Activation of Peroxymonosulfate by Co-Ni-Mo Sulfides/CNT for Organic Pollutant Degradation.

To explore advanced oxidation catalysts, peroxymonosulfate (PMS) activation by Co-Ni-Mo/carbon nanotube (CNT) composite catalysts was investigated. A compound of NiCo2S4, MoS2, and CNTs was successfully prepared using a simple one-pot hydrothermal method. The results revealed that the activation of PMS by Co-Ni-Mo/CNT yielded an exceptional Rhodamine B decolorization efficiency of 99% within 20 min for the Rhodamine B solution. The degradation rate of Co-Ni-Mo/CNT was 4.5 times higher than that of Ni-Mo/CNT or Co-Mo/CNT, and 1.9 times as much than that of Co-Ni/CNT. Additionally, radical quenching experiments revealed that the principal active groups were 1O2, surface-bound SO4•-, and •OH radicals. Furthermore, the catalyst exhibited low metal ion leaching and favorable stability. Mechanism studies revealed that Mo4+ on the surface of MoS2 participated in the oxidation of PMS and the transformation of Co3+/Co2+ and Ni3+/Ni2+. The synergism between MoS2 and NiCo2S4 reduces the charge transfer resistance between the catalyst and solution interface, thus accelerating the reaction rate. Interconnected structures composed of metal sulfides and CNTs can also enhance the electron transfer process and afford sufficient active reaction sites. Our work provides a further understanding of the design of multi-metal sulfides for wastewater treatment.

Tanshinone IIA Suppresses Glioma Cell Proliferation, Migration and Invasion Both in vitro and in vivo Partially Through miR-16-5p/Talin-1 (TLN1) Axis.

BACKGROUND: Tanshinone IIA (TIIA) is one of the active constituents derived from the rhizome of Danshen, a traditional Chinese herbal. Recently, microRNAs (miRNAs) have been suggested to be associated with the anticancer role of TIIA. However, it remains vague of the interaction between miRNAs and TIIA in glioma, a common aggressive brain tumor in humans. METHODS: Expression of miRNA (miR)-16-5p and talin-1 (TLN1) was detected using reverse transcription-quantitative polymerase chain reaction and Western blotting. Cell proliferation, migration and invasion were assessed with cell viability assay, transwell assay, Western blotting, and xenograft tumor experiment. The target binding between miR-16-5p and TLN1 was confirmed by dual-luciferase reporter assay and RNA pull-down assay. RESULTS: TIIA treatment inhibited cell viability, migration and invasion, and decreased Cyclin D1, matrix metalloproteinase (MMP)-9 and Vimentin expression in glioma T98G and A172 cells both in vitro and in vivo. Thus, TIIA induced anti-glioma role, wherein miR-16-5p was upregulated and TLN1 was downregulated. Moreover, silencing miR-16-5p could abate TIIA-mediated suppression on glioma cell proliferation, migration and invasion in vitro and in vivo. TLN1 overexpression also exerted tumor-promoting effect in TIIA-treated T98G and A172 cells. Mechanically, miR-16-5p could regulate TLN1 expression via target binding, and depleting TLN1 could counteract the inhibitory effect of miR-16-5p knockdown on the curative effect of TIIA in T98G and A172 cells. CONCLUSION: TIIA exerted the anti-proliferation, anti-migration and anti-invasion role in glioma cells both in vitro and in vivo partially through regulating miR-16-5p/TLN1 axis.