acrivastine + pseudoephedrine (Duact)

Mahuang Fuzi Xixin decoction attenuates allergic rhinitis by suppressing MHC-II-mediated antigen presentation in ovalbumin induced murine model.

Wei Xiaohan X, Ding Mengze M, Tan Xiaomei X

Allergic rhinitis (AR) is a chronic condition that impairs daily life and imposes economic burdens. Mahuang Fuzi Xixin Decoction (MFXD) is a commonly employed herbal formula in China for treating AR, owing to its established clinical efficacy. However, investigations into its underlying mechanisms remain limited. To evaluate the therapeutic effects of MFXD in a mouse model of AR and to investigate its influence on antigen presentation, thereby elucidating potential mechanisms of action. An ovalbumin (OVA)-induced murine AR model was established to assess the efficacy of MFXD. Subsequently, data-independent acquisition (DIA) proteomics characterized differentially expressed proteins (DEPs) in the nasal mucosa following MFXD treatment, followed by pathway enrichment analysis. Guided by the proteomic findings, we examined the regulatory effects of MFXD on antigen presentation molecules in AR mice. Finally, human nasal epithelial cells (HNEpCs), dendritic cells (DC2.4), and Naïve CD4+ T cells isolated from OT-II mice were used to confirm the inhibitory effect of MFXD on the antigen presentation pathway. Additionally, chemical characterization of MFXD was performed. MFXD alleviated AR symptoms, mitigated histopathological alterations, and regulated plasma histamine and IgE levels, as well as IL-4, IL-13, and IFN-γ levels in the nasal lavage fluid (NLF) in AR mice. MFXD significantly reduced the number of nasal DEPs between AR and control groups, with the antigen processing and presentation pathway being the most prominently enriched. MFXD modulated splenic histopathology and spleen index, and decreased major histocompatibility complex class II (MHC-II) expression in both the nasal mucosa and spleen of AR mice. In vitro, MFXD diminished the antigen phagocytic capacity of lipopolysaccharide (LPS)-stimulated DC2.4 cells and lowered MHC-II and CD86 expression on both HNEpCs and DC2.4 cells; It also suppressed DC2.4-induced proliferation and differentiation of naive OT-II CD4+ T cells. MFXD also downregulated CD74, cathepsin S (CTSS), and MHC-II; this effect was partially reversed by the CD74 agonist MIF and by CD74 overexpression. This study explores one potential therapeutic mechanism of MFXD in AR. The findings suggests that MFXD may exert its therapeutic effect against AR by suppressing CD74/CTSS/MHC-II axis, thereby inhibiting antigen presentation. This work provides mechanistic insights that could inform the clinical use of MFXD and highlights potential targets for future AR drug development. Ephedrine, Pseudoephedrine, Methylephedrine, Benzoylmesaconine, Benzoylhypacoitine, Benzoylaconine, Asarone.

Pseudoephedrine Improves Chronic Obstructive Pulmonary Disease by Regulating Airway Senescence and Mitochondrial Function through PI3K/AKT/mTOR Axis.

Wu Lijuan L, Chen Fenqiao F, Zhang He H, Xu Wenzhong W et al.

Ephedra can improve chronic obstructive pulmonary disease (COPD). Pseudoephedrine (PSE) is a main active ingredients of ephedra. It has anti-inflammatory pharmacological properties. Its effect on COPD and its possible mechanism have not been elucidated. The COPD rat model was constructed by systemic cigarette smoke exposure combined with lipopolysaccharide (LPS) tracheal instillation. BEAS-2B cells were treated using cigarette smoke extract; PSE was administered for treatment. The senescence level of rat lung tissue and bronchial epithelial cells was evaluated through staining, immunofluorescence and western blot. The mitochondrial damage of rats and BEAS-2B cells was detected by transmission electron microscopy, JC-1 probe, MitoSOX Red probe and kits. In addition, the lung function indexes of rats were detected by animal lung function analysis system. Hematoxylin and eosin (HE) staining analyzed the pathological damage. Enzyme-linked immunosorbent assay (ELISA), kit and immunohistochemistry were used to evaluate inflammation and oxidative stress. Western blot detected phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) axis protein. PSE significantly reduced senescent cells, apoptosis rate and P21 level in rat lung tissue and BEAS-2B cells, significantly increased the levels of zonula occludens-1 (ZO-1)and adenosine triphosphate (ATP), restored mitochondrial structure, and visible mitochondrial cristae. It also inhibited reactive oxygen species (ROS) levels and mitochondrial excessive fission. PSE also significantly improved lung function in rats, increased mean alveolar number (MAN), reduced pro-inflammatory factors, and increased superoxide dismutase (SOD) levels. PSE markedly suppressed p-p85, p-AKT and p-mTOR protein expressions. In addition, the PI3K/AKT agonist 740Y-P weakened the effect of PSE on improving COPD. PSE inhibited PI3K/AKT/mTOR axis, improved lung tissue senescence, mitochondrial dysfunction and pathological damage, and reduced airway inflammation and oxidative stress damage, thereby alleviating COPD.

A novel pharmacokinetics-pharmacodynamics strategy for effective components exploration combined with metabolomics and proteomics: Application to Xingbei Zhike granule.

Gao Xia X, Yin MingKe M, Liu Jing J, Feng Jian J et al.

Traditional Chinese medicine (TCM) is characterized by its complex and diverse components, difficult to identify the effective components. In this study, a pharmacokinetics (PK)-pharmacodynamics (PD) strategy, integrating chemical component profile, PK, metabolomics, and proteomics, was developed to explore the effective components of Xingbei Zhike granule (XBZKG) in treating post-infection cough (PIC). The quality consistency of XBZKG was confirmed by evaluating 78 components across 20 batches. And its good curative effect against PIC was verified through measurements of cough latency, cough frequency, and biochemical assays. Meanwhile, XBZKG was found to ameliorate PIC-induced metabolic disturbances, particularly in amino acid metabolism. Interestingly, the pathological state of PIC itself altered the absorption and metabolism of XBZKG in rats. Among ten components, ephedrine, pseudoephedrine, and amygdalin fitted good dose-effect models with three PD indicators, with the PIC pathological state appearing to enhance their efficacy. Spearman correlation analysis further revealed that 15 components alleviated PIC-induced amino acid imbalances, and some structurally similar components exhibited synergistic effects. Integrative proteomic and metabolomic analysis identified 28 potential pathway of XBZKG in the treatment of PIC, mainly related to inflammation. Finally, in vitro cellular assays confirmed 15 components exert good anti-inflammatory activity. This study provides a reproducible strategy for identifying effective components in TCM and offers new insights into its multi-component, multi-target, and multi-pathway therapeutic mechanisms.

Phenylephrine- and Pseudoephedrine-Associated Psychotic Relapse in Stable Schizophrenia on Long-Acting Injectables: A Case Series and Clinical Caution.

Liu Tsung-Lin TL, Lee Kuan-Lin KL, Lin Huang-Chi HC