1. Effects of the silicon-containing chemical species dissolved from chitosan–siloxane hybrids on nerve cells.
- Author
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Hattori, Kosei, Hayakawa, Satoshi, and Shirosaki, Yuki
- Abstract
Silicic acid components from bioactive glass activate osteoblasts gene for bone generation. Many studies have been reported on osteoblast compatibility and bone regeneration using composites and hybrids, including silica or siloxane units. We previously synthesized chitosan−siloxane hybrids via a sol-gel method and observed bone and nerve regeneration. However, it is not clear the structure of molecules involving silicon atoms that has a more effective role in the cell activity and their mechanisms of cell activation. In this study, we prepared hybrid materials from chitosan and different types of alkoxysilane, 3-glycidoxypropyltrimethoxysilane (GPTMS), 3-glycidoxypropyldimethoxymethylsilane (GPDMS), and tetraethoxysilane (TEOS), and investigated the structures of the silicon-containing species dissolved from each hybrid and their effect on the proliferation of nerve cells. The silicon-containing species in the extraction were mainly 100–600 molecular weight, indicating they were chitin/chitosan units and monomeric hydrolyzed GPTMS, GPDMS, and TEOS. The nerve cell proliferation was inhibited by the chitosan–GPTMS and GPDMS hybrid extractions. The silicon-containing species were not taken up by the cells. The silicon-containing species dissolved from the hybrids were adsorbed to the cells or they inactivated biomolecules in the culture medium, suppressing cell proliferation. Highlights: The silicon-containing species dissolved from chitosan–siloxane hybrid were corresponding to hydrolyzed GPTMS, GPDMS, and TEOS with chitosan oligomers. Nerve cells did not uptake the silicon-containing species. The silicon-containing species derived from Chitosan–GPTMS and –GPDMS hybrids inhibited nerve cell proliferation. The silicon-containing species derive the hybrids adsorbed to the cell surface or inactivated biomolecules in the medium. [ABSTRACT FROM AUTHOR]
- Published
- 2022
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