Lotus (Nelumbo nucifera) leaves, a traditional Chinese medicinal herb, are rich in flavonoids.In an effort to thoroughly analyze their flavonoid components, macroporous resin chromatography coupled with HPLC-MS/MS was employed to simultaneously enrich and identify flavonoids from lotus leaves. Flavonoids extracted from lotus leaves were selectively enriched in the macroporous resin column, eluted subsequently as fraction II, and successively subjected to analysis with the HPLC-MS/MS and bioactivity assays. Altogether, fourteen flavonoids were identified, four of which were identified from lotus leaves for the first time, including quercetin 3-O-rhamnopyranosyl-(1→2)-glucopyranoside, quercetin 3-O-arabinoside, diosmetin 7-O-hexose, and isorhamnetin 3-O-arabinopyranosyl-(1→2)-glucopyranoside. Further bioactivity assays revealed that these flavonoids from lotus leaves possess strong antioxidant activity, and demonstrate very good potential to be explored as food supplements or even pharmaceutical products to improve human health.

cRelatively little is known about the hepatotoxicity of pyrazinamide (PZA). PZA requires activation by amidase to form pyrazinoic acid (PA). Xanthine oxidase then hydroxylates PA to form 5-hydroxypyrazinoic acid (5-OH-PA). PZA can also be directly oxidized to form 5-OH-PZA. Before this study, it was unclear which metabolic pathway or PZA metabolites led to hepatotoxicity. This study determines whether PZA metabolites are responsible for PZA-induced hepatotoxicity. PZA metabolites were identified and cytotoxicity in HepG2 cells was assessed. Potential PZA and PA hepatotoxicity was then tested in rats. Urine specimens were collected from 153 tuberculosis (TB) patients, and the results were evaluated to confirm whether a correlation existed between PZA metabolite concentrations and hepatotoxicity. This led to the hypothesis that coadministration of amidase inhibitor (bis-p-nitrophenyl phosphate [BNPP]) decreases or prevents PZA-and PZA metabolite-induced hepatotoxicity in rats. PA and 5-OH-PA are more toxic than PZA. Electron microscopy showed that PZA and PA treatment of rats significantly increases aspartate transaminase (AST) and alanine aminotransferase (ALT) activity and galactose single-point (GSP) levels (P < 0.005). PA and 5-OH-PA levels are also significantly correlated with hepatotoxicity in the urine of TB patients (P < 0.005). Amidase inhibitor, BNPP, decreases PZA-induced, but not PA-induced, hepatotoxicity. This is the first report of a cell line, animal, and clinical trial confirming that the metabolite 5-OH-PA is responsible for PZA-induced hepatotoxicity.

Paroxysmal dyskinesias are a group of neurological diseases characterized by intermittent episodes of involuntary movements with different causes. Paroxysmal kinesigenic dyskinesia (PKD) is the most common type of paroxysmal dyskinesia and can be divided into primary and secondary types based on the etiology. Clinically, PKD is characterized by recurrent and transient attacks of involuntary movements precipitated by a sudden voluntary action. The major cause of primary PKD is genetic abnormalities, and the inheritance pattern of PKD is mainly autosomal-dominant with incomplete penetrance. The proline-rich transmembrane protein 2 (PRRT2) was the first identified causative gene of PKD, accounting for the majority of PKD cases worldwide. An increasing number of studies has revealed the clinical and genetic characteristics, as well as the underlying mechanisms of PKD. By seeking the views of domestic experts, we propose an expert consensus regarding the diagnosis and treatment of PKD to help establish standardized clinical evaluation and therapies for PKD. In this consensus, we review the clinical manifestations, etiology, clinical diagnostic criteria and therapeutic recommendations for PKD, and results of genetic analyses in PKD patients performed in domestic hospitals.

Background:The total flavonoid (TF) and total phenolic (TP) contents of the ethanol extracts of the whole plant, stem, leaf, and seed of Mimosa pudica Linn belonging to the genus Mimosa (Family: Fabaceae alt. Leguminosae), which originates from the subtropical regions of southern China, were determined in this experiment.Materials and Methods:The antioxidant activity of the extracts and 5 flavonoid monomers of M. pudica Linn. were also evaluated by 2 assays, the 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical-scavenging activity and ferric reducing/antioxidant power (FRAP) assays. In addition, correlation analysis was also made in the present study.Results:The results showed that leaf extracts contained the highest amount of TF and TP, and the content was significantly higher than that found in other parts of the plant. Moreover, the sequence of antioxidant activity of the ethanol extracts was as follows: leaf > the whole plant > seed > stem; the sequence of the 5 flavonoid monomers was as follows: 5,7,3´,4´-tetrahydroxy-6-C-[β-D-apiose-(1→4)]-β-D-glycopyranosyl flavone (1) > isorientin (2) > orientin (3) > isovitexin (4) > vitexin (5), and the antioxidant activity of compound 1 is equivalent to the synthetic antioxidant trolox or a bit stronger than trolox, and significant correlations were found among the active ingredient contents and the results of antioxidant activity.Conclusion:The present study suggested that M. pudica Linn. could be a potential rich source of natural antioxidants.