Journal of Food and Drug Analysis最新文献

Chronic obstructive pulmonary disease (COPD) is a chronic respiratory disease characterized by various pathological lesions and an imbalance in the microflora. The Yi-Qi-Xuan-Fei Formula (YQXF) is a clinically effective formula with pharmacological potential to delay the progression of COPD. This study aims to explore the relationship between the therapeutic mechanism of YQXF and the microflora in COPD. Our study found that YQXF reduces inflammatory injury and inflammatory cell infiltration in lung tissue, repairs the intestinal mucosal barrier, and enhances immune function. Additionally, YQXF regulates the pulmonary and intestinal flora by increasing the abundance of Alloprevotella, Roseburia, Oscillibacter, and Lactobacillus, while reducing the abundance of Fusobacterium, Escherichia/Shigella, and Clostridium sensu stricto. Moreover, YQXF elevates the levels of short-chain fatty acids, which are produced by the intestinal flora. In conclusion, our findings demonstrate that YQXF reduces inflammation levels in lung tissue and repairs the intestinal barrier in COPD rats. Furthermore, the anti-inflammatory and tissue damage prevention effects of YQXF are based on its intervention in the pulmonary and intestinal flora. These findings provide valuable insights into the fundamental mechanism of the herbal formula YQXF and suggest that specifically targeting the intestinal flora could be a potential therapeutic approach for COPD.

A series of chromatographic separation on the liquid-state fermented products of Didymocyrtis brachylaenae Km1530 derived from the littoral medicinal herb Atriplex maximowicziana Makino, resulted in the isolation of compounds 1-13. Their structures were determined by spectroscopic analysis as five previously unreported C₁₃ polyketides, namely brachylactones A-D (1-4) and brachic acid (5), along with eight known compounds 6-13. Among these, brachylactones A (1) and B (2) exhibited nitric oxide production inhibitory activity in lipopolysaccharide-induced murine BV-2 microglial cells at a concentration of 20 μM without any cytotoxicity.

Following the observed significant improvements in overall survival and progression-free survival in clinical trials, the combination of atezolizumab and bevacizumab has been recommended as a first-line therapy for patients with unresectable hepatocellular carcinoma. Despite its clinical benefits, the high cost associated with this treatment poses a substantial challenge in routine practice in Taiwan. This study aims to assess the cost-effectiveness of atezolizumab plus bevacizumab in comparison to sorafenib monotherapy. This study utilized partitioned survival analysis and extrapolated survival over a 20-year horizon to conduct a cost-effectiveness analysis from the perspective of the National Health Insurance Administration. Efficacy and utility data were directly extracted from the IMbrave150 trial, with input parameters adjusted to align with clinical practice in Taiwan. One-way deterministic and probabilistic sensitivity analyses were performed to assess the robustness of the results. Additionally, a scenario analysis was conducted to evaluate the impact of bevacizumab use on the outcomes. Compared to sorafenib, the combination of atezolizumab and bevacizumab resulted in an increase of 0.53 quality-adjusted life years (QALYs) and had an incremental cost of NT$1,867,151. The incremental cost-effectiveness ratio (ICER) was NT$3,523,768 per QALY, exceeding the commonly accepted willingness-to-pay threshold at NT$2,788,290 (three times Taiwan's gross domestic product per capita). One-way sensitivity analysis indicated that reducing the cost of atezolizumab plus bevacizumab to 70% would yield an ICER of NT$1,793,703. Scenario analysis demonstrated cost reduction in bevacizumab, either through the adoption of a biosimilar product or lower dosage, would make the combination cost-effective. Under Taiwan's National Health Insurance (NHI) system and based on the cost-effectiveness analysis in 2021, the combination of atezolizumab and bevacizumab is not cost-effective compared to sorafenib monotherapy for the treatment of unresectable hepatocellular carcinoma.

Synthetic cathinones are a widely abused class of new psychoactive substances that pose significant challenges in forensic toxicology owing to their complex metabolic pathways and lack of verified reference standards. This study investigated the in vitro metabolism of nine methylenedioxy-substituted synthetic cathinones, including methylone and eight structural isomers, which were categorized into three groups: Group 1 (dimethylone, ethylone, and butylone), Group 2 (dibutylone, pentylone, and eutylone), and Group 3 (N-ethylpentylone and dipentylone). Pooled human liver microsomes, cytosol, and uridine diphosphate glucuronic acid were used to identify phase I and II metabolites by liquid chromatography-quadrupole time-of-flight mass spectrometry. Key pathways included N-dealkylation, β-ketone reduction, aliphatic hydroxylation, demethylenation, and glucuronide conjugation, with the analytes containing N, N-dimethylamino moieties showing higher N-dealkylation and β-ketone reduction ratios. Metabolic differences were semiquantitatively assessed using peak area ratios, which revealed relative trends among the analytes. Differences in the retention times and mass spectral fragmentation patterns enabled effective isomer differentiation, which was validated using a metabolite database. Analysis of 29 urine samples confirmed that the metabolites generated from β-ketone reduction (M2) and demethylenation followed by O-methylation (M3-5) were reliable detection targets. For instance, even when the parent drug concentrations were as low as 11 ng/mL (semiquantitative peak area ratio ~70.0%) for methylone (M-6) and 23 ng/mL (semiquantitative peak area ratio ~2.9%) for dibutylone (DB-8), multiple metabolites were detected. These metabolites extended the detection window beyond Taiwan's legal threshold of 50 ng/mL. Overall, this study provides a unified comparison of the products of synthetic cathinone metabolism, and highlights the importance of metabolites as key markers for enhanced identification accuracy in forensic toxicology.

