体外丹酚酸B改善四环素致脂肪肝的作用及机制初探  

The amelioration of salvianolic acid B on tetracycline-induced hepatic steatosis

作　　者：郭文涛[1] 王来友[1] 郭姣[1] 

机构地区：[1]广东药学院中医药研究院/国家中医药管理局高脂血症"调肝降脂"重点研究室,广东广州510006

出　　处：《广东药学院学报》2014年第2期224-227,共4页Academic Journal of Guangdong College of Pharmacy

基　　金：广东省自然科学基金(10351022401000000;S2013010015021)

摘　　要：目的建立四环素诱导HepG2细胞药物性脂肪肝模型,研究丹酚酸B对此模型的作用,并初步探讨其机制。方法采用油红O染色观察细胞内脂质积聚情况,采用GPO·PAP法三酰甘油试剂盒定量检测细胞内三酰甘油的变化及Real-time PCR检测CD36 mRNA的表达。结果四环素处理后能够明显增强油酸诱导的HepG2细胞脂肪变性(P<0.05),同时75μmol/L四环素处理后显著提高CD36 mRNA的表达(P<0.05)。丹酚酸B能明显改善四环素油酸诱导的HepG2细胞脂肪积聚,且呈剂量依赖性(P<0.01);丹酚酸B高剂量组与造模组相比能显著降低CD36 mRNA的表达(P<0.05)。结论丹酚酸B能够改善四环素油酸诱导的HepG2细胞脂肪变性,其作用可能与抑制CD36的表达、影响脂肪酸转运有关。Objective To establish the model of tetracycline-induced hepatic steatosis in HepG2 ceils line, and study the effect and potential mechanism of salvianolic acid B on this model. Methods Intracellular lipid accumulation was stained by oil red O. Intracellular triglyceride was measured by triglycerides kits. CD36 mRNA expression was detected by real-time PCR. Results Tetracycline treatment remarkably enhanced the sodium oleate-induced steatosis in HepG2 cells （P〈 0.05）.The expression of intracellular CD36 mRNA significantly increased after treatment with 75 μmol/L tetracycline （P〈 0.05 ）. Salvianolic acid B attenuated HepG2 lipid accumulation induced by sodium oleate and tetracycline in a dose-dependent manner （ P〈 0. 01） . Compared with the model group, salvianolic acid B in high-dose group significantly suppressed the expression of CD36 mRNA （P 〈 0.05 ）. Conclusion Salvianolic acid B can alleviate tetracycline and sodium oleate-induced HepG2 cells steatosis, which may be associated with inhibition of CD36 expression.

关 键 词：药物性脂肪肝 四环素 HEPG2 丹酚酸B CD36 

分 类 号：R285.5[医药卫生—中药学]