摘要
目的测定不同饮食喂养大鼠和瑞舒伐他汀及替米沙坦干预后大鼠产生胰岛素抵抗(IR)的情况,观察大鼠肝脏中IKK、活性氧(ROS)表达的变化。方法 4周龄Wistar雄性大鼠40只,以高糖高脂饮食诱导建立IR模型,以高脂给药(ARB类、他汀类)诱导建立实验组,通过RT-PCR方法检测IR大鼠肝脏组织中IKK、ROS的表达水平。结果高糖高脂饲料组大鼠产生IR,给予瑞舒伐他汀干预后IR明显改善,高糖高脂饲料组大鼠ROS、IKK在肝脏中的表达明显高于对照组大鼠,瑞舒伐他汀药物可降低IR组大鼠ROS、IKK在肝脏中的表达。结论高脂高糖饲料喂养8 w可诱导大鼠产生IR。IR大鼠体内氧化应激增强ROS产生增加。过量的ROS通过激活IKK等通路,干扰细胞胰岛素受体信号转导,导致IR。通过瑞舒伐他汀、替米沙坦干预,可使ROS、IKK等表达水平下调,明显改善IR,其中瑞舒伐他汀降低更为明显。
Objective To observe the influence of rosuvastatin calcium and telmisartan on the expressions of IKK, ROS of insulin resistance （IR） rat liver. Methods 4-week-old Wistar male rats were given high-glucose and high-fat diet to build IR model. Rats in ex- perimental groups were given telmisartan or rosuvastatin calcium. Expressions of IKK and ROS in liver tissue were detected by RT-PCR. Re- sults Rats with high-glucose and high-fat diet were induced into IR. Rosuvastatin calcium could improve IR. Expressions of IKK and ROS in IR rat＇ s liver were higher than those of control group and rosuvastatin calcium could decrease the expressions of IKK and ROS. Conclu- sions Telmisartan and rosuvastatin calcium can down-regulate the expressions of KK and ROS and improve IR. Effect of rosuvastatin calci- um is more obvious.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2013年第2期332-334,共3页
Chinese Journal of Gerontology
基金
辽宁省科技厅技术基金(20102277)
辽宁省教育厅科研项目(LA2010647)
关键词
胰岛素抵抗
活性氧
核因子κ-B/IκB激酶
Insulin resistance （IR）
Reactive oxygen species （ROS）
Nuclear factor-KB/IKB kinase
