The American journal of Chinese medicine最新文献

Large language models (LLMs) are reshaping the landscape of Traditional Chinese Medicine (TCM). This review covers the latest applications of LLMs in TCM, including literature analysis, data mining, TCM knowledge management, diagnosis simulation and clinical decision making. LLMs can analyze large quantities of TCM literature and medical records to extract critical information, classify prescriptions, and build TCM knowledge maps to help researchers quickly grasp state-of-the-art and future research trends. LLMs can provide initial diagnostic recommendations by analyzing textual information such as a patient's symptom description and medical history, enabling the optimization of TCM therapy and the training of TCM practitioners. Compared with traditional tools, LLMs can significantly improve the efficiency and accuracy of bibliographic analysis and TCM prescription classification, and offer new potential for data-driven standardized TCM diagnosis. However, challenges remain, including the standardization of TCM terminology and data formats, integration of different data sources, timely knowledge updates, and the interpretability and credibility of results generated by LLMs. Future research on standardized templates for patient symptom description, multimodal data fusion techniques, and real-time knowledge update systems is warranted to improve the transparency and interpretability of LLMs. This review highlights the potential of LLMs to modernize TCM research and practice, providing an up-to-date reference for data scientists, biomedical engineers, and TCM practitioners.

SNHG5 serves as a key factor in regulating various cancers, and Dexmedetomidine (Dex) protects against myocardial ischemia/reperfusion (I/R) injury. However, the role of SNHG5 in Dex-mediated protection during myocardial I/R remains uninvestigated. In this study, models of rat myocardial I/R injury and hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury were generated. The infarct size, histological changes and apoptosis in heart tissues were evaluated by TTC, HE, and TUNEL staining. CCK-8, flow cytometry and immunofluorescence were employed to assess cell viability, apoptosis and autophagosome-lysosome fusion in H9c2 cells. The associations among SNHG5, LIN28A and BCAT1 mRNA were detected by RNA pull-down, RIP, and RNA fluorescence in situ hybridization (FISH) assays. Western Blot, qRT-PCR and immunohistochemistry were employed to detect the expression of key molecules. Our results revealed that Dex ameliorated myocardial I/R injury and H/R-induced impairments in H9c2 cells by enhancing autophagy. Moreover, Dex led to a rebound of SNHG5 in the heart tissues of I/R rats and H/R-treated H9c2 cells, and functional studies revealed that Dex protected against cardiac impairments through SNHG5-dependent autophagy in vitro and in vivo. Furthermore, SNHG5 alleviated H/R-induced impairments by recruiting LIN28A protein, which was subsequently bound to BCAT1 mRNA and maintained its stability. In conclusion, our findings demonstrated that SNHG5, when upregulated by Dex, alleviated myocardial I/R injury through LIN28A-mediated BCAT1 mRNA stabilization and autophagy enhancement.

Paeoniflorin (PF) is a key active ingredient with anti-inflammatory and antioxidant properties extracted from the root of Paeonia lactiflora. Non-alcoholic fatty liver disease (NAFLD), recently referred to as metabolic dysfunction-related fatty liver disease (MAFLD), is the leading cause of chronic liver disease worldwide. However, the potential mechanisms and targets of paeoniflorin's anti-inflammatory and antioxidant therapy for MAFLD remain to be thoroughly investigated. Thus, in cellular experiments, we added free fatty acids (P/O) to AML-12 cells and cultured them for 24 h. In animal experiments, mice were administered a high-fat diet (HFD) for a duration of 16 weeks in order to create an animal model of fatty liver disease. Our study confirmed that PF significantly reduced steatosis and alleviated oxidative stress and inflammation levels in P/O-induced AML-12 hepatocytes and mouse livers with HFD. Cellular experiments showed that PF-attenuated Phosphoric acid/Oleic acid (P/O) induced lipid deposition in AML-12 cells, indicators related to cellular focal death were downregulated, and mitochondrial oxidative damage was alleviated. In animal experiments, ALT, AST, TG, TC and the hepatic index were elevated in the model group, and lipid deposition and cell infiltration were shown by HE, Oil Red O staining. These were significantly reduced in the PF groups. Network pharmacology studies indicated PF may target the Stimulator of interferon genes (STING) as a crucial molecule for the treatment of MAFLD, and the validation of C-176 (STING inhibitor) and DXMAA (STING promoter) further supported that PF could target STING to regulate hepatocyte cellular pyroptosis.

