The American journal of Chinese medicine最新文献

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.

Inflammation is a pathological process implicated in a wide range of diseases, and is orchestrated by complex regulatory networks at both transcriptional and post-transcriptional levels. A growing body of evidence supports the understanding that numerous natural compounds exhibit robust anti-inflammatory activity, structural diversity, low toxicity, and minimal side effects. These qualities make them promising leads for therapeutic development. Within the framework of Traditional Chinese Medicine (TCM), which has been extensively applied in the management of chronic conditions, specific herbal remedies, such as Paeonia lactiflora for rheumatoid arthritis, and Angelica sinensis and Codonopsis pilosula for cardiovascular regulation, have clinically relevant efficacy. In recent years, bioactive peptides (BAPs) derived from Chinese medicinal herbs, including peptides from Cordyceps sinensis and Panax ginseng, have drawn considerable international attention for their anti-inflammatory potential. This review delineates the principal methodologies for the extraction, isolation, and purification of anti-inflammatory peptides derived from medicinal herbs, highlights recent advances in their therapeutic application for inflammatory disorders, critically assesses existing barriers to clinical translation, and outlines future research priorities.

Notoginsenoside R1 (NGR1), a natural triterpenoid saponin, is extracted from Panax notoginseng, and has cardiovascular and cerebrovascular protective effects due to anti-inflammatory, anti-oxidant, and anti-apoptotic properties. Previous research has suggested a protective role for NGR1 in myocardial ischemia/reperfusion (MI/R) injury. However, the potential mechanisms involved have not been fully elucidated. Thus, the objective of our study was to validate the protective role of NGR1 in MI/R injury and to investigate its underlying mechanisms. Results showed that, in mice, NGR1 substantially improved heart function, reduced infarct area, and inhibited cardiomyocyte apoptosis. Mechanistically, network pharmacological predictions suggested that NGR1 could inhibit apoptosis by activating the Wnt signaling pathway. Experimentally, the protective effects of NGR1 in inhibiting cardiomyocyte apoptosis, improving cardiac function, and reducing infarct size were significantly attenuated with the use of the Wnt signaling inhibitor XAV-939. Collectively, our investigation demonstrated that NGR1 improves myocardial injury triggered by ischemia/reperfusion (I/R) by enhancing Wnt/[Formula: see text]-catenin pathway activity, which in turn suppresses apoptosis.

The aim of this study was to evaluate the therapeutic effect of puerarin (PUE) on alcoholic liver disease (ALD) and elucidate the potential mechanism from the perspective of lipolysis and hepatic steatosis. Assessment of PUE efficacy against ALD was performed using serum biochemical parameters and the histological examination of liver and adipose tissue via Hematoxylin and eosin (H&E) staining. The potential mechanisms underlying the amelioration of ALD by PUE were investigated using Western blotting (WB) analysis and immunofluorescence (IHC) staining. We demonstrated that PUE attenuated steatosis in ALD by alleviating ethanol-induced liver damage and lipid accumulation, suppressing the expression of lipid synthesis genes, upregulating the expression of lipid metabolism genes, and reducing lipolysis by inhibiting adipose triglyceride lipase (ATGL) activation and the phosphorylation of hormone-sensitive lipase (HSL). In conclusion, PUE ameliorates ALD by inhibiting the sympathetic outflow-mediated activation of key lipolysis enzymes ATGL and HSL. These findings provide a solid theoretical foundation for the potential application of PUE in the clinical treatment of ALD.

