Journal
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
Volume 187, Issue -, Pages 651-663Publisher
ELSEVIER
DOI: 10.1016/j.ijbiomac.2021.07.138
Keywords
Auricularia auricula polysaccharides; Protease; C. elegans; Oxidative stress resistance; Lipid lowering effect
Funding
- National Natural Science Founda-tion of China [31871797]
- Key R & D Projects of Department of Science and Technology of Zhejiang Province [2020C02035]
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An efficient extraction method of Auricularia auricula polysaccharides by neutral protease was developed. The extracted AAPs showed significant antioxidant and lipid-lowering effects, prolonging the lifespan and enhancing antioxidant enzyme activity in Caenorhabditis elegans. The polysaccharides also demonstrated a protective effect against damage induced by intracellular free radicals.
An efficient extraction method of Auricularia auricula polysaccharides (AAPs) by neutral protease was developed and optimized by response surface methodology. AAPs were graded by stepwise ethanol precipitation, the fraction with high recovery rate and strong radical scavenging rate were obtained, then its antioxidant and lipid lowering effect were studied using Caenorhabditis elegans as model organism. The extract yield and ABTS(+) scavenging rates of AAPs could reach 14.90% and 86.0% at 50 degrees C, 75 mL/g of liquid-to-material ratio and pH 9.0. AAP3 obtained by 15% ethanol was a heteropolysaccharide comprised of mannose, glucose, glucuronic acid, xylose, galactose and glucosamine. AAP3 could significantly prolong the lifespan of C. elegans and enhance the activity of antioxidant enzymes including superoxide dismutase (SOD), catalases (CAT) at 0.25 mg/mL (p < 0.05). The qRT-PCR results showed that AAP3 could up regulate mRNA expression levels of daf-16 and skn-1 (>1.6 fold) at 0.25 mg/mL. Besides, AAP3 could significantly reduce the level of body fat and triglyceride in C. elegans (p < 0.05). These studies demonstrated that A. auricula polysaccharides prepared by neutral protease had a prominent protective effect to the damage induced by the intracellular free radical generating agents.
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