Largely Enhanced Surface Flashover Voltage of Poly(ether Imide) by Scalable and Durable ZnO Coating: A Gift from In Situ Growth.

Dielectric materials with high surface electric insulation strength are in great demand in a high-power space solar cell array (SSCA). A moderately conductive surface is favorable to inhibit charge accumulation and mitigate electric field distortion, thus improving the surface flashover voltage. Although numerous modification methods have been proposed to achieve this goal, the facile, efficient, scalable, and environmentally friendly modification strategy remains a critical challenge to date. Considering the excellent charge modulation ability of ZnO and its mild preparation conditions, a facile and economical hydrothermal strategy was proposed to fabricate in situ a durable poly(ether imide)/zinc oxide (PEI/ZnO) coating with a high charge decay rate. The blooming flower-like ZnO in the coating is proved to play a key role in enhancing lateral charge dissipation on the surface of PEI, thereby suppressing surface charge accumulation. It was also shown that the shielding effect of ZnO on high-energy photons during flashover and the catalytic effect of Zn2+ on PEI molecular chains during hydrothermal treatment had a facilitating and suppressing effect on outgassing, respectively, and consequently affected the flashover. Excitingly, the synergistic effects of both accelerated charge dissipation and suppressed outgassing helped to improve the flashover voltage of PEI by up to 36.7%. The strategy selected here is efficient, scalable, and facile, and the coating is durable, which makes sense for commercial promotion.

Pharmacokinetics-based comprehensive strategy to identify multiple effective components in Huangqi decoction against liver fibrosis.

BACKGROUND: Huangqi decoction (HQD) has been used to treat chronic liver diseases since the 11th century, but the effective components in HQD against liver fibrosis have not been definitively clarified. PURPOSE: To investigate and identify multiple effective components in HQD against liver fibrosis using a pharmacokinetics-based comprehensive strategy. METHODS: The absorbed representative components in HQD and their metabolites were detected in human plasma and urine using high-resolution mass spectrometry combined with a database-directed method, and then pharmacokinetics in multiple HQD components in human plasma was analyzed by ultra-performance liquid chromatography coupled with triple-quadruple mass spectrometry. Furthermore, the anti-fibrotic effect of potential effective HQD components was studied in LX-2 cells and that of a multi-component combination of HQD (MCHD) was verified in a mouse CCl4-induced hepatic fibrosis model. RESULTS: Twenty-four prototype components in HQD and 17 metabolites were identified in humans, and the pharmacokinetic characteristics of 14 components were elucidated. Among these components, astragaloside IV, cycloastragenol, glycyrrhizic acid, glycyrrhetinic acid, liquiritigenin, and isoliquiritigenin downregulated the mRNA expression of α-SMA; cycloastragenol, calycosin-7-O-ß-D-glucoside, formononetin, glycyrrhetinic acid, liquiritin, and isoliquiritin downregulated the mRNA expression of Col I; and calycosin, liquiritigenin, isoliquiritigenin, cycloastragenol, and glycyrrhetinic accelerated the apoptosis of LX-2 cells. MCHD reduced serum aminotransferase activity and hepatic collagen fibril deposition in mice with CCl4-induced hepatic fibrosis. CONCLUSION: Using the pharmacokinetics-based comprehensive strategy, we revealed that multiple effective HQD components act together against liver fibrosis.

Simultaneous quantification of multiple components in rat plasma by UPLC-MS/MS and pharmacokinetic study after oral administration of Huangqi decoction.