In a previous study, Eugenol (EU) has been demonstrated to alleviate DSS-induced experimental colitis, due to its anti-inflammatory, anti-oxidant, and immune regulatory efficacy, but its underlying molecular mechanism remains unknown. In this study, EU applications were combined with peroxisome proliferator-activated receptor-[Formula: see text] (PPAR-[Formula: see text]) agonist (rosiglitazone) and inhibitor (GW9662) in order to clarify the role of PPAR-[Formula: see text] in EU against UC by testing NF-κB and Nrf2 signaling pathway activation and the salient features of colitis. The binding activity and adjusting effect of EU on inflammation and oxidative stress were further investigated in vitro. Similar to rosiglitazone, the results illustrated that EU remarkably reversed DSS-induced weight loss, reversed colonic shrinkage and integrity damage, and inhibited the DAI scores increase, excessive inflammatory response, and oxidative stress. However, the combination with GW9662 noticeably restrained the protective effect on mice. Additionally, molecular docking and a surface plasmon resonance assay evidenced the direct binding activity of EU with PPAR-[Formula: see text]. EU's anti-oxidant and anti-inflammation bioactivities were evidenced again in vitro. Overall, the above results further demonstrated the molecular mechanism of EU's defensive effect, which is directly dependent on PPAR-[Formula: see text] activation, on experimental colitis. Therefore, this study may facilitate a better understanding of EU's protective action against UC.

Ulcerative colitis (UC) is a chronic, nonspecific inflammatory disorder characterized by symptoms such as abdominal pain, diarrhea, hematochezia, and urgency during defecation. While the primary site of involvement is the colon, UC can extend to encompass the entire rectum and colon. The causes and development mechanisms of UC are still not well understood; nonetheless, it is currently held that factors including environmental influences, genetic predispositions, intestinal mucosal integrity, gut microbiota composition, and immune dysregulation contribute to its development. Dysregulated immune responses are pivotal in the pathophysiology of UC, and these aberrant responses are considered key contributors to the disease onset. In patients with UC, immune cells become hyperactive and erroneously target normal intestinal tissue, resulting in inflammatory cascades and damage to the intestinal mucosa. The therapeutic strategies currently employed for UC include immunosuppressive agents such as aminosalicylates and corticosteroids. However, these treatments often prove costly and carry significant adverse effects - imposing a considerable burden on patients. Traditional Chinese Medicine (TCM) has attracted worldwide attention because of its multi-target approach, minimal side effects, cost-effectiveness, and favorable efficacy profiles. In this review, the ways in which TCM modulates inflammatory responses in the treatment of ulcerative colitis have been outlined. Research into TCM modalities for modulating inflammatory pathways in the treatment of UC, which has yielded promising advancements, including individual herbs, herbal formulations, and their derivatives, has been summarized. TCM has been utilized to treat UC and the immune system plays a key role in regulating intestinal homeostasis. It is imperative to facilitate large-scale evidence-based medical research and promote the clinical application of TCM in the management of UC.

Oxidative stress and pyroptosis have been established as key contributors to myocardial ischemia-reperfusion injury (MIRI). While previous studies reported that electroacupuncture (EA) preconditioning exerted cardioprotective effects, the underlying mechanisms remain elusive. Thus, this study aimed to investigate the effects of EA preconditioning on oxidative stress and pyroptosis in MIRI rats, and explore the role of nuclear factor E2-associated factor 2 (Nrf2) throughout that process. A MIRI model was constructed by ligating the left anterior descending coronary artery for 30 min, followed by 4 h of reperfusion in rats. Prior to modeling, rats were subjected to EA at the Neiguan Point for three days. Furthermore, ML385, a Nrf2 inhibitor, was administered in order to examine the role of Nrf2 in regulating oxidative stress and pyroptosis following EA preconditioning. The results revealed that EA preconditioning improved left ventricular function after MIRI and reduced both the myocardial infarction area and cTnT levels. Meanwhile, EA preconditioning alleviated MIRI-induced oxidative stress and pyroptosis, as evidenced by the downregulation of ROS, MDA, NF-κB p65, caspase-1, IL-1β, and GSDMD-N, and the upregulation of SOD and HO-1. Mechanistically, EA up-regulated enhanced the expression of Nrf2. However, its cardioprotective effects and ability to attenuate oxidative stress and pyroptosis were suppressed by the inhibition of Nrf2. Taken together, our study indicated that EA preconditioning attenuated MIRI in rats by mitigating oxidative stress and pyroptosis, with Nrf2 playing a vital role in this protective mechanism.

