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目的:研究氟西汀对小鼠肝脏脂质代谢的影响。方法:小鼠腹腔注射10 mg/kg或25 mg/kg氟西汀,对照组给予生理盐水,以25 mg/kg氯氮平作为阳性对照,注射6 h或24 h后处死小鼠,取肝脏组织。用油红O染色观察肝脏中性脂肪积累;用试剂盒测定肝脏甘油三酯和总胆固醇含量;用Western blot技术测定小鼠肝脏固醇调节元件结合蛋白1c(SREBP1c)、乙酰辅酶A羧化酶(ACC1)和脂肪酸合成酶(FAS)以及羧酸酯酶1和3(CES1和CES3)的蛋白表达水平。结果:氟西汀诱导小鼠肝脏脂质积累,增加肝脏甘油三酯含量;氟西汀显著增加小鼠肝脏SREBP1c、ACC1和FAS的蛋白表达,同时小鼠肝脏CES1和CES3的蛋白表达水平显著减少。结论:氟西汀可能通过增加脂质合成基因的表达及减少脂质分解基因的表达从而诱导小鼠肝脏的脂质积累。
Objective: To study the effect of fluoxetine on liver lipid metabolism in mice. Methods: The mice were intraperitoneally injected with 10 mg / kg or 25 mg / kg of fluoxetine, and the control group was given normal saline. Clozapine at 25 mg / kg was used as a positive control. After 6 or 24 hours of injection, mice were sacrificed and the liver organization. Oil red O staining was used to observe the accumulation of neutral fat in the liver. The contents of triglyceride and total cholesterol in the liver were determined by kit assay. The levels of hepatic sterol regulatory element binding protein 1c (SREBP1c), acetyl CoA carboxylase (ACC1) and fatty acid synthetase (FAS) as well as carboxylesterase 1 and 3 (CES1 and CES3). Results: Fluoxetine induced hepatic lipid accumulation in mice and increased hepatic triglyceride content. Fluoxetine significantly increased the protein expression of SREBP1c, ACC1 and FAS in mice liver, and significantly decreased the protein expression of CES1 and CES3 in mouse liver . Conclusion: Fluoxetine may induce lipid accumulation in mouse liver by increasing the expression of lipid synthesis genes and decreasing the expression of lipidolytic genes.