The American journal of Chinese medicine最新文献

The gut microbiota serves as a crucial modulator of host immunity and plays a pivotal role in regulating airway inflammation, maintaining immune balance, and affecting the course of associated diseases through gut-lung axis interactions. Recent studies increasingly demonstrate that patients with chronic inflammatory airway diseases (CIAD) commonly exhibit gut dysbiosis. This imbalance in gut microbiota can promote pulmonary inflammation and airway remodeling by affecting the synthesis of short-chain fatty acids (SCFAs), impairing intestinal mucosal barrier integrity, and disrupting immune regulation. With increasing attention to the gut-lung axis, microbiota-targeted therapeutic strategies have attracted growing attention. Traditional Chinese medicine (TCM), characterized by its multi-component composition, multi-target approach, and holistic regulatory properties, holds unique advantages in restoring gut microbial balance for the treatment of CIAD. This paper systematically reviews the therapeutic potential of TCMs and their bioactive constituents in managing CIAD through gut microbiota modulation. By regulating gut microbial composition and stimulating the generation of SCFAs, TCMs exert anti-inflammatory, immunomodulatory, and gut barrier-protective effects. TCMs thus offer novel perspectives and promising therapeutic strategies for CIAD treatment.

As cancer continues to pose a significant threat to human health, the search for effective therapeutic agents has become a critical focus in medical research. Cordyceps is a fungus used in traditional Chinese medicine (TCM) valued for its potential health benefits, which include boosting energy, supporting the immune system, and acting as an anti-oxidant. Cordycepin, also known as 3[Formula: see text]-deoxyadenosine, is a bioactive nucleoside derived from Cordyceps. This compound recently has garnered widespread attention for its potential anticancer properties. Through systematic integration of our prior experimental evidence with literature retrieval from PubMed, we confirmed its efficacy in inducing apoptosis, suppressing proliferation, and blocking metastasis across a broad range of cancer types. These effects are primarily attributed to its modulation of key signaling pathways, such as MAPK, AMPK, mTOR, and Wnt/[Formula: see text]-catenin, all of which play crucial roles in various malignant conditions. In addition, cordycepin's ability to modulate immune responses through the regulation of adenosine receptor (AR), and in particular the A3 adenosine receptor (A3AR), has gained attention as an innovative strategy for enhancing the effectiveness of immunotherapy. Recent advancements in improving cordycepin's biostability, bioavailability, and transport efficiency within the body system have further supported the clinical application of this compound in medical oncology. This review highlights key research findings and explores promising future directions with the aim of contributing to ongoing studies in cancer management.

Ischemic stroke seriously endangers both the health and quality of life of patients. The gut microbiota, which plays a crucial role in modulating communication between the gut and the nervous system, has emerged as a promising target for therapeutic interventions in stroke. Electroacupuncture (EA), which is associated with intestinal immunity, has been proven to exert significant beneficial effects in ischemic stroke, but its exact mechanism remains unclear. In this study, we investigated the regulatory mechanism of EA on the microbiome-gut-brain axis following ischemic stroke. In rat models of ischemic stroke, EA treatment significantly reduced cerebral infarct volume and neuronal damage following cerebral ischemia-reperfusion injury, and also modulated the composition, diversity, and taxonomic distribution of the gut microbiota. Fecal microbiota transplantation from EA-treated donors significantly reduced cerebral infarct volume and neuronal damage in the ischemic hemisphere of recipient mice, and likewise upregulated Treg cell expression to suppress immune-inflammatory responses in the brain. These results indicate that, through modulation of the gut microbiota, which in turn regulates Treg-mediated immune-inflammatory responses, EA ameliorates cerebral ischemic injury to thereby improve the prognosis of ischemic stroke patients. This study provides new perspectives on the efficacy of EA in the treatment of ischemic stroke.

