The American journal of Chinese medicine最新文献

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.

Astragaloside IV (ASIV), the main active component of the traditional Chinese medicine HuangQi, exhibits ameliorating effects on myocardial fibrosis through unclear mechanisms. To investigate the effects of ASIV on Endothelial-to-mesenchymal transition (EndMT) in myocardial fibrosis, 10 ng/mL TGF-β1 was used to induce EndMT in human umbilical vein endothelial cells (HUVECs) in vitro, and a 5 mg/kg/d subcutaneous injection of Isoproterenol (ISO) was used to induce myocardial fibrosis in mice in vivo. The drug affinity-responsive target stability (DARTS) was used to identify the target proteins of ASIV in endothelial cells. The results showed that ASIV could significantly inhibit the TGF-β1-induced EndMT, which includes changes in cytoskeletal structure, the expression of EndMT markers, cell migration potency, and cell glycolysis rate. ASIV significantly ameliorated ISO-induced myocardial fibrosis in mice and inhibited EndMT in heart tissues. The Ras homolog gene family member A (RhoA) protein was found to be a possible direct binding target of ASIV in endothelial cells. The binding affinity between ASIV and RhoA was confirmed by molecular docking and the cellular thermal shift assay (CETSA). ASIV inhibited the RhoA-related pathway in the heart tissues of myocardial fibrosis mice. In addition, siRNA knockdown of RhoA expression or treatment with RhoA agonists was found to significantly affect the inhibition of EndMT by ASIV. The results suggested that ASIV could significantly inhibit the EndMT by binding with RhoA, and that the inhibition of EndMT by ASIV contributed to its amelioratory effects on myocardial fibrosis. This discovery provided a theoretical basis for the application of ASIV and HuangQi in the treatment of myocardial fibrosis.

Chronic airway diseases are a group of diseases, such as chronic obstructive pulmonary disease (COPD) and bronchial asthma (BA), characterized pathologically by chronic airway inflammation, airway chronic mucus hypersecretion, and airway remodeling. Patients usually present with chronic coughing, expectoration, and dyspnea, and recurrent exacerbation is an important causative factor of increased mortality, along with the important triggers. Currently, existing treatment options cannot meet the clinical needs of chronic airway diseases. Ginseng's great potential for treating chronic airway diseases has been confirmed by various clinical and basic studies, and traditional Chinese medicine compounds composed mainly of ginseng can both improve the symptoms of coughing and expectoration and reduce the number of acute exacerbations. Ginseng and its main biologically active ingredients exhibit the multifaceted mechanisms of effectively improving airway inflammation, mitigating airway mucus secretion, and reducing airway remodeling, which underscores their effectiveness in airway disease treatment. This study was conducted for the further elucidation and extension of the possible value of ginseng in chronic airway diseases. This review summarizes recent studies on the efficacy of ginseng in chronic airway disease treatment, discusses the pharmacological effects of ginseng and ginsenosides, and highlights their roles in the prevention and treatment of chronic airway diseases, airway diseases caused by airway inflammation and high airway mucus secretion, and airway remodeling-induced lung diseases. Finally, this study also predicted future research directions. Findings in this study may lay a robust foundation for investigating ginseng in chronic airway diseases, its underlying mechanisms, and its clinical development and practical application.

Ferroptosis, an iron-dependent form of non-apoptotic cell death, has emerged as a critical process in cancer therapy. Sanguinarine chloride (S.C), an alkaloid that stimulates apoptosis by activating reactive oxygen species (ROS), has demonstrated significant anticancer potential, but its role in modulating ferroptosis remains unclear. The aim of the present study was to elucidate the effects of S.C on ferroptosis in gastric cancer (GC) progression and its mechanism. Here, we determined cell viability by CCK-8 and revealed that the most potent drug, S.C, which is a small molecule compound in the ferroptosis library, had the strongest killing effect on GC cells. S.C could trigger ferroptosis in GC cells by inhibiting glutathione levels through promoting malondialdehyde production and ROS accumulation. Interestingly, S.C was found to function as a pro-ferroptotic death by interacting with NOS2 through network pharmacological docking. Mechanistically, we observed the deacetylase SIRT1 to regulate the acetylation level of NOS2 and thus affect the expression of NOS2. In addition, S.C regulates the downregulation of SLC7A11 and GPX4 through the SIRT1/NOS2/SOD1 pathway, and thereby induces ferroptosis. In vivo experiments showed that S.C treatment significantly inhibited subcutaneous tumor growth in BALB/c nude mice. This was significantly rescued by injection of a ferroptosis rescue agent (AA9). Taken together, these findings demonstrate that S.C works through the SIRT1/NOS2/SOD1 pathway and suggest that targeting SLC7A11/GPX4 to cause ferroptosis in cancer cells has potential as an anticancer therapy.

This study aimed to clarify the protective effect of Glycyrrhizic acid (GL) against Diosbulbin B (DB) - induced liver injury in mice and investigate its mechanisms of action. A liver injury DB was established in mice through the oral administration of DB for 15 days. At the same time, GL was administered to the mice for treatment. After the experiment, the pharmacodynamics and mechanisms of GL in ameliorating DB-induced liver injury were explored using biochemical indexes, non-targeted metabolomics, targeted metabolomics, Western blotting analysis of protein expression, 16S rDNA sequencing, and Spearman correlation analysis. The results show reduced liver function indices and improved DB-induced hepatic pathological changes. It also attenuated DB-induced hepatic inflammation and oxidative stress. Hepatic metabolomics revealed that GL regulated ABC transporters and bile secretion. Targeted bile acid (BA) metabolomics and Western blotting demonstrated that GL improved DB-induced reduction in BA efflux by regulating FXR-mediated efflux transporters. Furthermore, analysis of 16S rDNA gene sequencing revealed that GL effectively restored the relative abundance of beneficial bacteria, reduced the relative abundance of harmful bacteria, and reinstated the structure of the intestinal flora. Additionally, correlation analyses between BA and intestinal flora indicated that Firmicutes, Bacteroidota, TDGA, DGA, UDGA, GDGA, THDGA, and HDGA could serve as major markers for DB-induced liver injury. In conclusion, GL significantly improved DB-induced liver injury by increasing the expression of Nrf2/FXR-BSEP/MRP2/P-gp/UGT1A1, promoting BA efflux, regulating intestinal flora, and alleviating inflammation and oxidative stress.

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.