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目的研究海参皂苷(sea cucumber saponins,SCS)对乳清酸诱导的大鼠非酒精性脂肪肝(nonalcoholic fatty liver disease,NAFLD)的改善及胆固醇代谢的影响。方法通过膳食乳清酸诱导产生NAFLD模型,将大鼠按体重随机分为正常对照(CN)、乳清酸模型(orotic acid,OA)、皂苷低剂量(0.01%SCS)、皂苷高剂量组(0.05%SCS)4组,饲喂10d后观察其血清、肝脏脂质及胆固醇代谢相关基因m RNA表达量。结果:相比对照组,模型组血清和肝脏中总胆固醇含量升高,喂食高剂量海参皂苷后,血清和肝脏总胆固醇浓度分别降低了27.0%(P<0.01)和24.7%(P<0.05)。海参皂苷显著抑制了胆固醇合成限速酶羟甲基戊二酸单酰辅酶A还原酶(HMG-Co A reductase)以及胆固醇调节元件结合蛋白-2(SREBP-2)的基因表达,但对低密度脂蛋白受体(LDLR)的基因表达无显著影响,对胆固醇7α-羟化酶(CYP7A)的基因表达并没上调。结论:海参皂苷可显著抑制肝脏胆固醇的合成,降低血中胆固醇浓度,改善乳清酸诱导的大鼠脂肪肝。
Objective To study the effect of sea cucumber saponins (SCS) on the improvement of apo-or-cholesterol metabolism in rats with orofacial-induced fatty liver disease (NAFLD). Methods The NAFLD model was induced by dietary orotic acid. The rats were randomly divided into normal control (CN), orotic acid (OA), low dose of saponin (0.01% SCS) and high dose of saponin 0.05% SCS) were given to the rats in each group for 10 days. The expression of m RNA in the serum and liver lipid and cholesterol metabolism genes were observed. Results: Compared with the control group, the serum and liver total cholesterol levels in model group were significantly increased by 27.0% (P <0.01) and 24.7% (P <0.05), respectively, . Ginseng saponin significantly inhibited the gene expression of cholesterol-producing rate-limiting enzyme HMG-Co A reductase and cholesterol regulatory element binding protein-2 (SREBP-2) The gene expression of lipoprotein receptor (LDLR) had no significant effect, and the gene expression of cholesterol 7α-hydroxylase (CYP7A) was not up-regulated. Conclusion: Ginsenoside can significantly inhibit hepatic cholesterol synthesis, reduce blood cholesterol levels, and improve orotate-induced fatty liver in rats.