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目的观察姜提取物改善果糖所致大鼠脂肪肝的作用,并探讨其可能的作用机制。方法取SD大鼠24只,随机分为4组,每组6只,即正常对照组(给予正常饮食饮水),模型组(给予10%果糖水),姜提取物低、高剂量组20,50 mg·kg~(-1),给予姜提取物灌胃,连续28 d。用酶法和ELISA检测血浆葡萄糖、甘油三酯(TG)、胆固醇(TC)和胰岛素含量,苏木精-伊红(HE)染色和油红-O染色观察肝脏组织中的脂肪沉积程度,RT-PCR和Western blot法检测肝脏相关基因和蛋白表达。结果姜提取物逆转了果糖过量消耗引起的大鼠肝脏甘油三酯的过度堆积(P<0.05)、肝细胞空泡化的增加和肝脏油红-O染色面积的增加(P<0.05)。然而,姜提取物并不影响大鼠食物摄入量和体质量。姜提取物能够抑制肝脏二脂酰甘油酰基转移酶(DGAT)-2 mRNA和蛋白的过表达(P<0.05),但对肝X受体(LXR)、DGAT-1、单酰甘油酰基转移酶(MGAT)-1、MGAT-2、激素敏感脂肪酶(HSL)和脂肪甘油三酯脂肪酶(ATGL)mRNA的表达无影响。结论姜提取物可能通过抑制介导肝脏甘油三酯生物合成的关键酶DGAT-2的过表达,从而改善果糖所致大鼠脂肪肝。
Objective To observe the effect of ginger extract on improving fatty liver caused by fructose in rats and to explore its possible mechanism. Methods Twenty-four Sprague-Dawley rats were randomly divided into 4 groups with 6 rats in each group, namely normal control group (given normal drinking water), model group (given 10% fructose water), ginger extract low and high dose group 20, 50 mg · kg -1, Ginger extract was given for 28 days. Plasma glucose, triglyceride (TG), cholesterol (TC), and insulin levels were measured by enzyme-linked immunosorbent assay (ELISA) and ELISA, and fat deposition in liver tissues was observed by hematoxylin-eosin (HE) The expressions of liver related genes and proteins were detected by PCR and Western blot. Results Ginger extract reversed the excessive hepatic triglyceride accumulation (P <0.05), hepatocytic vacuolization and hepatic red-O staining (P <0.05) caused by excessive consumption of fructose. However, ginger extract did not affect rat food intake and body weight. Ginger extract could inhibit the overexpression of DGAT-2 mRNA and protein in the liver (P <0.05), but had no effect on the liver X receptor (LXR), DGAT-1, monoacylglycerol acyltransferase MGAT-1, MGAT-2, hormone-sensitive lipase (HSL) and fat triglyceride lipase (ATGL) mRNA expression. Conclusion Ginger extract may improve fatty liver in rats induced by fructose by inhibiting the overexpression of DGAT-2, a key enzyme in hepatic triglyceride biosynthesis.