RÉSUMÉ
Aim To study the effects of Dicliptera chinensis polysaccharide(DCP)on alcoholic fatty liver disease(AFLD)in rats based on anti-inflammation and antioxidation.Methods 60 rats were randomly divid-ed into six groups:control group,model group,silybin group and DCP of high,medium and low dose groups. The control group was fed with normal diet, other groups were fed with high sugar and high fat diet,and given 5% alcohol 5 mL·kg-1 by gavage.The alcohol consistency increased 5%every week until AFLD mod-els in rats were made after 7 weeks.Except control group,other groups were fed with high sugar and high fat diet,and given 35% alcohol 5 mL · kg-1 and DCP.All rats were killed after five weeks,and blood and liver tissues were collected.The activity of alanine aminotransaminase (ALT),aspartate aminotransferase (AST ), alkaline phosphatase (AKP ), triglyceride (TG),total cholesterol (TC ),low-density lipoprotein cholesterol(LDL-C)and high-density lipoprotein cho-lesterol(HDL-C)in serum were detected by using bio-chemical method. The contents of malondialdehyde (MDA),superoxide dismutase (SOD),reduced gluta-thione(GSH)in liver tissues were detected.The con-tents of tumor necrosis factor-α(TNF-α),interleukin-6 (IL-6 )and transforming growth factor-β1 (TGF-β1 ) were determined by enzyme-linked immunosorbent as-say(ELISA)in liver tissues.The liver tissues were ob-tained and histologic analysis was done through HE. Results DCP reduced the activity or content of ALT, AST,AKP,TG,TC,LDL-C,HDL-C,TNF-α,IL-6, TGF-β1 in serum and liver tissues of rats(P<0.05 ), and increased the activity or content of HDL-C,SOD and GSH (P<0.05 ).DCP could remarkably inhibit the NF-κB expression in liver tissues(P<0.01 ).The pathological examination indicated that DCP could ob-viously alleviate the inflammation and fat denaturation of the liver cells.Conclusion DCP can inhibit the de-velopment of AFLD.The mechanism may be related to antioxidation,free radical scavenging, inhibition of lipidperoxidation,anti-inflammation,and inhibition of the TGF-β1 and NF-κB expression.