ABSTRACT
The use of natural starch as a replacement for petroleum-based packaging materials is limited due to its poor processability, weak mechanical properties, and strong moisture sensitivity. To address these limitations, this study adopts molecular design of hydroxypropylation and acetylation to sequentially modify natural starch, and material design of introducing acetylated cellulose nanofibers (ACNF) into the starch matrix to reinforce the material. Hydroxypropylation decreased the interaction force between the starch molecular chains, thereby reducing the glass transition temperature. Subsequent acetylation introduced hydrophobic acetyl groups that disrupted intermolecular hydrogen bonds, enhancing the mobility of the starch molecular chain, and endowed the hydroxypropyl starch acetate (HPSA) with excellent thermoplastic processability (melt index of 7.12 g/10 min) without the need for plasticizers and notable water resistance (water absorption rate of 3.0 %). The introduction of ACNF generated a strong interaction between HPSA chains, promoting the derived ACNF-HPSA to exhibit excellent mechanical strength, such as high impact strength of 2.1 kJ/m2, tensile strength of 22.89 MPa, elasticity modulus of 813.22 MPa, flexural strength of 24.18 MPa and flexural modulus of 1367.88 MPa. Its overall performance even surpassed that of polypropylene (PP) plastic, making it a potential alternative material for PP-based packaging materials.
ABSTRACT
<p><b>AIM</b>To investigate the protective role of HO/CO systems in IL-1beta induced islest apoptosis and to explore the mechanisms of the protective effect of fructose-1, 6-disphosphate (FDP).</p><p><b>METHODS</b>The pancreases of the rats were removed to collect islets cells. The cells were incubated with IL-1beta with/or FDP. Cell activity, insulin secretion, HO-1 activity, CO content and apoptotic percentage were detected.</p><p><b>RESULTS</b>HO-1 activity and CO content of the normal control group were low. IL-1beta induced a significant decrease of cell activity and insulin release, flow cytometry analysis showed that apoptotic percentage of islet cells remarkably increased following the addition of IL-1beta, FDP obviously improved the islets cellular activity damaged by IL-1beta, and basic amount of insulin secretion and stimulated by high glucose were improved (P < 0.01). Content of CO and activity of HO-1 were higher in the IL-1beta group than the normal control group (P < 0.05), and there were significant differences between the FDP groups and IL-1beta group. FDP decreased cell apoptotic percentage. Activities of HO-1 and content of CO were higher than that in the IL-1beta group (P < 0.01).</p><p><b>CONCLUSION</b>FDP can attenuate the IL-1beta induced apoptosis of cultured beta cells, the mechanism of which may be improved HO-1 activity and CO content.</p>