中文摘要：

目的 观察腹腔神经丛阻滞（NCPB）对2型糖尿病Goto-Kakizaki（GK）大鼠胰腺的影响。方法 25只2型糖尿病（T2DM）构模成功的雄性GK大鼠,随机抽取5只取胰腺组织（N0）,以观测基础状况;再随机将20只GK大鼠分为对照组和实验组,每组10只。实验组给予0.5%利多卡因行NCPB,1 ml/（次·d）,对照组以0.9%生理盐水替换。对照组和实验组分别于14次（N14）和28次（N28）NCPB后,各取5只GK大鼠,取胰腺组织。采用免疫组化和Western blot法检测各组胰腺组织中TNF-α、IL-1β水平和Bax、Bcl-2的蛋白表达。结果 HE染色和胰岛素免疫组化分析均可见对照组和实验组GK大鼠胰腺在N14、N28时病变持续加重,胰岛数及细胞数目减少,并可见被增生纤维组织分割包围的胰岛明显萎缩,但两组相比,实验组胰岛萎缩程度明显轻于对照组;在N14、N28时,对照组胰岛的TNF-α和IL-1β水平均有所升高,而实验组却明显下降,并显著低于对照组;实验组GK大鼠胰腺Bax蛋白表达水平在N14、N28时显著低于对照组（P〈0.01）,Bcl-2蛋白表达显著高于对照组（P〈0.01）,Bax/Bcl-2比值显著低于对照组（P〈0.01）。结论 延缓T2DM模型GK大鼠胰岛的病理改变,可能是NCPB减轻糖耐量受损程度的机制之一。

英文摘要：

Objective To observe the effects of neurolytic celiac plexus block （NCPB） on Goto-Kakizaki （GK） islets in rats with type 2 diabetes. Methods A total of 25 make GK rats successfully were modeled with type 2 diabetes mellitus （T2DM）. Five rats were randomly selected to get the pancreatic tissue （No） to observe basic conditions, and another 20 GK rats were randomly divided into a control group and an experiment group（n=10, respectively）. The experiment was administrated with 0.5% lidocaine for NCPB, 1 ml/（time.d） and the control group with 0.9% normal saline. After the 14th （N14） and 28th （N2s） NCPB, five GK rats were selected from the control group and the experiment group respectively to get the pancreatic tissue. Immunohistochemistry and Western blot were used to detect the levels of TNF-ct and IL-I- and the protein expression of Bax and Bcl-2. ll-ttlls Both HE staining and immunohistochemical analysis of insulin showed that the lesion of GK rat pancreas in the control group and the experiment group at N,4 and N-. The number of islet and cell reduced. The islet separated and surrounded by the hyperplastic fibrous tissue obviously receded, but the receding degree in the experiment group was lower than that in the control group; at N14 and N=, the TNF-α and IL-1β levels of islet in the control group increased, while those in the control group reduced obviously and were much lower than those in the control group; the GK rat islet Bax protein expression level was significantly lower than that in the control group at N14 and N28 （P 〈 0.01）, while Bcl-2 protein expression was significantly higher than that in the control group（P 〈 0.01） and Bax/Bcl-2 ratio much lower than that in the control group （P 〈 0.01）. Conclusion The delay of the pathological change in T2DM model GK rat islet may be one of the mechanisms of NCPB to reduce the degree of impaired glucose tolerance.