Effects of chitosan oligosaccharides on neutrophils from glycogen-induced peritonitis mice model

• Published in: Carbohydrate polymers Vol. 75; no. 1; pp. 119 - 124
• Main Authors: Dou, Jiangli, Xu, Qingsong, Tan, Chengyu, Wang, Wenxia, Du, Yuguang, Bai, Xuefang, Ma, Xiaojun
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.01.2009; Elsevier Science
• Subjects: Apoptosis; Applied sciences; Biological and medical sciences; Bones, joints and connective tissue. Antiinflammatory agents; Chitosan oligosaccharides; Exact sciences and technology; Inflammation; Medical sciences; Natural polymers; Neutrophil; Pharmacology. Drug treatments; Physicochemistry of polymers; Starch and polysaccharides; Superoxide; Chitosan oligosaccharides; Superoxide; Inflammation; Neutrophil; Apoptosis; Animal model; Hydrogen peroxide; Enzyme; Experimental study; Oligomer; In vitro; Biological activity; Non steroidal antiinflammatory agent; Hyperoxides; Peroxidases; Oside polymer; Peroxidase; Oxidoreductases; Chitosan
• ISSN: 0144-8617; 1879-1344
• DOI: 10.1016/j.carbpol.2008.07.005

To investigate the effects of chitosan oligosaccharides (COS) on the neutrophils from glycogen-induced peritonitis mice model, the production of superoxide and hydrogen peroxide, myeloperoxidase (MPO) release as well as apoptosis were measured. We found that 100 μg/ml COS supplementation could induce the production of superoxide and hydrogen peroxide by neutrophils, meanwhile, COS promoted the apoptosis of peritoneal neutrophils, whereas the MPO release was decreased. Furthermore, superoxide dismutase (SOD) administration could abolish the pro-apoptotic effects mediated by COS. These results demonstrated that COS exerted pro-apoptotic effects on neutrophils, and superoxide played an important role in neutrophil apoptosis caused by COS. By the use of inhibitors of PLD and PI3K respectively, administration of 1-butanol and wortamannin decreased the generation of superoxide stimulated by COS. The production of superoxide caused by COS resulted from the activation of PLD and PI3K to some extent.