San-huang dispersible tablet (SHDT) was designed with a patented technology to enrich the active ingredients in rhubarb and with a wide selection of excipients in the new manufacturing procedure. The total rhubarb anthraquinones were first enriched in the extract by our patented technology. Eudragit L100, S100 and PEG-6000 were used to release a part of the total rhubarb anthraquinones at the colon to induce the cathartic effect of the anthraquinones by another patented technology. Microcrystalline Cellulose (MCC), low-substituted hydroxypropyl cellulose (L-HPC), sodium carboxymethyl starch (CMS-Na), and hydroxypropyl methylcellulose (HPMC) were used to ensure quick release of baicalin and berberine hydrochloride in the stomach. The dissolution of SHDT was evaluated by a method in 2005 Chinese Pharmacopoeia along with San-huang tablet (SHT), and the results demonstrated that the dissolution of baicalin and berberine hydrochloride more than double that of SHT and release of half of the rhubarb anthraquinones in colon.

ObjectiveTo investigate the in vitro antivirus effect of total flavonoid from Trollius ledebouri Reichb (TFTLR).MethodsMadin-Darby canine kidney (MDCK) and Human epithelial type 2 (HEp-2) cell lines were used to test the antivirus effect of TFTLR on nine virus subtypes: four H1N1, one H3N2, and four other subtypes prevalent in North China. Tamiflu, Ribavirin and Lianhua Qingwen were used as active comparators. Comprehensive molecular pathway analyses of TFTLR-H1N1 and TFTLR-H3N2 relationships were also conducted.ResultsTFTLR inhibited MDCK cell lesions induced by H1N1 subtypes (A/FM1/1/47, A/Puerto Rico/8/1934 H1N1, A1/Tianjin Jinnan/15/2009, and A/Brisbane/59/2007) and by the H3N2 Brisbane/10/2009 strain. TFTLR inhibitory concentration (IC)50 values against these viruses were 0.13, 0.07, 0.06, 0.14, and 0.07 mg/ml, respectively; and therapeutic index (TI) values were 8.62, 16.0, 18.67, 8.0, and 16.0, respectively. TFTLR showed no effect on parainfluenza virus type 1, herpes simplex virus type 1, respiratory syncytial virus, and coxsackie group B virus type 4. Pathway analysis revealed possible functional therapeutic mechanisms for TFTLR against H1N1 and H3N2 infections.ConclusionTFTLR may represent a potential therapeutic agent against influenza A subtypes H1N1 and H3N2 that are prevalent in North China, and should be investigated further.

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Background: The seeds of Polygonatum cyrtonema Hua have dormancy phenomenon. Previous studies have shown that sand storage factors effects of the seed dormancy of P. cyrtonema Hua seeds and enhance the seed germination process. Subsequently, metabolic activities and different changes during the sand storage and germination process of P. cyrtonema Hua seed has not been heavily researched.Results: In this study the changes in the metabolites of P. cyrtonema Hua seeds at different sand storage times and germination stages, we used untargeted metabolomics to determine them. Most of the sugar and glycoside contents in seed coat increased after 30 d on the other hand, in peeled seeds increased at 30 d and decreased at 60 d after sand storage treatment. The content of proline and benzoic acid decreased in the seed coat after sand storage. PCA, OPLS-DA and HCA showed that the contents of most metabolites increased after 7 d and decreased after 14 d of seed germination. The process of 7 d to 14 d was the key stage of seed germination of P. cyrtonema Hua. Differential metabolic pathway analysis showed that seed germination was controlled by multiple metabolic pathways. Metabolic correlation revealed the interdependence between seed germination metabolites and metabolic pathways. Conclusion: Sand storage can significantly increase the rate of seed germination and play a vital role in seed dormancy of P. cyrtonema Hua. There was inherent differences in metabolites during different storage time and germination stages in P. cyrtonema Hua. Our work provides a first glimpse of the metabolome in seed germination of P. cyrtonema Hua, and provides a valuable informations for revealing the mechanism of breaking seed dormancy.