Jiao Sanxian (JSX) consists of three traditional Chinese medicine including charred hawthorn, malt and Liu Shen Qu, they are also from Chinese medicine homologous food. It is commonly used to relieve functional dyspepsia (FD). The present study aims to explore the mechanism of JSX (granule), with the addition of prebiotics for the treatment of FD using mice model. The network pharmacology and molecular docking were used to forecast therapeutic targets for JSX. Based on the protein-protein interaction (PPI) results, thirteen targets exhibited strong interactions with each other. The results of network pharmacology and molecular docking revealed therapeutic activity of JSX in FD regulated by its anti-inflammatory effect, improvement in gastrointestinal function and physiological activity in components-targets-pathways-disease. The pharmacological effects of JSX were further verified by rRNA gene sequencing, enzyme-linked immunosorbent assay (ELISA) and animal study. The in vivo results showed JSX, in combination with prebiotics, could mitigate FD symptoms. ELISA study showed that glyceraldehyde-3-phosphate dehydrogenase (GAPDH), AKT1 and tumor necrosis factor (TNF)-α played the roles in reducing the inflammatory response by downregulating inflammation content. The above results were coincided with the network pharmacology prediction. By 16S rRNA, the results showed JSX may alleviate the FD symptom by increasing the diversity of the intestinal flora, adjusting the dominant prebiotic. In conclusion, JSX can alleviate functional dyspepsia in mice. The mechanisms were related to regulating the secretion of inflammatory response, significantly improving the benefits of intestinal flora and ameliorating multi-metabolic pathways.

Diabetic nephropathy (DN) is one dominating reason for death in diabetic patients, and its incidence is high. It has been reported that Yiqi Yangyin Tongluo prescription (YYTP) can relieve inflammation, and it owns better clinical effects in the treatment of DN. However, the molecular mechanisms of YYTP in the treatment of DN still keep unclear, and deeply investigations are needed. In this study, it firstly was manifested that YYTP can repress the lncRNA VIM-antisense 1 (VIM-AS1) expression in high glucose (HG)-evoked HK-2 cells. Overexpression of VIM-AS1 roll-backed the inhibitive impacts of YYTP on cell apoptosis in HG-triggered HK-2 cells. Additionally, it was uncovered that the attenuated autophagy of LC3B in HG-triggered HK-2 cells was counteracted after 20% YYTP treatment, but this phenomenon was further attenuated after VIM-AS1 amplification. Besides, VIM-AS1 can pull down FOXK2 protein, and overexpression of VIM-AS1 counteracted the suppressive effects of YYTP on forkhead box K2 (FOXK2)/mammalian target of rapamycin (mTOR) in HG-mediated HK-2 cells. In conclusion, it was firstly disclosed that YYTP targeted lncRNA VIM-AS1 to regulate FOXK2/mTOR to promote autophagy and inhibit cell apoptosis in DN progression. This discovery hinted that YYTP may be one valid drug for DN therapy.

Aspergillosis stands as a primary opportunistic fungal infection which mainly results from Aspergillus fumigatus events that have gained more importance because of its multiple infection patterns and developing antifungal resistance. Healthcare providers identify two main ends of the aspergillosis spectrum which include allergic responses and invasive systemic infections that affect mainly immunocompromised subjects. This review presents a detailed summary for understanding the epidemiology of aspergillosis along with its risk factors as well as pathogenesis and host immune response and diagnostic difficulties. The analysis puts significant weight on increasing azole and echinocandin resistance that has become worse because of agricultural and environmental azole exposure and the development of multidrug-resistant strains. The mechanisms of action and restrictions together with resistance profiles differentiate different antifungal treatments like azoles and echinocandins in addition to polyenes from each other. The potential therapeutic benefits of using combination therapy with drug delivery targeting systems and developing new antifungal agents including rezafungin and ibrexafungerp are assessed. The review emphasizes relevant interactions between drugs when used together with food elements which affect antifungal safety and effectiveness specifically in patients with complex healthcare needs. The review analyzes newly developed diagnostic methods including PCR-based tests and biomarkers for their capability of improving fast and precise detection. The review presents immunomodulatory therapies as well as host-directed strategies which represent a set of emerging approaches. The clinical presentation of aspergillosis varies widely which case studies help doctors to understand better. Comprehensive management of aspergillosis necessitates cooperative medical care and precise medicinal interventions alongside continuous diagnostics improvements to achieve solutions for the worldwide health issue.

