Effects of ethanol exposure on the synthesis of hepatic lipid in mice
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摘要: 目的 观察小鼠不同时间乙醇暴露,其肝脏脂质合成情况。方法 8周龄雄性ICR小鼠随机分为空白对照组和乙醇实验组,实验组小鼠随机分为单次和连续4 d两个不同的时间组,均给予50%(V/V)乙醇溶液(4 g/kg体重)灌胃,对照组给予等体积的生理盐水。所有小鼠均于末次灌胃12 h后剖杀,取血清用于检测血液生化指标;取肝脏并称重,计算肝脏系数,检测甘油三酯(triglycerides,TG)和总胆固醇(total cholesterol,TCH)含量,苏木素伊红(hematoxylin and eosin,HE)染色观察其病理学改变,油红O 染色观察其脂质沉积;反转录酶-聚合酶链锁反应(reverse transcription-polymerase chain reaction,RT-PCR)检测乙酰辅酶A 羧化酶(acetyl coenzyme carboxylase,ACC)、脂肪酸合成酶(fatty acid synthase,FAS)和硬脂酰辅酶A去饱和酶-1(stearoyl coenzyme A desaturase-1,SCD-1)的mRNA水平。结果 与对照组相比,单次或4 d乙醇暴露小鼠肝脏系数均增加(均有P<0.05);血清和肝脏TG含量升高(均有P<0.05);HE染色和油红O染色显示,肝脏发生脂质沉积;FAS、ACC和SCD-1 mRNA水平上调(均有P<0.05)。结论 单次或连续4 d乙醇暴露均可导致肝脏脂质沉积,并通过增加小鼠肝脏TG合成来完成。
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关键词:
- 乙醇 /
- 肝细胞 /
- 生化现象,代谢和营养
Abstract: Objective To investigate the difference of hepatic lipid synthesis in mice that suffered from different ethanol exposure. Methods 8 weeks male ICR mice were randomly divided into control group and ethanol group. The mice of the ethanol group were administered a dose of 50%(V/V)ethanol solution (4 g/kg) for 1 and 4 d by gavage.Meanwhile,the mice in the control group were administered with saline of equal volume.The mice were sacrificed and used at 12 h after the last gavage. Blood samples and liver tissues were collected for detection of biochemical parameters and liver coefficient, respectively.The triglycerides(TG) and total cholesterol(TCH) in serum and liver were measured. The change of hepatic lipid accumulation was assessed by Hematoxylin and eosin(HE) staining and oil O staining. The mRNA levels of hepatic acetyl coenzyme carboxylase(ACC), fatty acid synthase(FAS) and stearoyl coenzyme A desaturase-1(SCD-1)were determined by the real-time quantitative reverse transcription-polymerase chain reaction(RT-PCR). Results In the single and four days' ethanol-treated mice, the liver coefficient was significantly increased(all P<0.05). The TG content was significantly increased both in serum and in liver, compared to the control group(all P<0.05). Oil O staining and Hepatic histology showed an obvious hepatic lipid accumulation. In addition, ethanol could significantly upregulate the levels of FAS, ACC and SCD-1 mRNA(all P<0.05). Conclusions A single or four ethanol exposures could promote hepatic TG accumulation through increasing hepatic TG synthesis.-
Key words:
- Ethanol /
- Hepatocytes /
- Biochemical phenomena, metabolism, and nutrition
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