Protective effect of Sam-Hwang-Sa-Sim-Tang against hepatic steatosis in mice fed a high-cholesterol diet
Protective effect of Sam-Hwang-Sa-Sim-Tang against hepatic steatosis in mice fed a high-cholesterol diet
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DOI：
10.1186/1472-6882-13-366
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发表时间：
2013-12-23
影响因子：
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通讯作者：
Kook, Yoon-Bum
中科院分区：
文献类型：
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作者：
Ahn, Tae-Gue;Lee, Joo-Young;Kook, Yoon-Bum
工作背景：三黄三心汤（SSST）是一种传统的东方药物，在韩国常用于治疗高血压、失眠和胸痛。此外，一些研究报告称，给予SHSST可抑制大鼠的高脂血症或降低血浆脂质水平，如总胆固醇（TC）。这些结果使我们发现并证明了SHSST的积极作用。本研究的目的是观察SHEST是否具有抗肝脂肪变性的作用，以及两种SHEST对肝脂肪变性的作用。正常饮食（CON）组、高胆固醇饮食（HC）组、处理组喂食含30%或80% SHSST乙醇提取物的高胆固醇饮食（HCD）（分别为SHSST-L和SHSST-H）。HCD给药9周。SHSST治疗组口服给药SHSST的剂量为150 mg/kg，而其他组接受生理盐水。结果：SHSST给药小鼠导致血清总胆固醇和低密度脂蛋白水平下降。组织学检查显示，SHSST治疗组的脂滴小于HC组。在蛋白质水平，固醇调节元件结合蛋白2（SREBP-2）的表达被抑制的SHSST。此外，胆固醇代谢相关分子如SREBP-2、肝X受体（LXR）、低密度脂蛋白受体（LDLR）和3-羟基-3-甲基戊二酰辅酶A（HMG-CoA）的mRNA表达在SHSST处理组中也受到抑制。在主动脉组织中，SHSST降低了肿瘤坏死因子-α的表达肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、细胞间粘附分子-1（ICAM-1）、血管细胞粘附分子-1（VCAM-1）、转化生长因子（TGF）-β 1和纤连蛋白。目前的研究表明，SHSST可防止肝脏脂肪变性，并保护血管免受因过度摄入胆固醇这些发现也可能表明，SHSST可用作预防肝脂肪变性的辅助治疗。
Background: Sam-Hwang-Sa-Sim-Tang (SHSST) is a traditional Oriental medication that has been commonly used in Korea for the treatment of hypertension, insomnia, and chest pain. In addition, some studies reported that administration of SHSST results suppression of hyperlipidemia in rats or lowering lipid plasma level such as total cholesterol (TC). Those results made us find and demonstrate positive effect of SHSST much more. The aim of the current study was to examine whether SHSST exerts an effect against hepatic steatosis and two type of SHSST has different efficacy on liver steatosis.Methods: Total 40 mice were divided randomly and equally into 4 groups: a normal diet (CON) group, high-cholesterol diet (HC) group, and treatment groups fed a high-cholesterol diet (HCD) with a 30% or 80% ethanol extract of SHSST (SHSST-L and SHSST-H, respectively). The HCD was given for 9 weeks. The SHSST-treated groups were orally administered SHSST at a dose of 150 mg/kg, whereas the other groups received physiological saline.Results: SHSST administration to mice resulted in a decline in serum levels of total cholesterol and low-density lipoprotein. Histological examination showed that lipid droplets were smaller in the SHSST-treated group than in the HC group. At the protein level, expression of sterol regulatory element-binding protein 2 (SREBP-2) was suppressed by SHSST. In addition, the mRNA expression of cholesterol metabolism-related molecules such as SREBP-2, liver X receptor (LXR), low-density lipoprotein receptor (LDLR), and 3-hydroxy-3methylglutary-CoA (HMG-CoA) was also suppressed in SHSST-treated groups in the liver. In the aorta tissue, SHSST decreased the expression of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1(VCAM-1), transforming growth factor (TGF)-beta 1, and fibronectin.Conclusions: The present study indicates that SHSST protects against liver steatosis and protects vessels against inflammation arising from excessive ingestion of cholesterol. These findings may also suggest that SHSST could be used as an adjuvant remedy for protection against liver steatosis.