吉林大学学报(医学版)

• 基础研究 • 上一篇    下一篇

赖氨大黄酸对糖尿病大鼠肝脏的保护作用及其机制

刘晓庆1,甄永占2,郝晓方1,王梅梅1,章广玲1   


  1. (1.河北联合大学基础医学院病原生物学与免疫学教研室,河北 唐山063000;2.河北联合大学基础医学院组织学与胚胎学教研室,河北 唐山063000)
  • 收稿日期:2013-09-23 出版日期:2014-05-28 发布日期:2014-05-28
  • 通讯作者: 章广玲 E-mail:(Tel:0315-3725918,E-mail:zhguangling@126.com)
  • 作者简介:刘晓庆(1986-),女,河北省唐山市人,在读医学硕士,主要从事糖尿病发病机制和治疗的研究。
  • 基金资助:

    国家自然科学基金资助课题(81001439,81201281);河北省科技厅自然科学基金资助课题(C2012401037,H2012401030,H2013209180)

Protective effect of rhein lysinate on liver of diabetic rats and its mechanism

LIU Xiao-qing1,ZHEN Yong-zhan2,HAO Xiao-fang1,WANG Mei-mei1,ZHANG Guang-ling1   

  1. (1.Department of Pathogen Biology and Immunology,College of Basic Medical Sciences,Hebei United University,Tangshan 063000,China;2. Department of Histology and Embryology,College of Basic Medical Sciences,Hebei United University,Tangshan 063000,China)
  • Received:2013-09-23 Online:2014-05-28 Published:2014-05-28

摘要:

目的: 探讨赖氨大黄酸(RHL)对糖尿病模型大鼠肝脏的保护作用,阐明RHL对肝脏的保护作用机制。方法:通过腹腔注射链脲佐菌素(STZ)建立大鼠糖尿病模型。将40只大鼠随机分为对照组、糖尿病模型组、25和50 mg•kg-1 RHL治疗组,每组10只。采用硫代巴比妥酸法检测肝脏组织中丙二醛(MDA) 水平,联苯三酚自氧化法和NADPH 偶联法分别检测超氧化物歧化酶(SOD) 和谷胱甘肽过氧化物酶(GSH-Px)活性;HE染色观察肝脏组织病理学变化;Nile red染色观察肝脏组织脂肪水平;Western blotting法检测脂肪合成相关蛋白表达水平。结果:与对照组比较,糖尿病模型组大鼠体质量减低,血糖、总胆固醇(TC)和甘油三酯(TG)水平升高(P<0.05),肝脏组织中SOD和GSH-Px活性降低(P<0.05),肝脏组织出现大量脂肪空泡和脂肪蓄积。糖尿病模型大鼠脂肪合成信号通路ERK1/2-SREBP-1c被激活;与模型组比较,25和50 mg•kg-1 1 RHL治疗组大鼠脂肪合成信号通路被抑制。与模型组比较,RHL治疗组大鼠体质量无显著变化,但血糖、TG和TC水平显著降低(P<0.05),SOD和GSH-Px活性显著升高(P<0.05)。与糖尿病模型组比较,RHL治疗组大鼠肝脏组织中的脂肪空泡和脂肪蓄积明显减少。结论:RHL能抑制氧化应激、肝脏脂肪变性和脂肪蓄积从而发挥对糖尿病大鼠肝脏的保护作用。

关键词: 赖氨大黄酸, 糖尿病, 肝脏, 脂肪肝

Abstract:

To investigate the protective effect of rhein lysinate (RHL) on the liver of the models with diabetic rats,and to provide basis for research on treatment of fatty liver in the patients  with  diabetes mellitus.Methods The models of diabetic rats were established by intraperitoneally injecting streptozotocin(STZ).40 rats were divided into control,model,25 mg•kg-1 RHL,and 50 mg•kg-1 RHL groups(n=10).The levels of malonaldehyde (MDA) and the
 activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were detected by  thiobarbituric acid method,pyrogallol autoxidation method,and NADPH coupling method,respectively.The pathological changes of liver tissue were observed by hematoxylin and eosin (HE) staining;the content of fat in liver tissue was observed by Nile red staining;the expression levels of fat synthesis-related proteins were detected by Western blotting method.Results  Compared with control group,the body weight of the rats in model group was decreased and the levels of blood glucose,total cholesterol(TC) and triglyceride(TG) were increased (P<0.05);the activities of SOD and GSH-Px in liver tissue were decreased (P<0.05);there were a plenty of fat vacuoles and fat accumulation in liver tissue.The signal pathway of fat synthesis-related ERK1/2-SREBP-1c was activated in model group;compared with model group,it was inhibited in 25 and 50 mg•kg-1 RHL groups (P<0.05).Compared with model group,the blood glucose,TC and TG of the rats in 25 and 50 mg•kg-1RHL groups were decreased (P<0.05);the activities of SOD and GSH-Px were increased (P<0.05);however the body weight had no change.Compared with model group,the fatty vacuoles and the fatty accumulation of liver tissue in 25 and 50 mg•kg-1 RHL groups were decreased.Conclusion The hepatic protection of RHL is correlated with the inhibition of oxidative stress,fat degeneration and fatty accumulation of liver tissues

Key words: rheinlysinate, diabetes mellitus, liver, fatty liver

中图分类号: 

  • R285.5