Liver cirrhosis is a critical stage in the progression of various chronic liver diseases, often leading to severe complications such as ascites, hepatic encephalopathy, and a high mortality rate, and it thus poses a serious threat to patient life. The activation of hepatic stellate cells is a central driver of disease progression. Cellular autophagy, a lysosome-mediated degradation process, plays a key role in maintaining cellular function and dynamic homeostasis. Research has shown that autophagy is closely associated with proteins like LC3, Beclin-1, P62, and mTOR, and is regulated through signaling pathways such as PI3K/Akt/mTOR, Ras/Raf/MEK/ERK, and AMPK/mTOR. Additionally, the relationship between autophagy and apoptosis, as well as between autophagy and exosomes, has been further demonstrated. While modern medicine has made progress in treating cirrhosis, it still faces significant limitations. By contrast, numerous studies have demonstrated the efficacy of traditional Chinese medicine in preventing and treating liver cirrhosis by regulating autophagy, with fewer adverse effects. Chinese herbal monomers and formulations can modulate various autophagy-related signaling pathways, including PI3K/Akt/mTOR, Ras/Raf/MEK/ERK, and AMPK/mTOR, and influence key autophagy proteins such as LC3 and Beclin-1. This modulation inhibits hepatic stellate cell activation, reduces extracellular matrix deposition, and exerts anticirrhotic effects. Moreover, Chinese medicine appears to reduce adverse reactions in cirrhosis treatment and lower the risk of disease recurrence. This review explores the mechanisms of autophagy in the prevention and treatment of liver cirrhosis through Chinese medicine, offering new insights for the development of Chinese medicinal therapies for cirrhosis and their rational clinical application.

The growing global burden of metabolic syndrome (MetS), a key driver of multiple chronic diseases, highlights the limited treatment options for its multifactorial pathophysiology. Tanshi-Tiaoti Decoction (TTD), a Chinese herbal formula comprised of Citri Reticulatae Pericarpium (Tangerine peel), Coicis Semen (Raw coix seed/Job's tears), Raphani Semen (Radish seed), Nelumbinis Folium (Lotus leaf), Eckloniae/Laminariae thallus (Kelp), and Crataegi Fructus (Raw hawthorn fruit), demonstrates efficacy in the clinical management of MetS. However, its underlying molecular mechanisms remain incompletely elucidated. This study indicates that TTD restored gut microbiota homeostasis and bile acid (BA) profiles in high-fat diet (HFD)-induced MetS mice. TTD significantly attenuated body weight gain, fasting glucose levels, serum triglycerides, and hepatic steatosis. TTD corrected gut microbiota dysbiosis, most notably by reducing the Firmicutes/Bacteroidetes ratio. Fecal microbiota transplantation (FMT) validated the fact that the gut microbiome mediates TTD's therapeutic effects. TTD regulated BA biosynthesis through this microbial modulation, and thus specifically increased hyodeoxycholic acid (HDCA). HDCA, which has been identified as the signature BA during TTD treatment, phenocopied TTD's therapeutic effects against MetS by both activating the BA receptor TGR5 and subsequently promoting beige adipocyte browning. Collectively, TTD ameliorates MetS by reshaping microbial-mediated BA pools, and in particular elevates HDCA levels to thereby activate TGR5 and induce beige adipocyte browning. These findings support TTD as a promising herbal-based therapeutic strategy for the treatment of MetS.

Myocardial infarction (MI) is a significant threat to human health worldwide. Following MI, cardiomyocytes (CMs) undergo pyroptosis, exacerbating the damage caused by infarction. Ginseng may play a role in alleviating CM pyroptosis. However, further exploration is needed regarding its main active ingredients and effects. By employing network pharmacology on the active ingredients of ginseng, MI and pyroptosis, and employing molecular docking between such ingredients and pyroptosis-related proteins, we screened for the main ingredient of ginseng. Through network pharmacology and molecular docking, we identified ginsenoside Rh2, which acts on MI and cell pyroptosis, as the most likely active ingredient that stably binds to pyroptosis-related proteins. We subsequently constructed a neonatal rat CM oxygen-glucose deprivation (OGD) model in vitro and an MI mouse model in vivo. Ginsenoside Rh2 was administered, with losartan used as a positive control. In the in vitro OGD model, ginsenoside Rh2 increased the viability of primary rat CMs and mitigated OGD-induced pyroptosis. In the in vivo MI model, ginsenoside Rh2 reduced CM pyroptosis, decreased infarct size, and subsequently improved cardiac function. Our study provides a novel therapeutic strategy for MI by attenuating CM pyroptosis.