American Journal of Chinese Medicine最新文献

Traditional Chinese Medicine (TCM) prescriptions are organically composed of compatible herbs according to the TCM theory. The complex ingredients of TCM could act on multiple targets through various pathways simultaneously to exert pharmacological effects, making TCM an unrivaled gem in the medical world. However, due to a lack of comprehensive and standard study methods, the research of TCM products has been quite limited. A novel paradigm that could aid in the discovery of the material basis and fully clarify the mechanism of TCM prescriptions is urgently needed. In this study, a similarity analysis based on molecular fingerprints was adopted to explore the representative molecules of the Tiaoxin recipe, a Chinese patent formula approved by the National Medical Products Administration (NMPA) for the treatment of mild-to-moderate Alzheimer's disease (AD), and 38 out of 1047 chemicals were finally screened out. Next, we tried to define a new concept of a "functional molecule cluster" for chemicals with similar pharmacological effects to elucidate how the chemical mixture from TCMs produce their therapeutic effects. Four anti-AD functional molecule clusters from the Tiaoxin recipe were identified: an anti-inflammatory cluster, an anti-ROS cluster, an anti-AChE activity cluster, and an anti-A[Formula: see text] aggregation cluster. Furthermore, the chemicals from the anti-inflammatory cluster and anti-ROS cluster were proved to display their multi-target and multi-pathway roles partially or mainly through molecules of the TLR4-MYD88-NF-[Formula: see text]B and Keap1-Nrf2-ARE pathways. The functional molecule clusters may be vital to the explanation of the efficacy of the Tiaoxin recipe, which could give us a more profound understanding of TCM prescriptions. Our paradigm may open a novel path for TCM research.

Fungi play an important role in the solution to important global problems. Making use of processes and goods that are based on fungi can help promote sustainability by making the most efficient use of natural resources. Fungi stand apart from other organisms due to their extraordinary capacity to generate organic compounds. They are necessary for the psychological and physiological well-being of people worldwide. They are excellent producers of vitamins, pigments, hydrolytic enzymes, biofuels, organic acids, polysaccharides, and secondary metabolites such as antibiotics, anticancer treatments, hypocholesterolemic pharmaceuticals, and immunosuppressants. Other secondary metabolites include biofuels. In addition, polysaccharides are produced by them. We provide a condensed explanation of the significance of secondary metabolites in a variety of industries, such as the pharmaceutical industry, the food industry, the textile industry, and the transportation industry. In addition to providing a better understanding of biosynthetic regulation and the possibilities of genetic engineering, improved laboratory processes for the selection of nontoxigenic fungal strains have permitted the manufacture of larger quantities of safe commercial items. The significance of fungi in industrial settings is the topic that will be investigated in this review.

Prostate cancer (PCa) is the second most prevalent cancer in men worldwide. The majority of PCa incidences eventually progress to castration-resistant PCa (CRPC), thereby establishing an urgent need for new effective therapeutic strategies. This study aims to examine the effects of morusin, a prenylated flavonoid isolated from Morus alba L., on PCa progression and identify the regulatory mechanism of morusin. Cell growth, cell migration and invasion, and the expression of EMT markers were examined. Cycle progression and cell apoptosis were examined using flow cytometry and a TUNEL assay, while transcriptome analysis was performed using RNA-seq with results being further validated using real-time PCR and western blot. A xenograft PCa model was used to examine tumor growth. Our experimental results indicated that morusin significantly attenuated the growth of PC-3 and 22Rv1 human PCa cells; moreover, morusin significantly suppressed TGF-[Formula: see text]-induced cell migration and invasion and inhibited EMT in PC-3 and 22Rv1 cells. Significantly, morusin treatment caused cell cycle arrest at the G2/M phase and induced cell apoptosis in PC-3 and 22Rv1 cells. Morusin also attenuated tumor growth in a xenograft murine model. The results of RNA-seq indicated that morusin regulated PCa cells through the Akt/mTOR signaling pathway, while our western blot results confirmed that morusin suppressed phosphorylation of AKT, mTOR, p70S6K, and downregulation of the expression of Raptor and Rictor in vitro and in vivo. These results suggest that morusin has antitumor activities on regulating PCa progression, including migration, invasion, and formation of metastasis, and might be a potential drug for CRPC treatment.

