The American journal of Chinese medicine最新文献

Colorectal cancer, characterized by its high incidence, concealed early symptoms, and poor prognosis at advanced stages, ranks as the third leading cause of cancer-related deaths worldwide. Astragalus membranaceus (AM) refers to the dried roots of Astragalus membranaceus (Fisch.) Bge. var. mongholicus (Bge.) Hsiao and Astragalus membranaceus (Fisch.) Bge. In the theory of Traditional Chinese Medicine (TCM), it is believed to have the functions of tonifying qi and lifting yang, as well as generating body fluids and nourishing blood. It can effectively treat cancer caused by the deficiency of vital energy and susceptibility to external diseases. Modern research has confirmed that the active components of AM, including Astragalus polysaccharides, flavonoids (formononetin and calycosin), Astragalus saponins (Astragaloside I and Astragaloside III), and Astragalus nanovesicles, are effective in the treatment of colorectal cancer. The mechanisms mainly involve inducing apoptosis, inhibiting tumor angiogenesis and the metastasis of cancer cells, regulating the cell cycle and tumor microenvironment, and reversing drug resistance. Moreover, it offers a synergistic enhancement when used in combination with chemotherapy, radiotherapy, targeted therapy, or surgical treatment. AM also has great potential in treating colorectal cancer when combined with other herbs. This review summarizes the relevant research findings on the treatment of colorectal cancer with AM, as well as its main pharmacological effects and molecular mechanisms, aiming to provide guidance for the development of new drugs, and offer direction for the conduct of more related research and promoting the development and application of AM.

Myocardial ischemia/reperfusion (I/R) injury is characterized by severe inflammation and oxidative stress, and involves the recruitment and activation of immune cells, the release of pro-inflammatory cytokines, and the generation of reactive oxygen species (ROS). The NOD-like receptor protein 3 (NLRP3) inflammasome, a multiprotein complex, is activated when exposed to different danger signals like excessive ROS, changes in ionic flux, and mitochondrial dysfunction. Once the NLRP3 inflammasome is activated, it promotes the maturation and release of pro-inflammatory cytokines such as interleukin-1β and interleukin-18, which contributes to the inflammatory storm in myocardial I/R injury. This inflammatory cascade not only leads to adverse cardiac remodeling but also impairs cardiac function, ultimately exacerbating the clinical outcomes of myocardial infarction. Despite the critical role of the NLRP3 inflammasome in myocardial I/R injury, there is a significant absence of effective therapeutic strategies to address it in clinical practice. In recent years, Chinese herbal medicine has emerged as a promising candidate in the therapeutic landscape of myocardial I/R injury. Chinese herbal medicine exerts its cardioprotective effects through various mechanisms of inhibiting NLRP3 inflammasomes, including enhancing mitochondrial function, reducing ROS generation, inhibiting the release of pro-inflammatory cytokines, and suppressing pyroptosis. This review emphasizes the therapeutic potential of Chinese herbal medicine and its extracts to inhibit NLRP3 inflammasomes in an effort to develop effective treatments for myocardial I/R injury. It likewise summarizes the research results of Chinese herbal medicine interventions for myocardial I/R injury by the mechanism of regulating the NLRP3 inflammasome, providing insights for the development of effective treatments for myocardial I/R injury.

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.

Ferroptosis has emerged as a critical contributor to the pathogenesis of chronic kidney disease (CKD). Quercetin, a promising therapeutic agent and flavonoid with potential antiferroptotic properties, has demonstrated renoprotective effects. However, its molecular mechanisms remain unclear. This study integrated bioinformatics, network pharmacology, and molecular docking to identify the epithelial growth factor receptor (EGFR) as a key target of quercetin. In folic acid (FA)-induced CKD mice, quercetin decreased renal fibrosis (reducing [Formula: see text]-SMA, collagen I, and fibronectin), suppressed ferroptosis markers (including iron accumulation, malondialdehyde [MDA] levels, and acyl-CoA synthetase long-chain family member 4 [ACSL4] expression), and downregulated EGFR. In FA-stimulated HK-2 cells, quercetin inhibited epithelial-mesenchymal transition (by decreasing N-cadherin and fibronectin) and ferroptosis (by lowering iron, MDA, and ACSL4) while suppressing EGFR expression. Pharmacological inhibition and genetic knockout of EGFR in HK-2 cells confirmed that EGFR blockade alleviated FA-induced renal fibrosis and ferroptosis. These findings demonstrate that quercetin mitigates FA-induced renal fibrosis by inhibiting tubular epithelial ferroptosis via the EGFR/ACSL4 signaling axis, and thus highlights its therapeutic potential in CKD.

Atherosclerosis (AS) is a risk factor for cardiovascular complications, induced by Type 2 diabetes mellitus (T2DM), which greatly increases the mortality of patients. Previous studies explored the potential molecular mechanism of Platycodin D (PD) in its capacity as a treatment of AS through network pharmacology, and obtained the potential targets of PD treatment of AS. Therefore, this paper conducted a more in-depth study on the anti-Type 2 diabetes mellitus-Atherosclerosis (T2DM-AS) activity of PD. By establishing a T2DM-AS mice model induced by high-fat diet (HFD) combined with streptozotocin (STZ), and human umbilical vein endothelial cell (HUVEC) injury models induced by lipopolysaccharide (LPS), both the NLRP3 inflammatory body and endoplasmic reticulum stress (ERS) were studied. This study focused on ERS activation to explore the regulatory effect and mechanism of PD on the inflammation and apoptosis of aorta and endothelial cells. It was found that PD (2.5[Formula: see text]mg/kg) could improve early AS inflammation and lipid translocation deposition in T2DM mice. PD could also alleviate the LPS-induced apoptosis of HUVECs at concentrations of 0.5, 1, and 2[Formula: see text][Formula: see text]M by regulating the PI3K/AKT pathway, and ameliorate inflammation by inhibiting the activation of the NLRP3 inflammasome and the NF-[Formula: see text]B pathway. Both in vivo and in vitro experiments showed that PD could regulate the activation of NLRP3 inflammasome, inhibit endothelial cell inflammation and cell apoptosis caused by ERS, and improve AS inflammation and lipid deposition in the early stage of T2DM by restoring damaged cell function. This study provided a theoretical reference for its clinical treatment and the development and application of health care products.

Sijunzi Decoction (SJZD), a classic traditional Chinese medicine formula, is primarily composed of Panax ginseng, Atractylodes macrocephala, Poria cocos, and Glycyrrhiza uralensis. This review aimed to provide a comprehensive overview of SJZD's traditional uses, chemical composition, pharmacological actions, and clinical applications, with a particular emphasis on its potential role in cancer therapy. The review also aims to identify the gaps in current knowledge and suggest directions for future research on SJZD. Research shows that this formula contains various chemical compounds, including saponins, flavonoids, and polysaccharides, which have significant pharmacological effects such as enhanced immune function, antitumor activity, and inhibition of tumor cell invasion and metastasis. Clinically, SJZD has evolved from its traditional gastrointestinal applications to demonstrate chemo-adjuvant potential by virtue of its characteristic detoxification-potentiation duality. Studies have revealed its ability to enhance patients' quality of life through immune modulation and the mitigation of chemotherapy-induced toxicity effects (e.g., myelosuppression and gastrointestinal reactions), while preclinical evidence suggests potential efficacy-enhancing synergies with conventional antitumor agents. However, further research on SJZD, and in particular, comprehensive studies of its chemical composition, large-scale clinical trials, and interdisciplinary collaboration, is needed. Future research is expected to reveal the underlying mechanisms of action, and provide new ideas and methods for cancer treatment.

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.