Inhibitory effect of Ephedra herba on human norovirus infection in human intestinal organoids.

Human norovirus (HuNoV) is a major cause of acute gastroenteritis and foodborne diseases worldwide with public health concern, yet no antiviral therapies have been developed. In this study, we aimed to screen crude drugs, which are components of Japanese traditional medicine, ''Kampo'' to see their effects on HuNoV infection using a reproducible HuNoV cultivation system, stem-cell derived human intestinal organoids/enteroids (HIOs). Among the 22 crude drugs tested, Ephedra herba significantly inhibited HuNoV infection in HIOs. A time-of-drug addition experiment suggested that this crude drug more preferentially targets post-entry step than entry step for the inhibition. To our knowledge, this is the first anti-HuNoV inhibitor screen targeting crude drugs, and Ephedra herba was identified as a novel inhibitor candidate that merits further study.

Comparative pharmacokinetic studies of Ephedra herba in common cold and nephrotic syndrome rat models.

Ephedra herba is a conventional Chinese medicine to treat cold, fever, asthma, edema, and lung diseases in the clinic. At present, most pharmacokinetic studies focus on the pharmacokinetic process of alkaloids in normal animals. However, the non-alkaloid components are also active. In addition, the pharmacokinetic studies under pathological state make more sense for clarifying the material basis of efficacy. In this study, a sensitive and rapid ultra-high-performance-tandem mass spectrometry method was developed and applied to determine nine bioactive components (ephedrine, pseudoephedrine, methylephedrine, (+)-catechin, epicatechin, vitexin, vicenin-2, cinnamic acid, and ferulic acid) in normal, common cold and nephrotic syndrome rats after the oral administration of Ephedra herba. Compared to the normal group, except for ferulic acid, the exposure levels of the other eight components were significantly increased and the plasma clearance clearly declined in common cold rats. Similarly, the exposure levels of seven components other than cinnamic acid and ferulic acid were also significantly augmented and the plasma clearance decreased significantly in nephrotic syndrome rats. In brief, the pathological conditions of the common cold and nephrotic syndrome could lead to alterations in the pharmacokinetics profiles of the nine components, which provide a reference for further exploration of the pharmacodynamics basis of Ephedra herba.

Molecular Mechanism of Belamcandae Rhizoma and Ephedrae Herba Couplet Medicines in Treating Asthma Based on Network Pharmacology / 中国实验方剂学杂志

Objective:To analyze the effective active ingredients of Belamcandae Rhizoma and Ephedrae Herba couplet medicines(BREH)in the treatment of bronchial asthma based on network pharmacology, in order to predict their potential targets and explore the mechanism. Method:Active ingredients and predict their targets were collected from traditional Chinese medicine system pharmacology(TCMSP) database. Drugs-components-targets network and Proteins interations network were built by STRING database and Cytoscape software. ClusterProfiler and ClueGO was used to enrich the biological function and metabolic pathway of core targets. Finally, candidate targets were mapped onto the pictures of correlative pathways. Result:The 38 effectively active ingredients were screened out, including luteolin, stigmasterol, diosmetin, naringenin, quercetin, iristectorigenin A, isorhamnetin. There were 214 candidate targets relating to bronchial asthma, and 55 core ones were selected to be mainly studied, including RAC-alpha serine/threonine-protein kinase (Akt1), tumor necrosis factor (TNF), mitogen-activated protein kinase 1 (MAPK1), vascular endothelial growth factor A (VEGFA), interleukin-10 (IL-10), NF-kappa-B inhibitor alpha (NFKBIA), and a number of relevant gene ontology(GO) functions and Kyoto Encyclopedin of Genes and Genomes(KEGG) pathways were enriched. Conclusion:BREH may regulate the Th1, Th2 and Th17 cell differentiations, Asthma, IL-17, phosphatidylinositol-3-kinases(PI3K)/Akt, MAPK, NF-κB, VEGF signaling pathways, so as to interfere the process of cell metabolism, and inhibit gene expression of proinflammatory factor in the treatment of bronchial asthma.