Qishun Liu

Conversion of biomass into 5-hydroxymethylfurfural using solid acid catalyst

5-Hydroxymethylfurfural (HMF) was produced from monosaccharide (fructose and glucose), polysaccharide (inulin) and the Jerusalem artichoke juice by a simple one-pot reaction including hydrolysis and dehydration using solid acid under mild condition. Hydrated niobium pentoxide (Nb(2)O(5)·nH(2)O(2)) after pretreatment showed high catalytic activities for dehydration of mono- and polysaccharide to HMF at 433 K in water-2-butanol (2:3 v/v) biphasic system, giving high HMF yield of 89% and 54% from fructose and inulin, respectively. The HMF yield was up to 74% and 65% when inulin and Jerusalem artichoke juice were hydrolyzed by exoinulinase. The solid acid made the process environment-friendly and energy-efficient to convert carbohydrates into bio-fuels and platform chemicals.

Chitosan Oligosaccharides Inhibit the Expression of Interleukin-6 in Lipopolysaccharide-induced Human Umbilical Vein Endothelial Cells Through p38 and ERK1/2 Protein Kinases

Chitosan oligosaccharides (COS) have been reported to exert anti-fungal activities, antitumour activities and immuno-enhancing effects. However, the potential roles of COS in the treatment of vascular inflammations remain unknown. In the present study, we examined the effects of COS on interleukin-6 (IL-6) production in human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS). Induction of HUVECs with LPS (100 ng/ml) increased the mRNA expression and protein secretion of IL-6 (versus the vehicle-treated group, p < 0.01), which were significantly reverted by the pre-treatment with COS (50-200 microg/ml) for 24 hr before LPS exposure (versus the LPS-treated group, p < 0.05 or 0.01). Signal transduction studies showed that the pre-treatment of HUVECs with COS (50-200 microg/ml) for 24 hr markedly inhibited the LPS-induced over-expression of phosphorylated p38 mitogen-activated protein kinase (MAPK), phosphorylated ERK1/2 and nuclear factor kappaB (NF-kappaB). Moreover, the LPS-induced NF-kappaB activation was suppressed by the specific ERK1/2 inhibitor PD98059 (30 microM) (versus the LPS-treated group, p < 0.01), but not by the specific p38 MAPK inhibitor SB203580 (25 microM). Additionally, both MAPK inhibitors markedly suppressed LPS-induced IL-6 mRNA expression in HUVECs (versus the LPS-treated group, p < 0.01). In conclusion, our results suggest that COS inhibit LPS-induced up-regulation of IL-6 in HUVECs, and this can be regulated by at least two parallel signalling pathways: one via p38 MAPK pathway independent of NF-kappaB activation and one via ERK1/2 pathway dependent on NF-kappaB activation.

Chitosan oligosaccharides suppress LPS-induced IL-8 expression in human umbilical vein endothelial cells through blockade of p38 and Akt protein kinases

Aim:To investigate whether and how COS inhibited IL-8 production in LPS-induced human umbilical vein endothelial cells (HUVECs).Methods:RT-PCR, enzyme-linked immunosorbent assays (ELISA) and Western blotting were used to study IL-8 expression and related signaling pathway. Wound healing migration assays and monocytic cell adhesion analysis were used to explore the chemotactic and adhesive activities of HUVECs.ResultsCOS 50–200 μg/mL exerted a significant inhibitory effect on LPS 100 ng/mL-induced IL-8 expression in HUVECs at both the transcriptional and translational levels. In addition, COS 50–200 μg/mL inhibited LPS-induced HUVEC migration and U937 monocyte adhesion to HUVECs in a concentration-dependent manner. Signal transduction studies suggest that COS blocked LPS-induced activation of nuclear factor-κB (NF-κB) and activator protein-1 (AP-1) as well as phosphorylation of p38 mitogen-activated protein kinase (MAPK) and phosphokinase Akt. Further, the over-expression of LPS-induced IL-8 mRNA in HUVECs was suppressed by a p38 MAPK inhibitor (SB203580, 25 μmol/L) or a phosphatidylinositol 3-kinase (PI3K) inhibitor (LY294002, 50 μmol/L).Conclusion:COS inhibited LPS-induced IL-8 expression in HUVECs through the blockade of the p38 MAPK and PI3K/Akt signaling pathways.

Conversion of saccharides into levulinic acid and 5-hydroxymethylfurfural over WO3–Ta2O5 catalysts

Bimetallic oxide catalysts WO3–Ta2O5 are active in converting saccharides into 5-hydroxymethylfurfural (HMF) and levulinic acid (LA) in one-pot reactions. The product selectivity varies at different WO3 to Ta2O5 ratios. FTIR measurements indicate the presence of Lewis acid sites and the strength of the Lewis acid sites varies when the WO3 to Ta2O5 ratio changes. The result suggests that conversion of carbohydrates into HMF and LA can be realized using a single catalytic system by adjusting the catalysts acidic properties.

The inhibition of LPS-induced inflammation in RAW264.7 macrophages via the PI3K/Akt pathway by highly N-acetylated chitooligosaccharide

Chitooligosaccharide (COS) has been shown to regulate many biological functions, such as antimicrobial effect and antitumor activity. In the present study, highly N-acetylated chitooligosaccharide (NACOS) was prepared by N-acetylation of COS, and the anti-inflammatory activity of NACOS in macrophages were evaluated. The results indicated NACOS significantly suppressed the LPS-induced pro-inflammatory cytokines interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) expression. Furthermore, the increased levels of reactive oxygen species (ROS) and nitric oxide (NO) were repressed by NACOS in a dose dependent manner. However, NACOS itself had no significant effect on the cell viability and cellular morphology. Signal transduction studies demonstrated that NACOS remarkably inhibited LPS-enhanced phosphorylation of phosphatidylinositol 3-kinase (PI3K) and Akt. These findings provide a possible molecular mechanism by which NACOS inhibit LPS-induced inflammatory response in macrophages, and a basis for utilizing NACOS in pharmaceutical therapy against inflammation.