Effects of carboxymethyl chitosan oligosaccharide on regulating immunologic function and inhibiting tumor growth.

Herein, the effects of carboxymethyl chitosan oligosaccharide (CM-COS) on regulating immunologic function and inhibiting hepatocellular tumor growth were evaluated. Results showed that CM-COS caused dramatic viability loss of hepatocellular carcinoma BEL-7402 with non-toxicity towards normal liver L-02 cells. CM-COS repressed tumor growth of hepatoma-22, and elevated the spleen index and thymus index of tumor-bearing mice. Contents of VEGF and MMP-9 were significantly down-regulated by CM-COS. Histological analyses revealed that CM-COS promoted tumor cell necrosis and produced no significant toxicity to spleen tissues. Moreover, expressions of Caspase-3 in tumor tissues and IL-2 in spleen tissues were significantly activated by CM-COS. Additionally, in vitro cell viability, phagocytic capability and NO production of mouse peritoneal macrophages exposed to CM-COS were significantly higher. CM-COS remarkably increased the in vivo phagocytosing capacity of peritoneal macrophages of Kunming mice. Taken together, our findings suggested that CM-COS might be potentially effective and non-toxic candidate as anti-hepatoma agents.

Preparation and renoprotective effects of carboxymethyl chitosan oligosaccharide on adriamycin nephropathy.

Carboxymethyl chitosan oligosaccharide (CMCOS), the hydrolytic product of carboxymethyl chitosan, is nontoxic, easily absorbable and good antioxidant. In this study, CMCOS was prepared and its properties in adriamycin nephropathy therapy were investigated. Our results showed that CMCOS had good curative effects on renal function and parenchymal injury induced by adriamycin. CMCOS administration significantly relieved symptoms of proteinuria, hypoalbuminemia, hyperlipidemia, renal hyperplasia and histological lesions in rats (P < 0.01). Further exploration for the underlying mechanisms indicated that CMCOS treatment reduced macrophage accumulation, myofibroblast transdifferentiation and podocyte apoptosis. CMCOS treatment could regulate secretions of cytokines (IL-1ß, TNF-ɑ and TGF-ß1) and improve activities of antioxidative enzymes (SOD, GSH-Px) (P < 0.01). In conclusion, therapeutic effects of CMCOS on renal injury mediated by inflammation, fibrosis and oxidative stress made it a good kidney health product and a promising candidate in clinical treatment of human chronic kidney disease.