腹腔神经丛阻滞对GK大鼠胰岛素受体底物的影响  

The Effects of Neurolytic Celiac Plexus Block ( NCPB) on Insulin Receptor Substrate in GK ( Goto-Kakizaki) Rats

作　　者：任尧[1] 牛杨 李军[2] 葛方兰[1] 杨芸[3] 李维[1] 杨永芝 文冬梅 REN Yao;NIU Yang;LI Jun;GE Fanglan;YANG Yun;LI Wei;YANG Yongzhi;WEN Dongmei(College of Life Sciences, Sichuan Normal University, Chengdu 610101, Sichuan;Department of Anesthesiology, Mianyang Central Hospital, Mianyang 621000 , Sichuan;State Key Laboratory of Biotherapy and Cancer center/Collaborative Innovation Center for Biotherapy, West China Hospital, Sichuan University, Chengdu 610064, Sichuan)

机构地区：[1]四川师范大学生命科学学院,四川成都610101 [2]绵阳市中心医院麻醉科,四川绵阳621000 [3]四川大学生物治疗国家重点实验室,四川成都610064

出　　处：《四川师范大学学报（自然科学版）》2018年第1期117-121,共5页Journal of Sichuan Normal University（Natural Science）

基　　金：国家自然科学基金面上项目(31271332);四川省教育厅重点项目(17ZA0323)

摘　　要：观察NCPB对GK(Goto-Kakizaki,GK)大鼠血糖及胰岛素受体底物的影响.构建25只非胰岛素依赖糖尿病(NIDDM)的雄性GK大鼠,随机抽取5只GK大鼠,以NCPB前表示,先进行口服葡萄糖耐受试验(OGTT),然后处死采取肝组织.其余20只GK大鼠随机分为对照组和NCPB组,每组10只.NCPB组给予双侧质量分数0.5%利多卡因进行NCPB,1 mL/侧,每天1次,而对照组以质量分数0.9%生理盐水替换.分别在14 d和28 d后取对照组和NCPB组各5只GK大鼠进行OGTT实验,通过Western Blot检测对照组和NCPB组肝组织中的胰岛素受体底物-1(IRS-1)、IRS-2表达以及IRS-1磷酸化情况.结果表明:NCPB组在14 d和28 d NCPB处理后,在0、60和120 min时的血糖均显著低于NCPB前(P<0.05或P<0.01)和对照组(P<0.01),而血清胰岛素水平与NCPB前和对照组相差不显著;在14、28 d NCPB后NCPB组肝组织IRS-1和IRS-2蛋白表达水平与NCPB前相比均显著增加(P<0.01),在相应时间点并显著高于对照组(P<0.01);而对照组的肝组织IRS-1丝氨酸307残基的磷酸化水平在14、28 d NCPB后与NCPB前均有所上调(P<0.05),NCPB组在相应时间点丝氨酸307残基的磷酸化程度均较NCPB前显著下降(P<0.01),且均显著低于对照组(P<0.01).NCPB可降低GK大鼠的空腹血糖,减轻GK大鼠糖耐量受损的程度,其机制可能与NCPB提高胰岛素受体底物的蛋白表达和抑制其丝氨酸磷酸化有关.To investigate the effects of neurolytic celiac plexus block（NCPB）on blood glucose and insulin receptor substrate in GK（Goto-Kakizaki）rats,the GK rats were used to establish a non-insulin dependent diabetes mellitus（NIDDM）model.5 GK rats before NCPB were randomly selected to be subjected to the oral glucose tolerance test（OGTT）and the liver tissue was excised.The remaining 20 GK rats were randomly divided into two groups：rats in the NCPB group were treated with 0.5% lidocaine（1 mL/1 time/day）for 28 consecutive days,while the control group received the same procedure with physiological saline injected instead of 0.5% lidocaine.The OGTT were performed after 14 and 28 days.Western blot assay was used to analyze the expression of insulin receptor substrate 1（IRS-1）,IRS-2 and phosphorylation of IRS-1 in the liver tissue.After 14 and 28 days of treatment with NCPB,the concentration of blood glucose in the NCPB group was significantly lower than before NCPB（P〈0.05 or P〈0.05）and the control group（P〈0.01）at 0,60 and 120 min of the OGTT,while the levels of serum insulin exhibited no statistical difference between the control group and the NCPB group.The IRS-1 and IRS-2 expression levels of liver tissue in the NCPB group were significantly higher than control group at the corresponding time points（P〈0.01）,which significantly increased compared to before NCPB（P〈0.01）.The phosphorylation level of Ser 307 of IRS-1 was significantly lower in the NCPB group than the control group（P〈0.01）at the corresponding time points,which declined significantly（P〈0.01）in the NCPB group,while were significantly increased（P〈0.05）in the control group compared with before NCPB.The NCPB treatment can decrease the fasting blood glucose level as well as reduce the degree of impaired glucose tolerance in GK rats.The mechanism may be related to increased protein expression and inhibition of the serine phosphorylation.

关 键 词：腹腔神经丛阻滞 GK大鼠 口服葡萄糖耐受试验 胰岛素受体底物 

分 类 号：R587.3[医药卫生—内分泌]