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作 者:刘博[1,2] 于春江 孟祥宝[4] 温富春[2] 赵宏伟 孙桂波[4] 丁涛[2] 徐惠波[2] 孙晓波[4]
机构地区:[1]黑龙江中医药大学,黑龙江哈尔滨150040 [2]吉林省中医药科学院,吉林长春130012 [3]吉林一正药业集团,吉林四平136001 [4]中国医学科学院药用植物研究所,北京100193
出 处:《中国中药杂志》2016年第11期1978-1982,共5页China Journal of Chinese Materia Medica
基 金:国家"重大新药创制"科技重大专项(2011ZX09201-201-31;2012ZX09501001-004)
摘 要:观察芪蛭降糖胶囊对2型糖尿病大鼠降糖的效果,并探讨其降糖的初步作用机制。该实验采用高糖高脂配合小剂量链脲佐菌素(STZ)制备成2型糖尿病大鼠模型,连续给药6周后,检测各组动物血糖、糖化血清蛋白(GSP)水平;免疫组化法检测胰腺组织中胰岛β细胞的数量;蛋白印迹法检测肝组织中胰岛素受体(InsR)、磷脂酰肌醇-3激酶(PI3K)、葡萄糖转运体2(GLUT2)及磷酸化的c-Jun氨基末端激酶(p-JNK)蛋白的表达。结果显示,芪蛭降糖胶囊能够降低糖尿病动物的血糖和血清GSP水平,提升血清中胰岛素含量和胰岛β细胞的数量,提高肝组织中InsR,PI3K,GLUT2蛋白表达,降低p-JNK蛋白的表达。总之,芪蛭降糖胶囊降糖的作用较为稳定,其降糖机制可能与增加胰岛β细胞的数量而提升血清中胰岛素的含量,提高肝组织中InsR,PI3K,GLUT2蛋白表达并降低p-JNK蛋白表达从而减少肝组织的胰岛素抵抗有关。To observe the hypoglycemic effect of Qizhi Jiangtang capsule in rats with type 2 diabetes, and investigate the preliminary mechanism of its hypoglycemic effect, type 2 diabetes rat models were established by high glucose and high fat combined with small dose of streptozotocin (STZ). After continuous administration for 6 weeks, blood glucose, and glycosylated serum protein (GSP) levels were detected in all of the animals; immunohistochemistry assay was used to detect the number of isletβ cells; Western blot assay was used to detect the protein expression levels of insulin receptor (InsR), phosphoinositide-3 kinases (PI3K) , glucose transporter-2 (GLUT2) and phosphorylated Jun N-terminal kinases (p-JNK) in hepatic tissues. The results showed that Qizhi Jiangtang capsule could reduce the blood sugar and GSP levels in serum in animals with type 2 diabetes mellitus, increase the level of insulin in serum and number of islet β cells, increase the protein expression levels of InsR, PI3K and GLUT2, and reduce the level of p-JNK protein expression. In conclusion, Qizhi Jiangtang capsule has relatively stable hypoglycemic effect, and the mechanism may be associated with increasing the number of isletβ cells and level of insulin in serum, up-regulating the protein expression levels of InsR, PI3K and GLUT2, down-regulating the level of p-JNK protein expression in hepatic tissues, and reducing the level of insulin in hepatic tissues.
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