Diabetic nephropathy (DN) is thought to be the major cause of end-stage renal disease. Due to its complicated pathogenesis and the low efficacy of DN treatment, a deep understanding of new etiological factors may be useful. Ferroptosis, a nonapoptotic form of cell death, is characterized by the accumulation of iron-dependent lipid peroxides to lethal levels. Ferroptosis-triggered renal tubular injury is reported to participate in the development of DN, and blocking ferroptosis might be an effective strategy to prevent the development of DN. Quercetin (QCT), a natural flavonoid that is present in a variety of fruits and vegetables, has been reported to ameliorate DN. However, its underlying nephroprotective mechanism is unclear. Herein, we explored the antiferroptosic effect of QCT and verified its nephroprotective effect using DN mice and high glucose (HG)-incubated renal tubular epithelial cell models. We found HG-induced abnormal activation of ferroptosis of renal tubular epithelial cells, and QCT treatment inhibited ferroptosis by downregulating the expression of transferrin receptor 1 (TFR-1) and upregulating the expression of glutathione peroxidase 4 (GPX4), ferritin heavy chain 1 (FTH-1), and the cystine/glutamate reverse antiporter solute carrier family 7 member (SLC7A11) in DN mice and HG-incubated HK-2 cells. Subsequently, both in vitro and in vivo results confirmed that QCT activated the NFE2-related factor 2 (Nrf2)/Heme oxygenase-1(HO-1) signaling pathway by increasing the levels of Nrf2 and HO-1. Therefore, this study supports that QCT inhibits the ferroptosis of renal tubular epithelial cells by regulating the Nrf2/HO-1 signaling pathway, providing a novel insight into the protective mechanism of QCT in DN treatment.

Several functional gastrointestinal disorders (FGIDs) have overlapping symptoms, and, consequently, developing treatment strategies based on symptomatology poses a challenge for the clinical management of complex FGIDs. The significant overlap in the symptoms of FGIDs caused by the shared pathophysiological mechanisms is both a challenge and an excellent target for therapeutic development, since treatment strategies focused on shared pathophysiological mechanisms can treat the associated underlying diseases rather than just alleviating the primary symptoms. Owing to its multi-targeted approach, traditional Chinese medicine (TCM) has garnered immense interest worldwide; however, the quality of the data demonstrating its effectiveness is generally weak. Additionally, the causal link between the intrinsic mechanisms of action of TCM and its clinical benefits remains obscure. Systems biology is characterized by holistic and dynamic research, which corresponds to the holistic, multi-targeted, and syndrome-based approach of TCM. Therefore, high-throughput analysis techniques can be employed to describe and comprehend the genesis and progression of diseases, as well as the impacts of TCM on the organism, which may aid in elucidating the pathogenic mechanisms of the diseases as well as the mechanism of action of TCM.

Salvia miltiorrhiza Bunge, called Danshen in Chinese, is the dried root and rhizome of S. miltiorrhiza, which is part of the mint family, Lamiaceae; it has chiefly been used to treat blood stasis and improve blood flow in cerebrovascular and cardiovascular diseases for over 2000 years. Recent preclinical studies have indicated that S. miltiorrhiza has a wide range of pharmacological properties making it useful for the treatment of diverse liver diseases. S. miltiorrhiza protects the liver from harmful hepatotoxins, reduces hepatic oxidative stress, ameliorates steatosis, and alleviates hepatic inflammation, fibrosis, and cancer. Moreover, several key mechanisms, including apoptosis, AMP-activated protein kinase, mitogen-activated protein kinase, and nuclear factor kappa B, may be involved in the benefits of S. miltiorrhiza in hepatic disorders. In particular, salvianolic acid B and cryptotanshinone, both compounds derived from S. miltiorrhiza, possess therapeutic activities similar to those of S. miltiorrhiza, and thus may play a crucial role in the therapeutic activity of S. miltiorrhiza in liver diseases. Because reports on the pharmacological effects of this herb are scattered, this review aimed to consolidate the available literature to allow the re-evaluation and identification of gaps to guide future research. This review focuses on the role of S. miltiorrhiza in improving the molecular pathology of liver diseases, as reported in in vitro and in vivo studies.

Pyroptosis, an apoptotic pathway for pro-inflammatory cells, has attracted attention from researchers because of its role in the development of cardiac inflammation reactions. Chinese medicine (CM) has been given more and more attention during the pursuit of a treatment for coronary heart disease (CHD). Evidence suggests that myocardial cell pyroptosis affects the progression of CHD. Pyroptosis pathways include the canonical pyroptosis pathway mediated by the caspase-1 inflammasome and the non-canonical pyroptosis pathway induced by cytoplasmic lipopolysaccharide-activated caspase-4/5/11. The frequently studied compounds that regulate pyroptosis in CHD include astragaloside IV (AS-IV), tanshinone IIA, aucubin, cinnamaldehyde (CD), ginsenoside Rb1, paeoniflorin, apigenin, berberine (BBR), ruscogenin (Rus), and total glucosides of paeonia (TGP). The patent drugs of CM that regulate pyroptosis in CHD include the Qishen granule (QSG), the Simiao Yong'an decoction (SMYAD), the Buyang Huanwu decoction (BYHWD), and the Shexiang Baoxin pill (SBP). Therefore, this paper reviews the pathogenesis of pyroptosis, the role of pyroptosis in CHD, and the potential therapeutic roles of CMs and their active ingredients targeting cell pyroptosis in the development of CHD.

