摘要
目的探索氧化苦参碱对胎龄新生大鼠代谢综合征氧化应激和糖脂代谢的影响及其作用机制。方法建立新生胎龄大鼠代谢综合征模型,检测血糖、胰岛素、血脂、肥胖指数、氧化应激水平和肝脏脂肪变性程度,检测AMPK、SIRT1、PGC1α蛋白表达。加入AMPK抑制剂后再次检测上述指标变化。结果与MS组比,各氧化苦参碱剂量组大鼠血糖、体重、肥胖指数、胰岛素水平降低,LDL、TG、TC、R0S、MDA、LDH含量降低,HDL、血糖、TG、R0S含量升高,肝脏脂肪变性得到不同程度的缓解,AMPK、SIRT1、PGC1α表达升高(P<0.05)。Compound C组AMPK、SIRT1、PGC1α表达降低。与Compound C组比,Compound C+Oxymatrine组中AMPK、SIRT1、PGC1α表达升高,血糖、TG、ROS含量降低(P<0.05).结论氧化苦参碱通过AMPK/SIRT1/PGC1α通路加强代谢综合征大鼠糖脂代谢,降低氧化应激水平。
Objective To explore the effect of oxymatrine on the oxidative stress and glucose and lipid metabolism in fetal neonatal rats with metabolic syndrome.Methods A neonatal fetal rat model of metabolic syndrome(MS)was established to detect blood glucose,insulin,blood lipid,obesity index,oxidative stress level and liver steatosis,and the expressions of AMPK,SIRT1 and PGC1α were determined.These parameters were re-measured after AMPK inhibitors were given.Results Compared with the MS group,the level of blood glucose,body weight,obesity index and insulin in the rats in each group receiving different doses of oxymatrine were decreased;the levels of LDL,TG,TC,ROS,MDA and LDH were lowered,the levels of HDL,blood glucose,TG and ROS were increased,liver steatosis was alleviated to different degrees,and the expression of AMPK,SIRT1 and PGC1α was up-regulated(P<0.05).The expression of AMPK,SIRT1 and PGC1 in Compound C group was down-regulated.Compared with Compound C group,the expression of AMPK,SIRT1 and PGC1α in Compound C+Oxymatrine group was increased,and the levels of blood glucose,TG and ROS were decreased(P<0.05).Conclusion Oxymatrine enhances glucose and lipid metabolism and reduces oxidative stress in rats with metabolic syndrome through THE AMPK/SIRT1/PGC1α pathway.
作者
苏志谦
刘赞丽
欧明
SU Zhiqian;LIU Zanli;OU Ming(Department of Neonatology,the First Affiliated Hospital of Hunan College of Traditional Chinese Medicine,Zhuzhou,Hunan,412000,China)
出处
《医学分子生物学杂志》
CAS
2021年第1期40-45,共6页
Journal of Medical Molecular Biology
基金
湖南省自然科学基金(No.2018 JJ6043)。
关键词
氧化苦参碱
代谢综合征
氧化应激
糖脂代谢
oxymatrine
metabolic syndrome
oxidative stress
glycolipid metabolism