Visible-Light-Driven Hydrogen Release from Dye-Sensitized Hydrogen Boride Nanosheets.

Hydrogen boride (HB) nanosheets are expected to be safe and lightweight hydrogen carriers because of their high gravimetric hydrogen density (8.5 wt %) and photon-driven hydrogen release under mild conditions. However, previously reported HB nanosheets respond only to ultraviolet (UV) light to release hydrogen. In this study, we develop dye-modified HB nanosheets that can release hydrogen under visible light irradiation (>470 nm) without heat input. Hydrogen generation is initiated by electron injection from excited dye molecules into the conduction band of the HB nanosheets. The conduction band of the HB nanosheets is formed by the antibonding states of the B 2py and H 1s atomic orbitals, and the electrons injected from the dye molecules react with the protons of the HB nanosheets to release gaseous hydrogen molecules. Although the hydrogen production is terminated after long-term light irradiation owing to dye oxidation and/or loss of protons in HB nanosheets, the total amount of the released hydrogen molecules corresponds to approximately 25% of the protons in HB nanosheets even under the extra mild conditions. The addition of a sacrificial agent like iodine ions and a proton source like formic acid sustained the H2 generation from the dye-modified HB nanosheets under visible light irradiation for long term.

Efficient cellular uptake of the novel NF-kappaB inhibitor (-)-DHMEQ and irreversible inhibition of NF-kappaB in neoplastic cells.

NF-kappaB is a transcription factor that induces the expression of inflammatory cytokines and antiapoptotic proteins. Earlier we designed a new NF-kappaB inhibitor, (-)-DHMEQ, and showed that it had potent anticancer and anti-inflammatory activities in various animal models without any toxicity. In the present research, we studied whether (-)-DHMEQ could be efficiently taken by cultured cells and irreversibly inhibit NF-kappaB by short time application to cultured cells. Even after mouse monocytic leukaemia RAW264.7 cells had been washed free of (-)-DHMEQ, lipopolysacharide (LPS)-induced activation of NF-kappaB in these cells was still inhibited. Moreover, topical application for 15 min was found to induce dormancy of the cells against LPS for 2-8 h. When it was topically added to RAW264.7 cells in which NF-kappaB was activated by LPS, the inhibition lasted at least for 2 h. NF-kappaB derectly upregulates expression of iNOS that produces NO. Short time application of (-)-DHMEQ also inhibited the function of cells in terms of NO production and iNOS induction in RAW264.7 cells. Thus, the fast incorporation of (-)-DHMEQ into the cells and irreversible inhibition of NF-kappaB by it were demonstrated, and this observation would explain its effective inhibition of certain functions in cellular and animal disease models.

A new NF-κB inhibitor based on the amino-epoxyquinol core of DHMEQ.

The amino-epoxyquinols 6a and 6b were synthesized as soluble derivatives of an NF-κB inhibitor DHMEQ (1). In spite of the opposite configuration from 1, 6b rather than 6a affected the deactivation of NF-κB, based on NO secretion and MALDI-TOF MS analysis. It was indicated that 6b inhibited the activation by different manner from that of 1.