Acetaminophen (APAP)-induced liver injury (AILI) is a universal liver disease and the predominant cause of acute liver failure in clinical practice. Autophagy is a highly conserved intracellular degradation pathway, with accumulating evidence indicating its involvement in APAP hepatotoxicity. Notably, the serine/threonine AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/unc-51-like kinase 1 (ULK1) pathway serves as the most classical autophagy pathway and engages in autophagy activation. Thus, pharmacological activation of the AMPK/mTOR/ULK1 pathway has emerged as a critical strategy for addressing AILI. Chlorogenic acid (CGA), a main bioactive constituent isolated from Lonicera japonica Thunb., is an autophagy regulator with potential for AILI therapy. However, whether and how CGA modulates autophagy to antagonize AILI has not yet been elucidated. In the present study, we aim to explore the impact of CGA on AILI, as well as the underlying mechanisms in vitro and in vivo. The results demonstrated that CGA could protect the mice and LO2 cells from oxidative stress and liver injury induced by APAP. Regarding mechanisms, CGA activated the AMPK/mTOR/ULK1 pathway, thereby promoting autophagy. This was evidenced by the degradation of p62/SQSTM1 (hereafter referred to as p62), as well as the up-regulation of LC3B, ATG5, and Beclin1. It is worth noting that the aforementioned, CGA-provided beneficial effects were abrogated by pharmacological inhibition of AMPK with Compound C (CC, an AMPK inhibitor). These [Formula: see text] that CGA alleviates oxidative stress and liver injury induced by APAP, which is contingent upon the regulatory effect of CGA on the AMPK/mTOR/ULK1 axis.

The pathogenesis of chronic hepatitis B (CHB) involves complex mechanisms, and hepatitis B virus (HBV)-induced immune responses play a central role in hepatocyte injury and inflammatory necrosis. CHB infection not only drives liver pathology but also demonstrates significant extrahepatic associations which include depression, cognitive dysfunction, diabetes mellitus, insomnia, non-alcoholic fatty liver disease, and thrombocytopenia. Conventional Western medicine primarily employs antiviral therapy but faces limitations which include low hepatitis B surface antigen clearance rates and frequent adverse drug reactions. In contrast, traditional Chinese medicine demonstrates therapeutic advantages in CHB management which are exemplified by Artemisia capillaris, Xiaochaihu Decoction and Fuzheng Huayu Tablet. Through its modulation of immune pathways and intervention in key HBV lifecycle targets, traditional Chinese medicine achieves a tripartite therapeutic synergy that combines immune reconstitution, viral suppression, and hepatic repair. Chinese medical interventions exhibit characteristic multi-ingredient, multi-target mechanisms that possess immunomodulatory effects in CHB management. Future research should employ modern technologies to elucidate these mechanisms further and thus facilitate the development of optimized treatment protocols. Standardized therapeutic approaches derived from such evidence will hold significant clinical value.

As reperfusion therapy becomes more common, cerebral ischemia-reperfusion (I/R) injury has emerged as a notable factor affecting the outcome of ischemic stroke. The intricate pathological mechanisms involved include oxidative stress, neuroinflammation, and various forms of cell death, characterized by interactions between multiple signaling pathways. Natural products, such as traditional Chinese medicines (TCMs), offer multi-targeted intervention effects through their diverse natural active compounds and integrate pharmacological and nutritional functions into 1 entity (Food and Medicine Homology), supporting their long-term use to prevent cerebral I/R injury. It was found that TCMs, such as Gastrodia elata Blume and Lycium barbarum L., potentially exert synergistic effects on redox imbalance, inflammation, apoptosis, and autophagy by concurrently modulating various pathways, including Nrf2/ARE, NF-κB, PI3K/Akt/mTOR, Bcl-2/Bax, and PARP-1. The prophylactic administration of TCMs may represent a novel approach for mitigating cerebral I/R injury. To advance the application of TCMs from the laboratory to clinical practice, it is essential to conduct clinical research to confirm their effectiveness and safety in preventing cerebral I/R injury.

Rhizoma Anemarrhenae, in which the primary active components are saponins, has shown potential in treating Alzheimer's disease (AD). However, the specific mechanisms of action and the active saponins responsible remain unclear. This study aimed to explore the mechanisms of action and identify the active components of Rhizoma Anemarrhenae saponins (RAS). First, 24 saponin components in RAS and eight absorbed saponins in rats were identified. Then, a component-target interaction network between eight saponins and 83 targets was constructed after target refinement and SPR validation. Bioinformatics analysis indicated that these targets were closely related to lipid metabolism, iron metabolism, and the AMPK signaling pathway. In addition, differentially expressed genes from RAS intervention were significantly enriched in the ferroptosis pathway. In vitro and in vivo assays demonstrated that RAS could inhibit neuronal ferroptosis and alleviate cognitive impairment. Notably, the ferroptosis inducer markedly reversed the neuroprotective effects of RAS. Moreover, silencing AMPK or Nrf2 using the siRNA or AMPK inhibitor abolished the neuroprotective and ferroptosis-inhibitory effects of RAS in vivo or in vitro. Silencing LKB1 reversed the RAS-induced activation of the AMPK/Nrf2 pathway, and co-immunoprecipitation assay revealed that RAS could promote the LKB1-AMPK interaction. Finally, a 2D comprehensive NC/CMC system was used to screen out four potential saponins that inhibit neuronal ferroptosis, with Timosaponin B-III, Timosaponin A-I, and Timosaponin A-III being validated. In conclusion, RAS exerts anti-AD effects by enhancing the LKB1-AMPK interaction, and activating the AMPK/Nrf2 pathway, inhibiting neuronal ferroptosis as a result. Three saponins are identified as the active components potentially responsible for this effect.

