黄芪多糖对KKAy小鼠骨骼肌蛋白激酶B丝氨酸磷酸化的影响  

Effect of Astragalus Polysaccharide on Ser Phosphorylation of Protein Kinase B in Skeletal Muscle of KKAy Mice

作　　者：刘敏[1] 欧阳静萍[1] 吴珂[1] 毛先晴[1] 李柯[1] 郭鹏[1] 叶彦[1] 杨海鹭[1] 徐怡[1] 

机构地区：[1]武汉大学医学院病理生理学教研室/湖北省过敏和免疫相关疾病重点实验室,武汉430071

出　　处：《武汉大学学报（医学版）》2006年第2期135-139,共5页Medical Journal of Wuhan University

基　　金：国家自然科学基金资助项目(编号:30370673)

摘　　要：目的:观察胰岛素刺激下蛋白激酶B(PKB)丝氨酸磷酸化水平在遗传性2型糖尿病小鼠(KKAy)骨骼肌组织的变化及黄芪多糖(APS)对其影响。方法:选取雌性KKAy16只,随机分为2组:糖尿病组和糖尿病黄芪多糖治疗组;选取雌性C57BL/6J小鼠20只作为对照组,随机分为正常对照组和黄芪多糖对照组。于黄芪多糖治疗前后观察体重、血糖、血胰岛素水平、胰岛素抵抗指数及口服葡萄糖耐量试验,治疗8周后用免疫印迹法检测骨骼肌组织胰岛素刺激的丝氨酸磷酸化PKB表达。结果:KKAy小鼠体重、血糖及胰岛素抵抗指数均显著高于C57BL/6J组,同时伴有明显的糖耐量异常(P<0.01),经APS治疗8周后,各项实验指标均明显降低(P<0.01)。KKAy小鼠骨骼肌组织胰岛素刺激的丝氨酸磷酸化PKB表达水平显著低于C57BL/6J小鼠(P<0.01),黄芪多糖可明显提高KKAy小鼠骨骼肌丝氨酸磷酸化PKB表达(P<0.05),但对C57BL/6J小鼠各项指标无显著影响。结论:胰岛素刺激下的PKB磷酸化障碍是2型糖尿病胰岛素抵抗的重要机制之一,黄芪多糖可增强胰岛素刺激的丝氨酸磷酸化PKB表达水平,从而改善KKAy小鼠胰岛素抵抗。Objective： To examine potential effects of astragalus polysaccharide （APS） treatment on glucose homeostasis and protein kinase B（PKB） Ser473 phosphorylation in skeletal muscle in vivo from KKAy diabetic mice and C57BL/6J non-dlabetic mice. Methods： Female KKAy （age eight weeks, n=16） and C57BL/6J mice（age eight weeks, n=20）were respectively randomized to the APS treated and control groups. In the groups with APS, KKAy and C57BL/6J mice were administered with APS[700 mg/（kg · d）] from the age of 12 weeks and lasted for eight weeks. Body weight, blood glucose level, plasma insulin concentration,insulin resistance index and oral glucose tolerance test（OGTT） were observed pre-and post-APS therapy. At the end of eightweeks treatment with APS, the insulin stimulated serine phosphorylation of serine/threonine protein kinase B in skeletal muscle was assessed. Results： Compared with C57BL/6J mice, there were significant increases in body weight, blood glucose level and insulin resistance index, and marked impaired in oral glucose tolerance test in KKAy mice（all P〈0.01） which were alleviated by treatment with APS for eight weeks（all P〈0.01）. Insulin stimulated serine phosphorylation of PKB was lower in KKAy compared to C57BL/6J （P〈0.01）and was enhanced in APS treated KKAy mice（P〈0.05）. While the above changes didn＇t occurred in C57BL/6J mice treated with APS. Conclusion： These data implicate decreased insulin stimulated PKB/Akt kinase phosphorylation as an important component underlying insulin resistance in skeletal muscle from KKAy mice. APS treatment attenuated hyperglycaemia with an increased PKB phosphorylation in KKAy mice.

关 键 词：糖尿病 2型 胰岛素抵抗 黄芪多糖 蛋白激酶B 

分 类 号：R587.1[医药卫生—内分泌]