Rhizoma coptidis (CR) is traditionally used for treating gastrointestinal diseases. Wine-processed CR (wCR), zingiber-processed CR (zCR), and evodia-processed CR (eCR) are its major processed products. However, the related study of their specific mechanisms is very limited, and they need to be further clarified. The aim of this study is to compare the intervening mechanism of wCR/zCR/eCR on rats via faecal metabolomics and 16S rDNA gene sequencing analysis. First, faecal samples were collected from the control and CR/wCR/zCR/eCR groups. Then, a metabolomics analysis was performed using UHPLC-Q/TOF-MS to obtain the metabolic profile and significantly altered metabolites. The 16S rDNA gene sequencing analysis was carried out to analyze the composition of gut microbiota and screen out the significantly altered microbiota at the genus level. Finally, a pathway enrichment analysis of the significantly altered metabolites via the KEGG database and a functional prediction of relevant gut microbes based on PICRUSt2 software were performed in combination. Together with the correlation analysis between metabolites and gut microbiota, the potential intervening mechanism of wCR/zCR/eCR was explored. The results suggested that wCR played a good role in maintaining immune homeostasis, promoting glycolysis, and reducing cholesterol; zCR had a better effect on protecting the integrity of the intestinal mucus barrier, preventing gastric ulcers, and reducing body cholesterol; eCR was good at protecting the integrity of the intestinal mucus barrier and promoting glycolysis. This study scientifically elucidated the intervening mechanism of wCR/zCR/eCR from the perspective of faecal metabolites and gut microbiota, providing a new insight into the processing mechanism research of Chinese herbs.

COVID-19 has posed unprecedented challenges to global public health since its outbreak. The Qing-Fei-Pai-Du decoction (QFPDD), a Chinese herbal formula, is widely used in China to treat COVID-19. It exerts an impressive therapeutic effect by inhibiting the progression from mild to critical disease in the clinic. However, the underlying mechanisms remain obscure. Both SARS-CoV-2 and influenza viruses elicit similar pathological processes. Their severe manifestations, such as acute respiratory distress syndrome (ARDS), multiple organ failure (MOF), and viral sepsis, are correlated with the cytokine storm. During flu infection, QFPDD reduced the lung indexes and downregulated the expressions of MCP-1, TNF-[Formula: see text], IL-6, and IL-1[Formula: see text] in broncho-alveolar lavage fluid (BALF), lungs, or serum samples. The infiltration of neutrophils and inflammatory monocytes in lungs was decreased dramatically, and lung injury was ameliorated in QFPDD-treated flu mice. In addition, QFPDD also inhibited the polarization of M1 macrophages and downregulated the expressions of IL-6, TNF-[Formula: see text], MIP-2, MCP-1, and IP-10, while also upregulating the IL-10 expression. The phosphorylated TAK1, IKK[Formula: see text]/[Formula: see text], and I[Formula: see text]B[Formula: see text] and the subsequent translocation of phosphorylated p65 into the nuclei were decreased by QFPDD. These findings indicated that QFPDD reduces the intensity of the cytokine storm by inhibiting the NF-[Formula: see text]B signaling pathway during severe viral infections, thereby providing theoretical and experimental support for its clinical application in respiratory viral infections.

Maslinic acid (MA) is a pentacyclic triterpene obtained from the peel of olives that exhibits anti-inflammatory and antioxidant properties in several conditions. Our previous study revealed that MA exerted a cardioprotective effect by repressing inflammation and apoptosis during myocardial ischemia-reperfusion injury (MIRI). However, data regarding the antioxidative effects of MA on MIRI remains limited. This study aims to elucidate the antioxidative roles and underlying mechanisms of MA on MIRI. The left anterior descending coronary artery of rats was subjected to ligate for the induction of the ischemia/reperfusion (I/R) model and the H9c2 cells were exposed to hydrogen peroxide (H₂O₂) to mimic oxidative stress. The results showed that MA reduced the I/R-induced myocardial injury and H₂O₂-induced cardiomyocyte death in a dose-dependent manner. Meanwhile, MA increased the activities of glutathione and superoxide dismutase both in vitro and in vivo while lowering the levels of reactive oxygen species and malondialdehyde. Mechanistically, MA could facilitate Nrf2 nuclear translocation, activate the Nrf2/HO-1 signaling pathway, and repress the NF-[Formula: see text]B signaling pathway both in I/R- and H₂O₂-induced oxidative stress. Besides, MA promoted the intranuclear Nrf2 and HO-1 expression, which could in part be improved by QNZ (NF-[Formula: see text]B inhibitor) in H₂O₂-insulted cells. Conversely, MA markedly reduced the intranuclear NF-[Formula: see text]B p65 and TNF-[Formula: see text] expression, which could be partially abolished by ML385 (Nrf2 inhibitor). Overall, our results indicate that MA, in a dose-dependent manner, mitigated I/R-induced myocardial injury and oxidative stress via activating the Nrf2/HO-1 pathway and inhibiting NF-[Formula: see text]B activation. Furthermore, MA exerts its cardioprotective effect through regulating the crosstalk between the Nrf2 and NF-[Formula: see text]B pathways.