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目的研究核黄素(Riboflavin)对高脂血症大鼠脂质代谢的影响,并探讨其机制。方法 70只SD雄性大鼠随机分为两组,10只大鼠作为正常对照组,60只大鼠给高脂饲料建立高脂血症模型,剔除造模失败的大鼠,最终造模成功高脂血症大鼠40只,分为模型对照组(HF)和低、中、高剂量组(分别为HF+LR、HF+MR、HF+HR组,核黄素剂量分别为0.667、3.385和6.670 mg/kg),每组10只。空白对照组正常饮食,其他组高脂饮食。实验末期(第60天)眼内眦采血(禁食)测卵磷脂胆固醇脂酰转移酶(LCAT);取肝组织HE染色观察肝组织病理学形态,并制作10%肝匀浆测肝组织中3-羟基-3-甲基戊二酰辅酶A还原酶(HMGR)、胆固醇和甘油三酯水平。结果 HF+LR组肝脏胆固醇水平[(1.07±0.14)mmol/L]与HF组[(1.37±0.36)mmol/L]差异有统计学意义(P<0.05);HF+LR组、HF+MR组肝脏甘油三酯水平[(1.73±0.28)、(1.82±0.38)mmol/L]明显低于HF组[(2.15±0.43)mmol/L],差异有统计学意义(P<0.05);HF+LR组肝脏HMGR水平[(1.82±0.72)ng/ml]明显低于HF组[(2.88±0.99)ng/ml],差异有统计学意义(P<0.05);核黄素干预组和HF组间血清LCAT水平差异无统计学意义(P>0.05)。结论核黄素可能通过降低HMGR的水平来调节肝脂水平,从而影响脂质代谢。
Objective To study the effect of Riboflavin on lipid metabolism in hyperlipidemic rats and to explore its mechanism. Methods Seventy male Sprague Dawley rats were randomly divided into two groups. Ten rats were used as normal control group. Sixty rats were given hyperlipidemia model for high fat diet. 40 rats were divided into model control group (HF) and low, medium and high dose groups (HF + LR, HF + MR, HF + HR group, riboflavin doses 0.667,3.385 and 6.670 mg / kg), 10 in each group. The blank control group normal diet, other groups of high-fat diet. At the end of the experiment (60 days), the leptin cholesterol acyltransferase (LCAT) was determined by blood sampling (fasting); the pathological morphology of liver tissue was observed by HE staining and the liver tissue was made by 10% 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR), cholesterol and triglyceride levels. Results The hepatic cholesterol level in HF + LR group was significantly higher than that in HF group (1.37 ± 0.36 mmol / L vs 1.07 ± 0.14 mmol / L, P <0.05) The levels of triglyceride in liver were significantly lower than those in HF group [(1.73 ± 0.28) and (1.82 ± 0.38) mmol / L], respectively (P <0.05) The serum levels of HMGR in + LR group were significantly lower than those in HF group [(1.82 ± 0.72) ng / ml vs [(2.88 ± 0.99) ng / ml, P <0.05) There was no significant difference in serum LCAT levels between groups (P> 0.05). Conclusion Riboflavin may regulate hepatic lipid levels by decreasing the level of HMGR, thus affecting lipid metabolism.