Article Summary
曹彦1 易艳荣2.非酒精性脂肪肝病大鼠肝脏SOCS-3 的表达与吡格列酮干预研究[J].现代生物医学进展英文版,2011,11(10):1817-1820.
非酒精性脂肪肝病大鼠肝脏SOCS-3 的表达与吡格列酮干预研究
Expression of SOCS-3 in the Liver of Rats with Nonalcoholic Fatty LiverDisease and Therapeutic Effects of Pioglitazone
  
DOI:
中文关键词: 非酒精性脂肪肝病  SOCS-3  吡格列酮
英文关键词: Nonalcoholic fatty liver  SOCS-3  Pioglitazone
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Author NameAffiliation
CAO Yan1, YI Yan-rong 2 湖南省人民医院急诊科 
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中文摘要:
      目的:探讨SOCS-3 在非酒精性脂肪肝病(NAFLD)发病中的作用以及吡格列酮的干预作用。方法:29 只雄性SD 大鼠随机分 为正常对照组(8 只),高脂饮食组(21 只)。饲养8 周后,从高质饮食组随机抽取5 只大鼠证实造模成功后,将该组余下的16 只大 鼠继续以高脂饲料喂养,并随机分为NAFLD 对照组(8 只);吡格列酮干预组(8 只),予以吡格列酮3mg·kg-1·d-1 灌胃。16 周末,处 死所有大鼠,检测血糖、血胰岛素、血脂、肝脏SOC S-3mRNA 和SREBP-1c mRNA 表达及肝脏病理学。结果:与正常对照组相比, NAFLD 组血糖、血胰岛素、血脂、肝脏脂肪变水平及肝组织SOCS-3mRNA、SREBP1c mRNA 表达显著上调。吡格列酮干预组 SOCS-3mRNA、SREBP-1cmRNA 表达较NAFLD 组下调,且血糖、血胰岛素、血脂、肝脏脂肪变水平下降。SOCS-3mRNA 表达水平 与胰岛素抵抗指数、SREBP-1c mRNA 表达水平、肝脂肪变成显著正相关。结论:SOCS-3 可能通过胰岛素抵抗及上调肝组织 SREBP-1c mRNA 表达参与NAFLD 发病,吡格列酮能抑制肝脏SOCS-3 的表达,对NAFLD 有一定治疗作用。
英文摘要:
      Objective: To investigate the role of suppressors of cytokine signaling protein(SOCS-3) in the pathogenesis of patients with nonalcoholic fatty liver as well as the effects of pioglitazone. Methods: Twenty-nine male SD rats were randomized into normal control group (n=8, fed with normal food), high fat diet group (n=21, fed with fat-rich food). Killed 5 rats of high fat diet group after 8 weeks, and confirmed that the model of NAFLD was successfully established. Then the remaining 16 rats were divided into 2 subgroups: NAFLD control group (n=8, fed with continuously with fat-rich food), pioglitazone intervention group (n=8, fed with continuously with fat-rich food and pioglitazone 3 mg·kg-1·d-1 by gastric perfusion). By the end of 16th week , all rats were killed to isolate the serum to test the levels of FBG, FINS, TG and TC. The SOCS-3 mRNA and SREBP-1c mRNA expression of rat liver were analyzed by RT-PCR. Results: Compared with control group, the serum levels of FBG, FINS, TC, TG and the liver SOCS-3 and SREBP-1c expression levels, liver fatty degeneration grades of NAFLD group were all up-regulated (P<0.05). The serum levels of FBG, FINS, TC, TG of pioglitazone intervention group were significantly lower than NAFLD control group (P<0.05); the liver SOCS-3 and SREBP-1c expression levels of pioglitazone intervention group were also lower than NAFLD control group(P<0.05). Meanwhile, the fatty degeneration grades of liver of pioglitazone intervention group was lower than NAFLD control group (P<0.05). The liver SOCS-3 mRNA expression levels positively correlated with HOMA-IR, the liver SREBP-1c mRNA expression levels and the fatty degeneration grades(P<0.05). Conclusion: SOCS-3 might be involved in nonalcoholic fatty liver through insulin resistance and up-regulating SREBP-1c mRNA expression, and pioglitazone therapy could decrease the SOCS-3mRNA expression and effectively treat nonalcoholic fatty liver.
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