Electro-response characteristic of starch hydrogel crosslinked with Glutaraldehyde.

The facile synthesis of the starch hydrogel with anisotropic microstructure and dynamic behaviors was developed in the presence (A-gel) and absence of DC electric field (B-gel). The microstructures of hydrogels were characterized by environmental scanning electron microscope. Their electro-responsive property of hydrogels was investigated with their storage modulus (G'). The result demonstrates that the G' of A-gel is greater than that of B-gel, and the modulus of A-gel increases along with the external field, which signifies positive electroresponse. In addition, the G' of A-gel and B-gel ((G'(A) and G'(B)) also continuously increases with increasing starch concentration, whereas both the maximum of modulus increment (ΔG' = G'(A)−G'(B) ) and that of modulus increment sensitivity (ΔG'/G'(B)) occur with the starch weight fraction at around 36.5%. To enhance the electro-responsive effects of the hydrogels, dielectric particles were dispersed in the hydrogel. It is found that BaTiO3/chitosan core-shell composite particles significantly enhance the electroresponse of the hydrogel. The mechanism of the electro-response mode is proposed.

Tempol, one of nitroxides, is a novel ultraviolet-A1 radiation protector for human dermal fibroblasts.

BACKGROUND: Nitroxide has been reported to have antioxidant and some photoprotective properties. Exposure of skin to ultraviolet-A1 (UVA1, 340-400 nm) can lead to formation of reactive oxygen species, reduction in collagen, and increased expression of matrix metalloproteinases (MMPs). OBJECTIVE: The goal of this research was to determine the effects of 4-hydroxy-Tempo (Tempol), one of nitroxides, in the presence of UVA1 on cytotoxicity, superoxide dismutase enzyme (SOD) activity, lipid peroxidation, and expression of collagen I, collagen III and MMP-1, MMP-3 in human dermal fibroblasts in vitro. METHODS: Fibroblasts were irradiated by a single exposure to UVA1 and at the same time incubated with, or without, Tempol and detected twenty-four hours later. SOD activity and lipid peroxidation, as shown by accumulation malonyldialdehyde (MDA), were detected by biochemical assay. Expressions of collagen I, collagen III (protein levels) and MMP-1, MMP-3 (mRNA level) were detected by ELISA and semi-quantitative reverse transcriptase-PCR separately. RESULTS: Cell survival curve after UVA1 irradiation showed dose dependent decrement pattern and Tempol, between 0.03 and 8 mM, increased cell viability in a dose-effect manner when the cells were exposed to 20 J/cm(2) UVA1. Fifteen Joule per centimetre square of UVA1 significantly inhibited SOD activity and collagen I, collagen III protein levels, while increased MDA level and stimulated MMP-1 and MMP-3 mRNA expression. Tempol reversed these effects caused by UVA1 in some degree or completely and in proper concentration, the results were statistically significant compared with irradiated group. CONCLUSIONS: Tempol had photoprotective properties against UVA1 irradiation in vitro. With antioxidant ability, Tempol inhibited extracellular matrix degradation and preserved collagen production in dermis and may be used as an anti-photoaging agent.