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Inhibitory effect of exopolysaccharide from Achromobacter piechaudii NRC2 against cyclooxygenases and acetylcholinesterase with evaluation of its antioxidant properties and structure elucidation | Abstract
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Abstract

Inhibitory effect of exopolysaccharide from Achromobacter piechaudii NRC2 against cyclooxygenases and acetylcholinesterase with evaluation of its antioxidant properties and structure elucidation

Author(s): Mohsen M. S. Asker1,*, Manal G. Mahmoud1, Abeer Y. Ibrahim2 and Saher S. Mohamed1

Research in Alzheimer’s disease (AD) currently includes various cellular, molecular, genetic, clinical and therapeutic approaches. Many epidemiological studies suggest that use of non-steroidal antiinflammatory drugs (NSAIDs) with their antioxidant properties delay or slow the clinical expression of AD. Therefore, in this study we have isolated and characterized both of Achromobacter piechaudii NRC2 by 16S rRNA and its exopolysaccharide (APEPS) by HPLC, GPC chromatography and FT-IR spectroscopy. The role of APEPS as cyclooxygenase COX-1 and COX-2 inhibitors (NSAIDs) and as acetyl cholinesterase inhibitor with evaluation of its antioxidative stress effects to mimic AD-like conditions in an in-vitro model at different concentrations was examined. Our results indicated that identified bacterial strain was A. piechaudii NRC2 and APEPS composed of arabinose, xylose, fructose, and galactouronic acid with a relative ratio of 4.5: 4.0: 1.0: 0.3, respectively, with molecular weight of 5.67´103 g/mol. APEPS showed potent inhibitory effect on COX-2 (inhibition ranged 21 to 92%) and COX-1 (7.77 to 36.22%) as compared to reference tested drug, celecoxib (28 to 100% for COX-2 and 6.11 to 34.12% for COX-1). It also inhibited acetyl cholinesterase concentration dependently, inhibition percentages ranged from 12.36 to 38.35%. These inhibition activities were accompanied with antioxidant effects including radical scavenging effect, IC50 were 170.00, 199.31, 205.12 and 73.58 μgmL-1 for DPPH, superoxide radical, H2O2 and total antioxidant capacity, respectively. IC50 was 100 μgmL-1 for metal chelation which appeared in inhibition of lipid peroxidation at IC50, 112.41 μgmL-1. These activities may led to slow down or treating Alzheimer disease by different mechanisms.