Faculty of Basic Medical Sciences, Chongqing Medical University, Chongqing, China.
J Ethnopharmacol. 2013 Dec 12;150(3):1045-52. doi: 10.1016/j.jep.2013.10.020. Epub 2013 Oct 21.
Salacia oblonga root (SOR) is a traditionally herbal medicine for obesity and diabetes, which are closely associated with fatty liver. To investigate the molecular mechanisms of SOR in the treatment of dietary-induced fatty liver.
Male rats were co-administered with fructose in drinking water and vehicle or the aqueous-ethanolic extract of SOR (by gavage, once daily) for 10 weeks. Biochemical variables were determined enzymatically or by ELISA. Gene expression was analyzed by Real-Time PCR and/or Western blot.
SOR treatment (20mg/kg) diminished fructose-induced fatty liver indicated by decreases in excess triglyceride accumulation and the increased vacuolization and Oil Red O staining area in the livers of rats. Importantly, Hepatic gene expression profile revealed that SOR suppressed fructose-stimulated overexpression of sterol regulatory element-binding protein (SREBP)-1/1c mRNA and nuclear protein. In accord, overexpression of SREBP-1c-responsive genes, such as fatty acid synthase, acetyl-CoA carboxylase-1 and stearoyl-CoA desaturase-1, was also downregulated. In contrast, overexpressed nuclear protein of carbohydrate response element binding protein and mRNA of its target gene liver pyruvate kinase were not altered. Additionally, SOR also did not affect expression of peroxisome proliferator-activated receptor-gamma- and -alpha, as well as their target genes, such as carnitine palmitoyltransferase-1a, acyl-CoA oxidase and CD36.
These results suggest that modulation of hepatic sterol regulatory element-binding protein-1c-mediated gene expression contributes to SOR-elicited improvement of fructose-induced fatty liver in rats. Our findings provide a better understanding of SOR in the treatment of obesity and diabetes.
匙羹藤根（SOR）是一种传统的草药，用于治疗肥胖症和糖尿病，这些病症与脂肪肝密切相关。为了研究 SOR 治疗饮食诱导性脂肪肝的分子机制。
雄性大鼠同时给予饮用水中的果糖和载体或 SOR 的水-乙醇提取物（灌胃，每天一次）共 10 周。通过酶法或 ELISA 测定生化变量。通过实时 PCR 和/或 Western blot 分析基因表达。
SOR 治疗（20mg/kg）可减轻果糖诱导的脂肪肝，表现为大鼠肝脏中甘油三酯蓄积过多减少，空泡化和油红 O 染色面积增加。重要的是，肝基因表达谱显示 SOR 抑制了果糖刺激的固醇调节元件结合蛋白（SREBP）-1/1c mRNA 和核蛋白的过度表达。相应地，SREBP-1c 反应基因如脂肪酸合酶、乙酰辅酶 A 羧化酶-1 和硬脂酰辅酶 A 去饱和酶-1 的过度表达也被下调。相反，糖反应元件结合蛋白的核蛋白过度表达及其靶基因肝丙酮酸激酶的 mRNA 没有改变。此外，SOR 也不影响过氧化物酶体增殖物激活受体-γ和-α的表达及其靶基因，如肉碱棕榈酰转移酶-1a、酰基辅酶 A 氧化酶和 CD36。
这些结果表明，调节肝固醇调节元件结合蛋白-1c 介导的基因表达有助于 SOR 改善果糖诱导的大鼠脂肪肝。我们的研究结果为 SOR 治疗肥胖症和糖尿病提供了更好的理解。