A rapid, sensitive and accurate UPLC-MS/MS method was developed for the simultaneous quantification of components of Huangqi decoction (HQD), such as calycosin-7-O-ß-d-glucoside, calycosin-glucuronide, liquiritin, formononetin-glucuronide, isoliquiritin, liquiritigenin, ononin, calycosin, isoliquiritigenin, formononetin, glycyrrhizic acid, astragaloside IV, cycloastragenol, and glycyrrhetinic acid, in rat plasma. After plasma samples were extracted by protein precipitation, chromatographic separation was performed with a C18 column, using a gradient of methanol and 0.05% acetic acid containing 4mm ammonium acetate as the mobile phase. Multiple reaction monitoring scanning was performed to quantify the analytes, and the electrospray ion source polarity was switched between positive and negative modes in a single run of 10 min. Method validation showed that specificity, linearity, accuracy, precision, extraction recovery, matrix effect and stability for 14 components met the requirements for their quantitation in biological samples. The established method was successfully applied to the pharmacokinetic study of multiple components in rats after intragastric administration of HQD. The results clarified the pharmacokinetic characteristics of multiple components found in HQD. This research provides useful information for understanding the relation between the chemical components of HQD and their therapeutic effects.

Chicken bile powder protects against α-naphthylisothiocyanate-induced cholestatic liver injury in mice.

This study explored the effects of chicken bile powder (CBP), a 2000-year-old Chinese medicine, on α-naphthyl isothiocyanate (ANIT)-induced intrahepatic cholestasis in mice. CBP treatment for 14 days significantly ameliorated ANIT-induced changes in serum alanine aminotransferase, aspartate aminotransferase, bile acids, bilirubin, γ-glutamyl transpeptidase, alkaline phosphatase, and liver tissue morphology. Serum metabolomics showed changes in 24 metabolites in ANIT-exposed mice; 16 of these metabolites were reversed by CBP treatment via two main pathways (bile acid biosynthesis and arachidonic acid metabolism). Additionally, CBP administration markedly increased fecal and biliary bile acid excretion, and reduced total and hydrophobic bile acid levels in the livers of cholestatic mice. Moreover, CBP increased liver expression of bile acid efflux transporters and metabolic enzymes. It also attenuated ANIT-induced increases in hepatic nuclear factor-κB-mediated inflammatory signaling, and increased liver expression of the nuclear farnesoid X receptor (FXR) in cholestatic mice. CBP also activated FXR in vitro in HEK293T cells expressing mouse Na+-taurocholate cotransporting polypeptide. It did not ameliorate the ANIT-induced liver injuries in FXR-knockout mice. These results suggested that CBP provided protection from cholestatic liver injury by restoring bile acid homeostasis and reducing inflammation in a FXR-dependent manner.

[Effect of Huangqi decoction on entecavir pharmacokinetics in rat plasma].

Entecavir (ETV), a guanosine nucleotide antiviral agent with activity against hepatitis B virus (HBV) and Huangqi decoction (HQD) that exerts significant therapeutic effects in liver cirrhosis are used as an effective drug combination in the treatment of liver cirrhosis with HBV. Therefore, this study was designed to assess the effect of HQD on ETV pharmacokinetics in rat plasma. Spraque-Dawley (SD) rats were randomized into single- and 7-day-dose experimental groups. The ETV and ETV-HQD groups were administered ETV and a simultaneous combination of ETV and HQD, respectively while the ETV-HQD-2h group received HQD 2 h after ETV treatment, all administered via intragastric (i.g.) gavage. A rapid, sensitive, and efficient ultra-high- performance liquid chromatography-linear trap quadrupole (UHPLC-LTQ)-Orbitrap method was developed and validated to determine ETV in rat plasma from blood samples collected at different time points following treatment. The linearity, accuracy, precision, recovery, matrix effects and stability of ETV were all satisfactory. The ETV-HQD group exhibited a decrease in the maximum plasma concentration (Cmax), and a delay in time to achieve Cmax (tmax) following single- and multi-dose administrations, and decreased area under the concentration- time curve (AUC0­t) following single dosing. ETV pharmacokinetics did not change significantly between the ETV and ETV-HQD-2h groups. In vitro everted intestinal sac models experiments indicated that HQD decreased the absorption of ETV. HQD prevented ETV from accessing the intestinal mucosa epithelial surface, thereby decreasing its absorption in rats.