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中华肝脏外科手术学电子杂志 ›› 2014, Vol. 03 ›› Issue (02) : 112 -116. doi: 10.3877/cma.j.issn.2095-3232.2014.02.012

所属专题: 文献

基础研究

CD36在小鼠非酒精性脂肪性肝病形成中的意义
尉秀清1,(), 林颖1, 何卉欣1, 蒋梦萍1, 吴斌1   
  1. 1. 510630 广州,中山大学附属第三医院消化内科
  • 收稿日期:2014-01-15 出版日期:2014-04-10
  • 通信作者: 尉秀清
  • 基金资助:
    国家自然科学基金(81272640); 广东省科技计划项目(2010B031200008,2012B031800043)

Role of CD36 in the formation of non-alcoholic fatty liver disease in mice

Xiuqing Wei1,(), Ying Lin1, Huixin He1, Mengping Jiang1, Bin Wu1   

  1. 1. Department of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, China
  • Received:2014-01-15 Published:2014-04-10
  • Corresponding author: Xiuqing Wei
  • About author:
    Corresponding author: Wei Xiuqing, Email:
引用本文:

尉秀清, 林颖, 何卉欣, 蒋梦萍, 吴斌. CD36在小鼠非酒精性脂肪性肝病形成中的意义[J/OL]. 中华肝脏外科手术学电子杂志, 2014, 03(02): 112-116.

Xiuqing Wei, Ying Lin, Huixin He, Mengping Jiang, Bin Wu. Role of CD36 in the formation of non-alcoholic fatty liver disease in mice[J/OL]. Chinese Journal of Hepatic Surgery(Electronic Edition), 2014, 03(02): 112-116.

目的

探讨分化群(CD)36在小鼠非酒精性脂肪性肝病(NAFLD)形成中的意义。

方法

SPF级8周龄健康雄性C57BL/6J小鼠20只,平均体重为(18.8±2.3)g,按照随机数字表法将小鼠随机分成NAFLD组和对照组,每组各10只。NAFLD组给予高脂饲料喂养10周,对照组给予正常饮食10周。处理结束后脱颈处死小鼠,留取心脏血和肝组织标本。观察两组小鼠血清ALT、总胆固醇(TC)、甘油三酯(TG)水平,肝组织TC、TG水平,肝组织病理学改变,肝组织CD36蛋白表达及其信使核糖核酸(mRNA)含量。两组实验数据的比较采用t检验。

结果

NAFLD组小鼠血清ALT水平为(49±6)U/L,对照组为(45±7)U/L,两组比较差异无统计学意义(t=1.70,P>0.05)。NAFLD组小鼠血清TC、TG水平分别为(4.42±0.09)、(0.45±0.04)mmol/L,对照组分别为(2.42±0.05)、(0.32±0.03)mmol/L,NAFLD组小鼠血清TC、TG水平明显高于对照组(t=21.90,8.22;P<0.05)。NAFLD组小鼠肝组织TC、TG水平分别为(1.18±0.09)、(1.75±0.08)mmol/L,对照组分别为(0.55±0.06)、(1.28±0.06)mmol/L,NAFLD组小鼠肝组织TC、TG水平明显高于对照组(t=18.42,14.86;P<0.05)。NAFLD组肝细胞明显脂肪变性、气球样变。对照组肝细胞形态、大小正常。NAFLD组小鼠肝组织CD36蛋白表达明显强于对照组。NAFLD组小鼠肝组织CD36 mRNA含量为2.75±0.26,对照组为1.00±0.08,NAFLD组小鼠肝组织CD36 mRNA含量明显高于对照组(t=21.16,P<0.05)。

结论

CD36可能参与小鼠NAFLD形成,降低CD36表达可能成为防治NAFLD的新靶点。

Objective

To investigate the role of cluster of differentiation (CD) 36 in the formation of non-alcoholic fatty liver disease (NAFLD) in mice.

Methods

Twenty specific pathogen free healthy male C57BL/6J mice [8 weeks old, average weight: (18.8±2.3)g] were randomly divided into NAFLD group and control group according to the random number table method with 10 mice in each group. Mice in NAFLD group was fed with high-fat diet for 10 weeks, while mice in control group was fed with normal diet for 10 weeks. The mice were sacrificed after the processing, and samples of cardiac blood and liver tissue were collected. The levels of serum alanine transaminase (ALT), total cholesterol (TC) and triglyceride (TG), levels of TC and TG in liver tissue, pathological changes of liver tissue, expression of CD36 protein and content of its messenger ribonucleic acid (mRNA) in liver tissue of 2 groups were observed. Experimental data of 2 groups were compared using t test.

Results

The level of serum ALT was (49±6)U/L in NAFLD group and (45±7)U/L in control group, where no significant difference was obsersed (t=1.70, P>0.05). The levels of serum TC and TG were (4.42±0.09), (0.45±0.04)mmol/L in NAFLD group and (2.42±0.05), (0.32±0.03)mmol/L in control group respectively. The levels of serum TC and TG in NAFLD group were significantly higher than those in control group (t=21.90, 8.22; P<0.05). The levels of TC and TG in liver tissue were (1.18±0.09), (1.75±0.08)mmol/L in NAFLD group and (0.55±0.06), (1.28±0.06)mmol/L in control group respectively. The levels of TC and TG in liver tissue in NAFLD group were significantly higher than those in control group (t=18.42, 14.86; P<0.05). Obviously fatty degeneration and ballooning degeneration were observed in hepatocytes of NAFLD group, while hepatocytes were normal in morphology and size in control group. The expression of CD36 protein in liver tissue in NAFLD group was significantly stronger than that in control group. The content of CD36 mRNA in liver tissue was 2.75±0.26 in NAFLD group and 1.00±0.08 in control group. The content of CD36 mRNA in liver tissue in NAFLD group was significantly higher than that in control group (t=21.16, P<0.05).

Conclusions

CD36 may play a role in the formation of NAFLD in mice. To decrease its expression can be a new target for the prophylaxis and treatment of NAFLD.

图1 两组小鼠饲养10周后肝组织病理学改变(HE ×200)
图2 两组小鼠肝组织CD36蛋白表达的电泳图
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