-related disorders.

Diabetic kidney disease (DKD) is one of the most common microvascular complications associated with diabetes mellitus. However, the existing treatment approaches, aimed at delaying the onset of DKD, exhibit limited efficacy. The flavonoid nobiletin has demonstrated substantial lipid-lowering and insulin-sensitizing effects in mice exhibiting metabolic dysfunction, but the therapeutic potential and mechanism of nobiletin in the context of DKD remains to be comprehensively elucidated. In this study, the active components of polymethoxylated flavonoids (PMFs) were identified via UPLC. A DKD rat model was established through a high-fat diet and the administration of streptozotocin via intraperitoneal injection. The effect and mechanism of nobiletin on DKD was evaluated by histological, biochemical, molecular, and multi-omics analysis. We found that treatment with PMFs and nobiletin inhibited ferroptosis and EMT in high glucose and insulin-induced models, protected the glomerular filtration barrier integrity, and concurrently suppressed ROS, Fe[Formula: see text], and MDA while increasing the GSH level. Animal experiments indicated that nobiletin treatment markedly impeded the progression of DKD and alleviated both EMT and endothelial dysfunction. Moreover, nobiletin significantly preserved the integrity of the intestinal barrier and enriched the diversity of gut microbiota. In conclusion, our findings indicate that nobiletin could attenuate DKD and concomitantly limit ferroptosis and EMT, and that the gut-kidney axis played an important role in its effects.

Type 2 diabetes mellitus (T2DM), a globally prevalent chronic metabolic disorder, imposes a significant worldwide public health burden. As a vital "microbial organ" within the human body, the balance of the gut microbiota (GM) structure and function is crucial for maintaining host metabolic health. Short-chain fatty acids (SCFAs), the metabolic products of GM, serve as key signaling molecules that play central roles in maintaining intestinal homeostasis, regulating systemic energy metabolism, and improving insulin sensitivity. Dysregulation of the "GM-SCFA axis" has emerged as a core pathological mechanism in the onset and progression of T2DM. Traditional Chinese Medicine (TCM) possesses unique advantages in T2DM treatment through its "holistic regulation and multi-targeted intervention," which enables precise modulation of the GM-SCFA axis. This paper provides a systematic review of the pathological mechanisms by which dysregulation of the GM-SCFA axis induces T2DM, and specifically covers energy metabolism disorders, insulin resistance, intestinal barrier impairment, chronic low-grade inflammatory activation, abnormal bile acid metabolism regulation, and disrupted gut-pancreatic axis and gut-brain axis signaling. Using keywords such as TCM, GM, SCFAs, and T2DM, we conducted an extensive literature search across databases including PubMed, Google Scholar, and Web of Science for publications from the past decade. This systematic review examines the application of TCM in regulating the "GM-SCFA axis" from multiple perspectives: Chinese herbal compounds (e.g., Zuogui Jiangtang Qinggan Formula, Gegen Qinlian Decoction), Chinese patent medicines (e.g., Shouhui Tongbian Capsules, Compound Danshen Dripping Pills), single-herb Chinese medicines (e.g., Edgeworthia gardneri, Alpinia oxyphylla), single-component compounds from TCM (e.g., Cyclocarya paliurus polysaccharide, Achyranthes bidentata polysaccharide water-soluble 1), and other TCM therapies (e.g., tuina, acupuncture). This study aims to systematically explore the mechanisms by which dysregulation of the "GM-SCFA axis" induces T2DM while providing novel therapeutic strategies for T2DM prevention and treatment using TCM. It also seeks to establish scientific foundations for developing novel TCM intervention strategies targeting the "GM-SCFA axis" in T2DM management.

Polygonati Rhizoma (PR), a plant with dual medicinal and edible properties, has been utilized for over two millennia, and is widely distributed across temperate to frigid zones in the Northern Hemisphere. In ancient China, it was revered as the "immortals' surplus grain," and the classical medical text "Ming Yi Bie Lu" documents its health benefits. These benefits include "tonifying the middle jiao, replenishing qi, dispelling rheumatism, and harmonizing the five viscera," which particularly emphasizes the efficacy of PR in both nourishing the liver and kidneys and prolonging lifespan. Modern studies reveal that PR rhizomes are rich in fructans, non-starch polysaccharides, amino acids, and other nutritional components, and their primary active constituents include polysaccharides, saponins, flavonoids, and polyphenols. These compounds exhibit anti-aging, antidepressant, anti-osteoporotic, and neuroprotective activities. Notably, raw PR contains calcium oxalate raphides, which induce an irritating sensation in the throat. However, processing can not only mitigate this irritation but also enhance its anti-oxidant and anti-aging capacities. Although progress has been made toward understanding its polysaccharides and saponins, the mechanisms underlying its other critical components, such as flavonoids, polyphenols, and oligosaccharides, remain underexplored. This review systematically examines the geographic distribution, traditional and modern applications, and pharmacological activities of PR, and the transformation patterns of key bioactive constituents that occur during its processing. Furthermore, it critically addresses research gaps, and particularly addresses both the relative lack of mechanistic studies on functional components and the lack of correlation between processing-induced compositional changes, pharmacological efficacy, and quality control. These insights contribute to advancing PR exploration, promoting sustainable utilization, and establishing scientific evidence-based quality standards.

Liver diseases pose a significant challenge in global public health, and scientific prevention and treatment strategies have become particularly crucial. Silybin, a flavonoid and active ingredient extracted from the traditional Chinese medicinal herb milk thistle, is the most critical effective component in silymarin, and has clearly demonstrated potent anti-oxidative stress capabilities. This unique attribute makes it a highly promising drug candidate for treating acute hepatitis, chronic hepatitis, cirrhosis, liver cancer, and other liver diseases. In the progression of liver diseases, silybin exerts significant therapeutic effects via dual anti-oxidant and anti-inflammatory mechanisms through which it alleviates the inflammatory response in acute hepatitis, stabilizes the progression of chronic hepatitis, and promotes the benign transition from decompensated to compensated cirrhosis. This study comprehensively reviews research findings on silybin in treating liver diseases via this anti-oxidative stress mechanism over the past few decades, and offers a particular focus on the development of novel drug formulations based on the oxidative stress pathogenesis of liver diseases. These formulations target the CD44 receptor, retinol/vitamin A, CXCR4 receptor, glycyrrhetinic acid receptor, GLUT4 protein, NS5B protein, and SPARC. It also examines the current status of the anti-oxidant and anti-inflammatory applications of silybin formulations in global liver disease treatments. However, more high-quality, detailed experimental studies are needed to explore its exact efficacy and safety so as to provide a stronger scientific basis for the widespread application of silybin in liver disease treatment.