Effects of ZnO/trimethylsilyl cellulose nano-composite coating on anti-UV and anti-fungal properties of papers.

Trimethylsilyl cellulose (TMSC) was employed as the coating matrix for the application of zinc oxide nanoparticles (ZnO) onto paper surfaces and the protections of ZnO/TMSC coating against UV-induced damages and fungal spoilage were evaluated. Filter papers were immersed in 2% w/v TMSC solution loaded with ZnO and air-dried. Three ZnO/TMSC suspensions were prepared with 0.1, 0.5, and 1% w/v ZnO NPs. The presences of ZnO/TMSC protective layers were confirmed with ATR-IR spectroscopy. The coated papers exhibited high surface hydrophobicities. After the coated papers were subject to 365-nm UV irradiation at 400 W for 3 h, the contact angles dramatically dropped. The trimethylsilyl (TMS) groups exposed on the surface formed a moisture barrier and were partially removed on UV exposure. ATR-IR revealed that more TMS groups were removed in the protective layer with no ZnO. UV-irradiated papers turned yellow and papers protected with 1% ZnO/TMSC exhibited significantly lower color changes than that of the uncoated one. Compared to the TMSC-coated paper, the addition of ZnO resulted in a significant reduction in tensile strength at maximum. However, after UV irradiation, significant increases in both the strain at break and strength at maximum were only observed in 1% ZnO/TMSC-protected papers. Regarding their anti-fungal properties, the 1% ZnO/TMSC films were effective in growth inhibitions of Aspergillus sp. and Penicillium sp. on the nonirradiated papers. Despite being hydrophilic after UV-irradiation, growths of the molds were severely suppressed on the UV-irradiated paper.

Acemannan increased bone surface, bone volume, and bone density in a calvarial defect model in skeletally-mature rats.

BACKGROUND/PURPOSE: Acemannan, a ß-(1-4)-acetylated polymannose extracted from Aloe vera gel, has been proposed as biomaterial for bone regeneration. The aim of this study was to investigate the effect of acemannan in calvarial defect healing. MATERIALS AND METHODS: Acemannan was processed to freeze-dried sponge form and disinfected by UV irradiation. Thirty-five female Sprague-Dawley rats were used in the in vivo study. Seven-mm diameter mid-calvarial defects were created and randomly allocated into blood clot control (C), acemannan 1 mg (A1), 2 mg (A2), 4 mg (A4), and 8 mg (A8) groups (n = 7). After four weeks, the calvarial specimens were subjected to microcomputed tomography (microCT) and histopathological analysis. RESULTS: MicroCT revealed a significant increase in bone surface and bone volume in the A1 and A2 groups, and tissue mineral density in the A4 and A8 groups compared with the control group (p < 0.05). Histologically, the acemannan-treated groups had denser bone matrix compared with the control group. CONCLUSION: Acemannan is an effective bioactive agent for bone regeneration, enhancing bone growth as assayed in two- and three-dimensions.

Acemannan increases NF-κB/DNA binding and IL-6/-8 expression by selectively binding Toll-like receptor-5 in human gingival fibroblasts.

Acemannan, an acetylated polymannose from Aloe vera, has immunomodulatory effects. We investigated whether acemannan induces IL-6 and -8 expression and NF-κB/DNA binding in human gingival fibroblasts. IL-6 and -8 expression levels were assessed via RT-PCR and ELISA. The NF-κB p50/p65-DNA binding was determined. The structures of acemannan mono-pentamers and Toll-like receptor 5 (TLR5) were simulated. The binding energies between acemannan and TLR5 were identified. We found that acemannan significantly stimulated IL-6/-8 expression at both the mRNA and protein level and significantly increased p50/DNA binding. Preincubation with an anti-TLR5 neutralizing antibody abolished acemannan-induced IL-6/-8 expression and p50/DNA binding, and co-incubation of acemannan with Bay11-7082, a specific NF- κB inhibitor, abolished IL-6/-8 expression. The computer modeling indicated that monomeric/dimeric single stranded acemannan molecules interacted with the TLR5 flagellin recognition sites with a high binding affinity. We conclude that acemannan induces IL-6/-8 expression, and p50/DNA binding in gingival fibroblasts, at least partly, via a TLR5/NF-κB-dependent signaling pathway. Furthermore, acemannan selectively binds with TLR5 ectodomain flagellin recognition sites.

Deacetylation affects the physical properties and bioactivity of acemannan, an extracted polysaccharide from Aloe vera.

Acemannan, an acetylated polymannose from Aloe vera, induces tissue repair. We investigated the role of acemannan's acetyl-groups on its physical and biological properties. Deacetylated acemannan (DeAcAM) was prepared and characterized. The physical properties and microscopic structure of DeAcAM were evaluated using water solubility, contact angle, X-ray diffraction, and scanning-electron microscopy. The activity of DeAcAM on cell proliferation and gene expression were assessed. Acemannan and DeAcAM structures were simulated and the acemannan tetramer diad and its completely deacetylated structure were also determined. Increased acemannan deacetylation reduced its water solubility and hydrophilicity. Complete deacetylation altered acemannan's conformation to a partial crystal structure. The bioactivity of acemannan was reduced corresponding to its deacetylation. Acemannan induced cell proliferation, and VEGF and Collagen I expression; however, 100% DeAcAM did not. The simulated structures of the acemannan diad and the completely deacetylated diad were different. We conclude acetyl-groups affect acemannan's structure and physical/biological properties.