基础医学与临床 ›› 2015, Vol. 35 ›› Issue (5): 642-647.

• 研究论文 • 上一篇    下一篇

L-谷氨酰胺治疗大鼠非酒精性脂肪肝病

张黎1,牛世伟1,李晓波1,刘华1,黄红1,李燕1,李树德2   

  1. 1. 云南省第一人民医院
    2. 昆明医科大学基础医学院
  • 收稿日期:2014-11-13 修回日期:2015-01-26 出版日期:2015-05-05 发布日期:2015-04-28
  • 通讯作者: 李燕 E-mail:liyanken@126.com
  • 基金资助:
    云南省科技厅—昆明医科大学联合专项基金项目(2011FB225);云南省科技厅应用基础研究(2013FZ183);云南省第一人民医院王陇德院士工作站基金项目;云南省老年病防治研究中心基金项目。

L-Glutamine Treats Non-Alcoholic Fatty Liver Disease in rats

  • Received:2014-11-13 Revised:2015-01-26 Online:2015-05-05 Published:2015-04-28

摘要: 目的 观察L-谷氨酰胺对非酒精性脂肪肝病大鼠的作用。方法 将大鼠随机分为对照组,高脂饮食组及L-谷氨酰胺治疗组,高脂饮食组与L-谷氨酰胺治疗组,高脂饮食建立非酒精性脂肪肝病模型,造模成功后给予相应治疗,8周后,处死大鼠,检测相关指标。结果 治疗组相较高脂饮食组有显著性改变,其中肝脏组织学治疗组相较于高脂饮食组有明显的炎症减轻,脂肪空泡减少;LDL、AST、TBA、 CHOL、TG、LDL-C、IL-6、TNF-α、IL-α、IL-β、MDA及CRP治疗组较高脂饮食组明显降低(P<0.05);GSH、T-AOC、HDL-C、明显升高(P<0.05);SREBF1和ACCα mRNA与蛋白表达明显下降 (P<0.05),PPARα mRNA及蛋白表达明显升高(P<0.05)。结论 L-谷氨酰胺可缓解大鼠非酒精性脂肪肝病症状,其机理可能是通过降低SREBF1及ACCα表达,同时增加PPARα表达实现的。

关键词: 非酒精性脂肪肝, L-谷氨酰胺, 肝功能, 血清生化指标, 氧化及抗氧化能力, 过氧化物酶体增殖物激活受Alphα, 乙酰辅酶A羧, 固醇原件调节因子1c

Abstract: Objective Observe the effect of L-Glutamine on fat- induced nonalcoholic fatty liver disease (NAFLD) in rat. Methods Rats were randomly divided into control group, model group and L-glutamine treatment group, model group and L-glutamine treatment group build nonalcoholic fatty liver disease model after the high-fat diet, modeling success given the appropriate treatment, after 8 weeks, rats were sacrificed to detect relevant indicators. Results Treatment group compared with the model group were significantly changed, liver histology treated group compared with the model group significantly reduced, fat vacuoles reduced; LDL, AST, TBA CHOL, TG, LDL-C, IL-6, TNF-α, IL-α, IL-β, MDA and CRP treatment group compared with the model group was significantly lower (P<0.05); GSH, T-AOC , HDL-C was significantly higher (P<0.05); SREBF1 ACCα and mRNA and protein expression was significantly decreased (P<0.05), PPARα mRNA and protein expression was significantly increased(P<0.05). Conclusion L-glutamine can alleviate the symptoms of nonalcoholic fatty liver disease in rats, the mechanism may be by reducing SREBF1 and ACCα expression, while promoting PPARα expression achieved.

Key words: Non-Alcoholic Fatty Liver Disease, L-Glutamine, Liver Function, Blood Biochemical Parameters, Oxidation and Antioxidant Capacity, Peroxisome Proliferator Activated Receptor Alphα, Acetyl-CoA Carboxylase Alphα, Sterol Regulatory Element binding Transcription Factor 1

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