体外丹酚酸B改善四环素致脂肪肝的作用及机制初探

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R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＆#183;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75 μmol/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.

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

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.