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Abstract: In the present research, chitooligosaccharides (COS) with molecular weight 800–3000Da and 90% of deacetylation were chemically modified by grafting 2-chloroethylamino hydrochloride at C-6 position to synthesize angiotensin I converting enzyme (ACE) inhibitory chitin derivatives based on the properties of ACE inhibitors. The synthetic product was designated as aminoethyl chitooligosaccharide (AE-COS) with molecular weight 800.79–4765Da. Its IC50 value on ACE was 0.8017μg/mL. Furthermore, Lineweaver-Burk plots revealed that the inhibition was competitive via obligatory binding site of ACE. Therefore, these results exhibited that substitution of the hydrogen atom at the C-6 position of pyranose residue by the aminoethyl group promotes ACE inhibitory effects of COS. [Copyright &y& Elsevier]

Unregulated activation of microglia is the major cause of neuronal degeneration in Alzheimer’s and Parkinson’s diseases. Excessive reactive oxygen species (ROS) generation is a common risk factor for chronic diseases, including neurodegeneration. In this study, N -acetyl chitooligomers (NA-COS, below 1 and 1–3 kDa) were produced from crab chitin using an ultrafiltration membrane system and investigated for their capabilities against H 2 O 2 -induced oxidative stress in murine microglia (BV-2 cells). NA-COS significantly decreased the oxidation of DNA by diminishing the intracellular ROS production. Furthermore, NA-COS upregulated the protein and gene expressions of antioxidant enzymes (superoxide dismutase and glutathione), thereby enhancing the intracellular antioxidant. Notably, NA-COS inhibit NF-κB activation by blocking degradation of the inhibitor of kappaB-alpha (IκB-α) and translocation of nuclear factor NF-κB (p65 and p50). Collectively, NA-COS could be potential agents for the prevention of neurodegenerative diseases. [ABSTRACT FROM AUTHOR]