Hybrid dynamic coating using n-dodecyl beta-d-maltoside (DDM) and methyl cellulose (MC) has been developed for suppression of analyte adsorption and electroosmotic flow (EOF) in a poly(methyl methacrylate) (PMMA) channel. The adsorption of APTS-labeled sugars in a PMMA channel was obviously suppressed with DDM dynamic coating; however, EOF was reduced only by a factor of approximately 25%, resulting in irreproducible separations. In contrast, both analyte adsorption and EOF in a PMMA channel were efficiently minimized with MC coating; however, concentrated MC above 0.3% was required to achieve high-performance separations, which greatly increased viscosity of the solution and caused difficulties during buffer loading and rinsing. In addition, n-dodecyltrimethylammonium chloride did not show observable effects on reducing analyte adsorption, although it has the same hydrophobic alkyl chain as DDM. These results strongly indicated that the polysaccharide moiety of surface modifiers has a specific affinity to surface charges and is crucial to achieving efficient and stable dynamic coating on the PMMA surface. Hybrid dynamic coating with 0.25% DDM and 0.03% MC was found to minimize both analyte adsorption and EOF in a PMMA channel to a negligible level, while still keeping a low viscosity of the solution. High-speed and high-throughput profiling of the N-linked glycans derived from alpha1-acid glycoprotein, fetuin, and ribonuclease B was demonstrated in both single-channel and 10-channel PMMA chips using DDM-MC hybrid coating. We propose that DDM-MC hybrid coating might be a general method for suppressing analyte adsorption and EOF in polymer MCE devices. The current MCE-based method might be a promising alternative for high-throughput screening of carbohydrate alterations in glycoproteins.
Alisol B 23-acetate (AB23A) is a natural triterpenoid isolated from Chinese herbal medicine and has a variety of biological functions, especially anti-cancer e ects. However, the e ects and mechanisms of AB23A in hepatocellular carcinoma (HCC) remain unclear. Cell viability, invasion and migration were measured by MTT, Transwell and wound healing assays, respectively. To detect cell cycle and apoptosis, a ow cytometry assay was used. Tumor xenogra experiment was performed to measure tumor growth. e enzymatic assay was used to determine the activity of matrix metalloproteinase (MMP)-2 and-9. Furthermore, the mRNA and protein levels of Bcl-2, Bax, Caspase-3/-9, MMP-2/-9 and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) were detected by RT-PCR and Western blotting assays. AB23A suppressed cell viability in a concentration-dependent manner, blocked cell cycle, and induced apoptosis via up-regulating Bax, Caspase-3 and Caspase-9, and down-regulating Bcl-2 in HCC cells both in vitro and in vivo. In addition, AB23A inhibited cell invasion and migration through down-regulating MMP-2/-9 activities. e e ects of AB23A might be associated with the PI3K/Akt signaling pathway in HCC cells. Taken together, the present data demonstrated that AB23A might play a role in suppressing the progression of HCC, revealing the value of AB23A for hepatocellular carcinoma treatment in clinic.
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