| Hesperidin is a flavonone derivant, by the formative glycoside of Hesperetin and rhamnosidoglucose. Hesperidin is widely present in legumes, white birch, Labiatae, Papilionaceae, Rutaceae, Citrus Plants. And it is an important element of citrus pulp and peel. Domestic and international previous study found that the main pharmacological effects of Hesperidin are Anti-inflammatory, immunomodulatory, antioxidant protection from damage, scavenging oxygen free radicals, lowering blood pressure, protecting liver function, etc.Non-alcoholic fatter liver disease (NAFLD) is a clinical syndrome with lesion of steatosis and fat storage in hepatic lobules but without alcohol abuse. The pathological features are fatty degeneration of hepatocytes, injury and inflammatory cells infiltration. In recent years, non-alcoholic fatty liver disease rates were increasing. Research has shown that, NAFLD rat liver showed high expression of COX-2, which can aggravate liver injury. HDN can also inhibit the expression of COX-2 in vitro significantly in previous report. The aim of the present study is to explore the possible mechanism of HDN effects in rats fed with high fat diet and sucrose on the base of previous study. We have studied the inhibition of HDN on the activity and expression of COX-2 in vivo, and tested the related COX-2 catalyzed.Histological examination revealed that HDN (160mg/kg, 320mg/kg) compared with the model of fatty lesions had a certain role in the improvement, while reducing liver inflammation. Compared to the model, HDN can decrease the level of ALT, AST, TC, TG in serum. All of these suggest that HDN can improve liver function and lower blood lipid levels. Radioimmunoassay results of 6-Keto-PGF1α and TXA2 in plasma suggest that the levels of 6-Keto-PGF1α and TXA2 in model are higher compared to normal. After administration of HDN(160, 320mg/kg), the levels of 6-Keto-PGF1α and TXA2 decreased. Furthermore, HDN can inhibit the expression of COX-2, IL-8mRNA and the protein of COX-2 in liver tissue. |