消渴灵片对2型糖尿病大鼠JNK信号通路的影响

Effects of Xiaokeling tablet on JNK signaling pathway with type 2 diabetic

关键词:  消渴灵片  糖尿病大鼠  JNK信号通路  PDX-1蛋白

Key words:  Xiaokeling tablets  diabetic rats  JNK signaling pathway  PDX-1 protein

摘要:

[目的] 研究消渴灵片（XKL）对2型糖尿病大鼠JNK信号通路的影响。[方法] 将2型糖尿病模型大鼠，按随机数字表法随机分为正常组、模型组、XKL低、中、高组[分别以2、4、8 g/kg XKL作为低、中、高剂量灌胃）、阳性对照组（以0.8 g/kg盐酸二甲双胍灌胃），测定各组大鼠空腹血糖（FBG）、空腹胰岛素（FINS）、丙二醛（MDA）水平、超氧化物歧化酶（SOD）活性、磷酸化c-Jun氨基末端激酶（p-JNK）及胰十二指肠同源盒-1（PDX-1）蛋白相对表达情况及JNK mRNA表达情况。[结果] XKL各剂量组均可有效降低模型大鼠FBG水平；XKL中高剂量组可降低MDA水平，提高FINS水平及SOD活性（P<0.05）；XKL中、高剂量p-JNK蛋白及JNK mRNA表达量显着下降（P<0.05），PDX-1蛋白表达量显着升高（P<0.05）.[结论] XKL的降糖作用，可能与抑制JNK信号通路的激活有关。

Abstract:

[Objective] To study the effect of Xiaokeling tablets (XKL) on JNK signaling pathway in type 2 diabetic rats. [Method] Preparation of type 2 diabetic rat model by using high-sugar and high-fat food feeding combined with low-dose streptozotocin (STZ). Experimental animals were divided into normal control group, model group, XKL low, medium and high dose group (intragastric administration in low, medium and high dose group as 2, 4, 8 g/kg respectiely), positive control group (intragastric administration by 0.8 g/kg metformin hydrochloride). Fasting blood glucose (FBG), fasting insulin (FINS), malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, phosphorylation of c-Jun N-terminal kinase (p-JNK), pancreas duodenal homeobox-1 (PDX-1) protein relative expression and JNK mRNA expressionrats were measured in each groups of rats. [Result] The level of FBG and MDA were effectively reduced and the level of FINS and SOD activity were improved in XKL each dose groups. The middle and high dose group had statistical significance compared with the model group (P<0.05). The expression of p-JNK protein and JNK mRNA was significantly decreased in middle and high dose compared with the model group (P<0.05). The expression of PDX-1 protein increased significantly in middle and high dose compared with the model group (P<0.05). [Conclusion] The hypoglycemic effect of XKL may be related to inhibiting the activation of JNK signaling pathway.