Anti-oxidative and immunological role of Cyclocarya paliurus polysaccharide on the liver injury of diabetic rats.

Objective: To investigate the effects of Cyclocarya paliurus (C. paliurus) polysaccharide on the liver injury of diabetic rats.

Methods: Rats were divided into 6 groups, including normal group, model group, control group, low-dose group of C. paliurus polysaccharide treatment, middle-dose group of C. paliurus polysaccharide treatment and high-dose group of C. paliurus polysaccharide treatment. Histological analysis of liver was analyzed using hematoxilin and eosin. Levels of plasma biological parameters and anti-oxidative enzymes were determined by spectrophotometry. Nuclear factor kappa-B-p65 (NF-κB p65), tumor necrosis factor-α (TNF-α), interleukins 6 (IL-6), IL-1β were measured by real-time polymerase chain reaction and enzyme-linked immunosorbent assay.

Results: Compared with that of model group, the glucose level of plasma decreased 62.32% (P < 0.01), but glycogen and insulin level increased 1.51 times and 1.27 times in the high-dose group of C. paliurus polysaccharide treatment, respectively. Plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) level decreased 47.47% (P < 0.05), 43.65% (P < 0.05) and 50.51% (P < 0.05) in the high-dose group of C. paliurus polysaccharide treatment, respectively. Superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase level increased 1.16 times (P < 0.01), 71.28% (P < 0.05), 1.29 times (P < 0.01) and 87.46% (P < 0.05) in the high-dose group of C. paliurus polysaccharide treatment, respectively. Enzyme activities of NF-κB, TNF-α, IL-1β and IL-6 were decreased 39.29% (P < 0.05), 51.11% (P < 0.05), 37.42% (P < 0.05) and 36.50% (P < 0.05), respectively.

Conclusions: Administration of C. paliurus polysaccharide may play a protecting role for liver injury of diabetic rats through lowering glucose, ALT, AST, ALP level, increasing glycogen and insulin level, enhancing the anti-oxidative ability and down-regulating the inflammatory factors expression.