In this article, ZnO nanostructures were synthesized via the hydrothermal method which used ZnCl(2) and HMTA mixed solution as the precursor. A multistep growth was adopted to improve the growth restriction of a closed system, not only the length but also the aspect ratio were increased with steps of growth, and the shape of nanorods maintained integrity. Furthermore, photoluminescence spectra which have the near-band-edge-emission (∼3.37 eV) and defect-related emission show the optical properties of ZnO nanostructures. The defect-related emission intensity was greatly enhanced with the increasing surface area of ZnO nanowires. The level of the OH group was attributed to the yellow-light emission (∼580 nm) and the red-shift phenomenon. In addition, we fabricated two types of ultraviolet photodetectors: a single nanowire device and a nanowire-array device, operating at a low bias (less than 5 mV). With the lower energy consumption and the weaker persistent photoconductive effect, our ultraviolet photodetectors have better performance, exhibiting a short response time and higher sensitivity.

An EtOH extract of the dried aerial parts of Ruta graveolens was suspended in water and then partitioned with EtOAc. Three new glycosides, 3'-sinapoyl-6-feruloylsucrose (4), methylcnidioside A (5), and methylpicraquassioside A (6), together with four known glycosides, 3',6-disinapoylsucrose (1), cnidioside A (2), rutin, and picraquassioside A (3), were isolated from the water-soluble part. Their structures were elucidated by interpretation of IR, MS, and 1D and 2D NMR spectra and comparison with literature data.

The Na 1 /glucose cotransporter 1 (SGLT1) is responsible for glucose uptake in intestinal epithelial cells. It has been shown that the intestinal SGLT1 level is significantly increased in diabetic individuals and positively correlated with the pathogenesis of diabetes. The development of targeted therapeutics that can reduce the intestinal SGLT1 expression level is, therefore, important. In this study, we showed that ginsenoside Rg1 effectively decreased intestinal glucose uptake through inhibition of SGLT1 gene expression in vivo and in vitro. Transient transfection analysis of the SGLT1 promoter revealed an essential cAMP response element (CRE) that confers the Rg1-mediated inhibition of SGLT1 gene expression. Chromatin immunoprecipitation assay and targeted CRE-binding protein (CREB) silencing demonstrated that Rg1 reduced the promoter binding of CREB and CREB binding protein associated with an inactivated chromatin status. In addition, further studies showed that the epidermal growth factor receptor (EGFR) signaling pathway also plays an essential role in the inhibitory effect of Rg1; taken together, our study demonstrates the involvement of the EGFR-CREB signaling pathway in the Rg1-mediated downregulation of SGLT1 expression, which offers a potential strategy in the development of antihyperglycemic and antidiabetic treatments.

Scope:The Na + /glucose cotransporter 1 (SGLT1) plays a crucial role in glucose uptake in intestinal epithelial cells (IECs), which has been shown essential in ameliorating intestinal inflammation. Ginseng has historically been used to treat inflammatory disorders. Understanding the regulatory mechanism of ginseng-mediated induction of SGLT1 gene expression in human intestinal cells is therefore important. Methods and results:We demonstrate that ginsenoside compound K (CK) enhances SGLT1-mediated glucose uptake in mice and human intestinal Caco-2 cells. Transient transfection analysis using SGLT1 promoter-luciferase reporters demonstrated that the presence of an essential cAMP response element (CRE) is required for CK-mediated induction of SGLT1 gene expression. The ChIP assays indicated that increased CRE-binding protein (CREB) and CREBbinding protein (CBP) binding to the SGLT1 promoter in CK-treated cells is associated with an activated chromatin state. Our result showed that the increased CREB phosphorylation is directly correlated with SGLT1 expression in IECs. Further studies indicated that the epidermal growth factor receptor (EGFR) signaling pathway is involved in the CK-mediated effect. Conclusion: These findings provide a novel mechanism for the CK-mediated upregulation of SGLT1 expression through EGFR-CREB signaling activation, which could contribute to reducing gut inflammation.