Effects of Hesperidin on the Progression of Hypercholesterolemia and Fatty Liver Induced by High-Cholesterol Diet in Rats
Effects of Hesperidin on the Progression of Hypercholesterolemia and Fatty Liver Induced by High-Cholesterol Diet in Rats
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DOI：
10.1254/jphs.11097fp
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发表时间：
2011-11-01
影响因子：
3.5
通讯作者：
Kimura, Koji
中科院分区：
文献类型：
--
作者：
Wang, Xinhui;Hasegawa, Junichi;Kimura, Koji
橙皮苷对高胆固醇血症和脂肪肝的保护作用，在雄性Wistar大鼠喂养高胆固醇饮食12周。与标准饮食相比，高胆固醇饮食不仅增加体重、肝脏重量和血清胆固醇浓度，而且还诱导肝脏脂肪变性。橙皮苷（0.08%）可降低高胆固醇饮食大鼠肝脏脂肪变性程度、脂肪组织和肝脏重量（P < 0.05）、血清总胆固醇和视黄醇结合蛋白（RBP）4浓度（P < 0.05），而对低密度脂蛋白胆固醇水平和甘油三酯浓度的降低不显著。它还减弱了肝脏和脂肪组织中脂质代谢相关蛋白RBP、心脏脂肪酸结合蛋白（H-FABP）和皮肤脂肪酸结合蛋白（C-FABP）mRNA表达的显著变化。气相色谱分析结果显示，橙皮苷组大鼠血清总胆固醇、胆固醇合成生物标志物（胆甾醇）和胆固醇吸收生物标志物（菜油甾醇、β-谷甾醇）浓度较低，粪便中胆固醇浓度较高（P < 0.05）。橙皮苷可能通过抑制胆固醇的合成和吸收，调节RBP、C-FABP和H-FABP mRNA的表达，改善高胆固醇血症和脂肪肝。
The protective effects of hesperidin against hypercholesterolemia and fatty liver were examined in male Wistar rats fed a high-cholesterol diet for 12 weeks. Compared with a standard diet, a high-cholesterol diet not only increased body weights, liver weights, and serum concentration of cholesterol, but also induced the fatty degeneration (steatosis) of liver. Hesperidin (0.08%) reduced levels of hepatic steatosis, adipose tissue and liver weights (P < 0.05), serum total cholesterol and retinol binding protein (RBP) 4 concentrations (P < 0.05) in rats fed with high-cholesterol diet, while reduction in low-density lipoprotein cholesterol levels and triglyceride concentrations was not significant. It also attenuated the marked changes in mRNA expression of lipid metabolism related proteins: RBP, heart fatty acid binding protein (H-FABP), and cutaneous fatty acid-binding protein (C-FABP), in liver and adipose tissue. According to the results of gas chromatography, serum concentrations of total cholesterol and biomarkers of cholesterol synthesis (lathosterol) and absorption (campesterol, beta-sitosterol) were lower, and concentrations of cholesterol in feces were higher in the rats given hesperidin (P < 0.05). Hesperidin may improve hypercholesterolemia and fatty liver by inhibiting both the synthesis and absorption of cholesterol and regulating the expression of mRNA for RBP, C-FABP, and H-FABP.