Glutathione-mediated intracellular release of anti-inflammatory N-acetyl-L-cysteine from mesoporous silica nanoparticles
표제/저자사항
Glutathione-mediated intracellular release of anti-inflammatory N-acetyl-L-cysteine from mesoporous silica nanoparticles / Ahn Na Koo, Hwa Pyeong Rim, Dong Jin Park, Jong-Ho Kim, Seo Young Jeong, Sang Cheon Lee
형태사항
p. 809-814 ; 29 cm
주기사항
수록자료: Macromolecular research. Polymer Society of Korea. Vol.21 no.7(2013 July), p. 809-814 21:7<809 ISSN 1598-5032 저자: Ahn Na Koo, Department of Maxillofacial Biomedical Engineering & Institute of Oral Biology, School of Dentistry, Kyung Hee University 저자: Hwa Pyeong Rim, Department of Life and Nanopharmaceutical Science, Kyung Hee University 저자: Dong Jin Park, Department of Life and Nanopharmaceutical Science, Kyung Hee University 저자: Jong-Ho Kim, Department of Pharmaceutical Science, College of Pharmacy, Kyung Hee University E-MAIL: jonghokim@khu.ac.kr 저자: Seo Young Jeong, Department of Life and Nanopharmaceutical Science, Kyung Hee University 저자: Sang Cheon Lee, Department of Maxillofacial Biomedical Engineering & Institute of Oral Biology, School of Dentistry, Kyung Hee University E-MAIL: schlee@khu.ac.kr
We report on a smart mesoporous silica nanoparticle (MSN) that can trigger the release of anti-inflammatory N-acetyl-L-cysteine (NAC) within the intracellular environment. NAC was conjugated to the pore surfaces of MSNs through glutathione (GSH)-cleavable disulfide linkages. Solid-state nuclear magnetic resonance (NMR), Fourier-transform infrared (FTIR) spectroscopy, and Brunauer-Emmett-Teller (BET) analyses confirmed the successful NAC conjugation to the pore walls. The release of NAC from the NAC-conjugated MSN (MSN-NAC) could be controlled by adjusting the concentration of GSH regarding the release media. At an extracellular level of GSH (10 μM), the NAC release was greatly inhibited, whereas, at an intracellular level of GSH (2 mM), MSN-NAC facilitated the release of NAC. Confocal laser scanning microscopy (CLSM) studies showed that the NAC release was effectively triggered by intracellular GSH after uptake by BV-2 microglial cells. The MSN developed in this work may serve as the efficient intracellular carriers of NAC for the treatment of neuroinflammation.