Chronic atrophic gastritis (CAG) is precancerosis with limited treatment options. This study investigated the therapeutic effects of velvet antler (VA), a traditional natural medicine, on CAG, with a focus on ferroptosis. In vivo experiments demonstrated the efficacy of VA in alleviating CAG, and network pharmacology analysis revealed its involvement in related terms, including inflammation, oxidative stress, and cell proliferation. Analyses further confirmed the modulation of ferroptosis by VA, particularly via the Keap1-Nrf2/HO-1/GPX4 pathway. In vitro assays supported these findings, demonstrating the ability of VA to reduce methylnitronitrosoguanidine-induced inflammation, oxidative stress, and ferroptosis in GES-1. This study provides a basis for exploring VA as a potential treatment for CAG, and offers new therapeutic strategies targeting ferroptosis.

The Ping-Chong-Jiang-Ni Formula (PCJNF), a compound of Traditional Chinese Medicine (TCM), has demonstrated remarkable clinical effectiveness and is widely utilized in the treatment of endometriosis (EMs). Previous studies have shown that PCJNF inhibits the proliferation and induces the apoptosis of ectopic endometrial stromal cells (EESCs) by modulating the JNK signaling pathway. In our most recent study, published in January 2024, we found that PCJNF effectively alleviates EMs-associated pain by reducing inflammatory mediators, including tumor necrosis factor-alpha (TNF-α) and nerve growth factor (NGF). Furthermore, PCJNF down-regulates the expression of transient receptor potential vanilloid 1 (TRPV1), phosphorylated TRPV1 (p-TRPV1), and protein kinase C (PKC). To further investigate the therapeutic potential of PCJNF, we conducted a comprehensive tandem mass tag (TMT) proteomics analysis, identifying 4984 proteins co-expressed in human EESCs treated with PCJNF and control serum. Based on these findings, this study explored the inhibitory effects of PCJNF on the migration and invasion of EMs cells in vitro. Reverse transcription-polymerase chain reaction (RT-PCR) analysis of 12 genes revealed a significant upregulation of FER and TRIP13 in ectopic lesions, which was further validated by immunohistochemistry. Given the crucial role of TRIP13 in EMs, we employed small interfering RNA (siRNA) to knock down its expression, observing a marked reduction in the migration and invasion abilities of EMs cells. Conversely, overexpression of TRIP13 using short hairpin RNA (shRNA) enhanced these processes. Additionally, after PCJNF treatment, we observed significant alterations in the expression of migration-and invasion-related proteins, such as vimentin and E-cadherin. In conclusion, these findings suggest that TRIP13 may serve as a potential therapeutic target for EMs and that PCJNF offers a promising new approach for integrating Traditional Chinese Medicine with modern medical treatments.

Products containing live microorganisms may be classified as food or drugs depending on their intended use; live biotherapeutic products (LBPs) with therapeutic claims are defined as medicinal products containing live bacteria or yeasts intended to prevent or treat disease. Based on their characteristics, LBPs are classified as biological drugs and must be registered as biological drugs before they can enter the Taiwanese market. As research into the microbiota and its role in health and disease continues to advance, LBPs are expected to play an increasingly important role in medicine and biotechnology. With the growing popularity of microbial applications in recent years, there is still a lack of awareness regarding the management and regulation of such products. This article outlines the development, manufacturing, and marketing requirements of LBPs in Taiwan. After searching relevant literature, we summarized the regulations or related guidelines on LBPs from regulatory agencies such as the U.S. FDA, EMA, PMDA, and ICH. And compare the current requirements for LBPs in Taiwan. Key regulatory aspects of LBPs in Taiwan include definitions and classifications, quality and manufacturing requirements, clinical evidence, labeling and packaging information, post-marketing surveillance, etc. Regulations of LBPs in Taiwan align with international standards, but Taiwan authorities must be more inclusive in addressing new challenges facing LBPs innovation. This highlights the importance of continuous regulatory adaptation to foster innovation while ensuring safety and efficacy. Collaboration between regulatory bodies, industry stakeholders, and scientific communities will be essential to promoting innovation while maintaining robust regulatory oversight in the LBPs sector. In summary, while LBPs have significant therapeutic potential, addressing the regulatory challenges associated with their development, approval, and post-marketing surveillance is critical to ensure their safety, efficacy, and successful integration into clinical practice.