[Effects of alcohol extract of radish seed on blood lipid, glucose and liver steatosis in ApoE mice].

To investigate the effects and mechanisms of alcohol extract of Raphani seed (AERS) on blood lipid, blood glucose and hepatic steatosis in ApoE mice. Sixty ApoE mice were randomly divided into control group (CG), normal saline group (NG), rosiglitazone group (RG) and AERS treatment groups (AERS-L / M / H). Except CG, other groups were fed with high-fat, high-sugar and high-salt diet for 9 weeks. The mice in RG were treated with rosiglitazone (1.33 mg·kg, 0.2 ml ·10 g) by gavage daily. The mice in CG and NG were treated with equal volume of NS by intragastric administration daily. The mice in AERS groups were treated with AERS at the doses of 100, 300 and 900 mg·kg for 9 weeks, respectively. FPG and Fins were detected. Insulin resistance index (IRI) and liver coefficient (LC) were calculated. The levels of ALT, AST, Leptin (LEP), TNF - α and blood lipid (TC, FFA, etc.) were tested. The expressions of proteins related to liver lipid metabolism (HMG-R、LDL-R、LEP-R) were detected by Western blot. Compared with NG or RG, CG showed significant changes in liver appearance (color, swelling, etc.) and pathology (steatosis, hepatocyte necrosis, etc.), while AERS-M/H groups were similar to CG. Compared with CG, the serum levels of FPG, Fins, IRI, ALT, AST, TNF-α, LC, TG, LDL-C, FFA and LEP were increased significantly (＜0.05) . Compared with NG, AERS could decrease the above mentioned indicators in a dose-dependent manner (＜0.05). Compared with RG, the levels of FPG and Fins of AERS-H were increased significantly, while the level of IRI was decreased (＜0.05). Compared with NG and RG, the protein expressions of HMG-R and LEP-R in AERS groups were decreased, while the protein expression of LDL-R was increased in a dose-dependent manner (＜0.05). AERS can prevent the increase of blood lipid, glucose and hepatic steatosis induced by high-fat and high-sugar diet in ApoE mice. The mechanism is related to the decrease of FFA and LEP, the inhibition of TNF-α, HMG-R, LEP-R protein expressions and the promotion of LDL-R protein expression.