More than one billion people worldwide suffer from hypertension, and essential arterial hypertension is in particular a major risk factor for cardiovascular diseases. These conditions can lead to complications such as stroke, renal failure, cardiac hypertrophy, and heart failure. Despite extensive research on various antihypertensive drugs, an increasing number of people are unable to effectively control their hypertension. Further optimization of their treatment is required. Given the pathogenesis of hypertension, natural products (NPs) have emerged as a promising source of potential antihypertensive agents. NPs can prevent the development of hypertension by targeting oxidative stress, inflammation, vascular remodeling, and neurohormonal pathways. These targets provide the foundation for the application of NPs in clinical treatment. This review assesses NPs with potential antihypertensive activities published between 2019 and 2024. A total of 70 unique NPs were identified through PubMed and Web of Science. Seventy unique NPs were categorized into flavonoids (20 compounds), terpenoids (24 compounds), alkaloids (17 compounds), and plant-derived extracts (9 species). These products were classified according to their structural frameworks, and their bioactivities were briefly summarized. Future research should prioritize NPs with dual anti-oxidant/anti-inflammatory properties for clinical experiments, advanced delivery systems for improved bioavailability, and interdisciplinary approaches integrating synthetic biology for scalable production.

With the continuous advancements in modern medicine, significant progress has been made in the treatment of lung cancer. Current standard treatments, such as surgery, chemotherapy, radiotherapy, targeted therapy, and immunotherapy, have notably improved patient survival. However, the adverse effects associated with these therapies limit their use and impact the overall treatment process. Traditional Chinese medicine (TCM) has shown holistic, multi-target, and multi-level therapeutic effects. Numerous studies have highlighted the importance of TCM's role in the comprehensive management of lung cancer, demonstrating its benefits in inhibiting tumor growth, reducing complications, mitigating side effects, and enhancing the efficacy of conventional treatments. Here, we review the main mechanisms of TCM in combating lung cancer, inducing cancer cell cycle arrest and apoptosis. These include inhibiting lung cancer cell growth and proliferation, inhibiting cancer cell invasion and metastasis, suppressing angiogenesis and epithelial-mesenchymal transition (EMT), and modulating antitumor inflammatory responses and immune evasion. This paper aims to summarize recent advancements in the application of TCM for lung cancer, emphasizing its unique advantages and distinctive features. In promoting the benefits of TCM, we seek to provide valuable insights for the integrated treatment of lung cancer.

Diabetic kidney disease is one of the most significant comorbidities of diabetic patients, and has become the second cause of end-stage renal disease. Current clinical management programs have difficulty in reducing morbidity and poor prognosis, and thus new treatment options and concepts need to be developed. Traditional Chinese medicine formulae and Chinese patent medicines contain a variety of medicinal flavors, laying the material foundation for the multi-target, multi-level therapeutic features. This study describes the main pathologic features of DKD as well as its pathogenesis. Additionally, the categorization of TCM according to its different therapeutic mechanisms is discussed, and the signaling pathways targeted and corresponding biological effects are described in detail. For example, TCM formulae can alleviate oxidative stress through pathways such as Nrf2 and NOX4, can inhibit the development of inflammation through pathways such as TGF-β and NF-κB, and can ameliorate DKD by inhibiting endoplasmic reticulum stress and apoptosis. Moreover, it highlights the superior efficacy of the combined application of TCM formulae and Western medicine over Western medicine alone, which can compensate for the shortcomings of existing DKD treatment methods to a certain extent. TCM formulae and CPMs are promising candidates for the auxiliary treatment of DK, however, the lack of clarity regarding the active ingredients intensifies the difficulty of integrating TCM formulae and CPMs into clinical practice. Further research is warranted to explore the material basis and molecular mechanisms of action of TCM formulae against DKD.