• Clean Technology
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• v.27 no.2
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• pp.115-123
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• 2021

This study demonstrates a new method for the synthesis of organic-inorganic hybrid particles composed of an inorganic silica shell and organic core particles. The organic core particles are prepared with a uniform size using droplet-based microfluidic technology. In the process of preparing the organic core particles, uniform droplets are generated by independently controlling the flow rates of the dispersed phase containing photocurable resins and the continuous phase. After the generation of droplets in a microfluidic device, the droplets are photo-polymerized as particles by ultraviolet irradiation at the ends of microfluidic channels. The core particle is coated with a nano complex composed of polyallylamine hydrochloride (PAH) and phosphate ion (Pi) through strong non-covalent interactions such as hydrogen bonding and electrostatic interaction under optimized pH conditions. The polyamine nano complex rapidly induces the condensation reaction of silicic acid through the arranged amine groups of the main chain of PAH. Therefore, this method enabled the preparation of organic-inorganic hybrid particles coated with inorganic silica nanoparticles on the organic core. Finally, we demonstrated the synthesis of organic-inorganic hybrid particles in a short time under ambient and environmentally friendly conditions, and this is applicable to the production of organic-inorganic hybrid particles having various sizes and shapes.

• Yonsei Medical Journal
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• v.59 no.9
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• pp.1096-1106
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• 2018

Purpose: Alzheimer's disease (AD) is the sixth most common cause of death in the United States. MicroRNAs have been identified as vital players in neurodegenerative diseases, including AD. microRNA-128 (miR-128) has been shown to be dysregulated in AD. This study aimed to explore the roles and molecular mechanisms of miR-128 in AD progression. Materials and Methods: Expression patterns of miR-128 and peroxisome proliferator-activated receptor gamma ($PPAR-{\gamma}$) messenger RNA in clinical samples and cells were measured using RT-qPCR assay. $PPAR-{\gamma}$ protein levels were determined by Western blot assay. Cell viability was determined by MTT assay. Cell apoptotic rate was detected by flow cytometry via double-staining of Annexin V-FITC/PI. Caspase 3 and $NF-{\kappa}B$ activity was determined by a Caspase 3 Activity Assay Kit or $NF-{\kappa}B$ p65 Transcription Factor Assay Kit, respectively. Bioinformatics prediction and luciferase reporter assay were used to investigate interactions between miR-128 and $PPAR-{\gamma}$ 3'UTR. Results: MiR-128 expression was upregulated and $PPAR-{\gamma}$ expression was downregulated in plasma from AD patients and $amyloid-{\beta}$ $(A{\beta})-treated$ primary mouse cortical neurons (MCN) and Neuro2a (N2a) cells. Inhibition of miR-128 decreased $A{\beta}-mediated$ cytotoxicity through inactivation of $NF-{\kappa}B$ in MCN and N2a cells. Moreover, $PPAR-{\gamma}$ was a target of miR-128. $PPAR-{\gamma}$ upregulation attenuated $A{\beta}-mediated$ cytotoxicity by inactivating $NF-{\kappa}B$ in MCN and N2a cells. Furthermore, $PPAR-{\gamma}$ downregulation was able to abolish the effect of anti-miR-128 on cytotoxicity and $NF-{\kappa}B$ activity in MCN and N2a cells. Conclusion: MiR-128 inhibitor decreased $A{\beta}-mediated$ cytotoxicity by upregulating $PPAR-{\gamma}$ via inactivation of $NF-{\kappa}B$ in MCN and N2a cells, providing a new potential target in AD treatment.