ABSTRACT
Cellulose nanocrystals (CNCs) with silver nanoparticles (AgNPs) are used for applications ranging from chemical catalysis to environmental remediation, and generation of smart electronics and biological medicine such as antibacterial agents. To reduce the synthesis cost of AgNPs and environmental pollution, microwave-assisted generation of AgNPs on the CNC surface (AgNPs@CNC) has been found to be useful, because microwave reaction has the advantages of simple reaction conditions, short reaction time and high reaction efficiency. The silver ions (Ag+) could be added to the CNC suspension and placed in the microwave reactor for a few minutes to produce AgNPs. AgNP generation was affected by factors such as the concentrations of Ag+ and CNC, and the power of the microwave, as well as the time of reaction. In this study, we used trace amounts of AgNO3 to rapidly synthesize AgNPs using a green microwave-based method instead of Tollen's reagent, and the antibacterial activity of the T1 sample showed that only using 0.03 mM (â¼0.01 wt%) AgNO3 to synthesize AgNPs@CNC could achieve good antibacterial properties.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the relationship between and underlying mechanistic pathway of clusterin (CLU) and chemo-resistance ofhepatocellular carcinoma (HCC) cells.</p><p><b>METHODS</b>CLU protein expression in HCC cell lines (Hep3B, SMMC7721, PLC, and HepG2) and HepG2/ADM cells was quantified by western blotting. Four short-hairpin (sh)RNAs designed to block CLU-mRNA were generated, screened by RT-PCR, and transfected into the cells to determine effects of CLU on cell viability and apoptosis. Effects of CLU blockade on drug efflux pump activity were measured by flow cytometry.</p><p><b>RESULTS</b>CLU was found to be over-expressed in HCC cell lines and HepG2/ADM cells. The four shRNAs inhibited CLU-mRNA as follows (vs. levels in untransfected cells): shRNA-1: 73.68% (q =23.011, P < 0.01), shRNA-2: 39.26% (q =11.991, P < 0.01), shRNA-3: 62.36% (q =19.392, P < 0.01), and shRNA-4: 55.35% (q =17.149, P < 0.01). shRNA-mediated depletion of CLU led to increased sensitivity to anti-cancer drugs and increased doxorubicin-induced apoptosis in HepG2/ADM cells, as evidenced by the apoptosis ratio of the shRNA-1 group of 39.28% vs. the apoptosis ratio of the untransfected control group of 4.92%. Silencing of CLU also decreased drug etflux pump activity, and the level of MDR1/P-gp expression was significantly reduced (shRNA-1 group vs.untransfected control group: q =14.604, P < 0.01).</p><p><b>CONCLUSION</b>CLU repression may enhance sensitivity of HCC cells to anti-cancers drugs and represents a potential molecular-target for reversal of multidrug-resistant HCC.</p>