Colorectal cancer (CRC) remains a major threat to health worldwide, partly due to the lack of effective treatments targeting the transition from inflammatory bowel disease (IBD) to malignancy. Astragaloside IV (AS-IV) is a major bioactive component from the traditional herb Astragalus membranaceus, and it has strong immunomodulatory and gastrointestinal protective effects. In this review, we evaluate the therapeutic potential and mechanisms of AS-IV in addressing the three hallmark pathological phases of colorectal cancer development: IBD-related inflammation, the transition from inflammation to cancer, and IBD-associated colorectal cancer (IBD-CRC). During the inflammatory phase, AS-IV promotes M2 macrophage polarization, reducing mucosal inflammation and repairing the intestinal barrier. In the transition from inflammation to cancer, AS-IV prevents IBD-CRC transition by targeting immune signaling pathways (e.g., NF-κB and PPAR[Formula: see text] signaling pathways), gut microbiota, and oxidative stress. At the IBD-CRC stage, AS-IV can promote the polarization of M1 macrophages, thereby suppressing tumor growth, inducing apoptosis, inhibiting metastasis, and enhancing chemosensitivity. These findings highlight the potential of AS-IV to bidirectionally modulate the M1/M2 macrophage ratio and its role in the prevention and treatment of IBD-CRC. The multi-target therapeutic effects of AS-IV at various stages of IBD also provide new strategies to guide future drug development.

Sepsis is a life-threatening condition characterized by systemic inflammatory response syndrome, and often results in cardiac damage and poor prognosis. This study aimed to explore the protective effects of Poria cocos polysaccharides (PCP) on sepsis-induced cardiac injury and elucidate the underlying molecular mechanisms. An in vivo sepsis model was established, and an in vitro myocardial cell model was induced using lipopolysaccharide (LPS) to mimic a sepsis environment. Histopathological analysis revealed morphological changes in the myocardial tissue, while apoptosis and oxidative stress in the myocardial cells were assessed using immunofluorescence staining. The Western blot assay was employed to measure the expression levels of CaMKII, NF-[Formula: see text]B, and NLRP3, and myocardial cell apoptosis was quantified by flow cytometry. Inflammatory cytokine levels were determined via ELISA. The results indicated that PCP treatment significantly alleviated myocardial injury, reduced myocardial apoptosis, and lowered the levels of inflammatory markers when compared to the sepsis group. Mechanistic studies revealed that PCP inhibited the P38/NF-[Formula: see text]B/NLRP3 signaling pathway activation induced by CaMKII to thereby mitigate apoptosis and the inflammatory response in sepsis-induced cardiomyocytes. In conclusion, PCP exerts a protective effect against sepsis-induced cardiac injury by inhibiting the CaMKII-mediated P38/NF-[Formula: see text]B/NLRP3 signaling pathway. This study provides a novel theoretical framework and identifies potential therapeutic targets for the prevention and treatment of sepsis-associated cardiac injury.

Valeriana jatamansi Jones (V. jatamansi) has a long history of medicinal use owing to its significant therapeutic effects, particularly in the treatment of mental diseases such as depression, and on account of its cytotoxicity against various cancer cells. The chemical composition, pharmacological properties, and mechanisms of V. jatamansi have been extensively explored in various studies published between 2017 and 2023 on major databases such as Web of Science, PubMed, and CNKI[Formula: see text] Investigations have identified 128 compounds including iridoids, sesquiterpenoids, volatile oils, lignans, and miscellaneous compounds based on their structural characteristics. Pharmacological research has documented its impact on the central nervous system, and its antitumor, gastroprotective, antioxidant, and anti-inflammatory effects. In particular, iridoids stand out among these compounds, and iridoid-enriched fraction from V. jatamansi (IEFV), identified by several pharmacological experiments, exhibits notable protective properties against diseases of the central nervous system and several cancers. In summary, V. jatamansi holds potential as an adjunct in cancer treatment, enhancing its therapeutic efficacy.

Osteoarthritis (OA) is the most common chronic degenerative joint disease, characterized by cartilage damage, synovial inflammation, subchondral bone sclerosis, marginal bone loss, and osteophyte development. Clinical manifestations include inflammatory joint pain, swelling, osteophytes, and limitation of motion. The pathogenesis of osteoarthritis has not yet been fully uncovered. With ongoing research, however, it has been gradually determined that OA is not caused solely by mechanical injury or aging, but rather involves chronic low-grade inflammation, metabolic imbalances, dysfunctional adaptive immunity, and alterations in central pain processing centers. The main risk factors for OA include obesity, age, gender, genetics, and sports injuries. In recent years, extensive research on gut microbiota has revealed that gut dysbiosis is associated with some common risk factors for OA, and that it may intervene in its pathogenesis through both direct and indirect mechanisms. Therefore, gut flora imbalance as a pathogenic factor in OA has become a hotspot topic of research, with potential therapeutic connotations. In this paper, we review the role of the gut microbiota in the pathogenesis of OA, describe its relationship with common OA risk factors, and address candidate gut microbiota markers for OA diagnosis. In addition, with focus on OA therapies, we discuss the effects of direct and indirect interventions targeting the gut microbiota, as well as the impact of gut bacteria on the efficacy of OA drugs.