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作 者:赵晓伟[1] 刘宇[1] 李铁[1] 邸蕴华[1] 李楠[2] ZHAO Xiao-wei;LIU Yu;LI Tie;DI Yun-hua;LI Nan(Department of Endocrinology,Affiliated Central Hospital of Shenyang Medical College,Shenyang 110024;Department of Endocrinology,Affiliated Hospital of Liaoning University of Traditional Chinese Medicine,Shenyang 110033,China)
机构地区:[1]沈阳医学院附属中心医院内分泌一科,辽宁沈阳110024 [2]辽宁中医药大学附属医院内分泌科,辽宁沈阳110033
出 处:《解剖科学进展》2022年第1期109-112,共4页Progress of Anatomical Sciences
基 金:辽宁省自然科学基金(20180551277)。
摘 要:目的探讨杨芽黄素对糖尿病大鼠胰岛素敏感性的作用及可能机制。方法40只雄性SD大鼠随机分为对照组(Control组)、糖尿病组(DM组)、杨芽黄素低剂量组(TEC-L组)和杨芽黄素高剂量组(TECH组),每组10只。检测大鼠空腹血糖和口服糖耐量;ELISA方法检测大鼠血清胰岛素水平,计算胰岛素抵抗指数和胰岛素敏感指数;HE染色观察胰腺组织形态学变化;Western blot方法检测骨骼肌IRS-1/Akt信号通路相关蛋白及脂肪组织NF-κB蛋白表达水平。结果杨芽黄素降低糖尿病大鼠空腹血糖和血清胰岛素水平,改善口服糖耐量,降低胰岛素抵抗指数,增加胰岛素敏感指数,增加骨骼肌IRS-1/Akt信号通路相关蛋白表达,降低脂肪组织NF-κB表达,对胰腺组织病理损伤无显著影响。结论杨芽黄素可增加糖尿病大鼠胰岛素敏感性,其机制可能与抑制NF-κB信号通路有关。Objective To explore the ameliorating effect and possible mechanism of tectochrysin on insulin sensitivity of diabetic rats.Methods 40 male SD rats were randomly divided into control group,diabetes group,tectochrysin low-dose group(TEC-L group)and tectochrysin high-dose group(TEC-H group)with 10 rats in each group.Fasting blood glucose and oral glucose tolerance of rats were measured.Serum insulin level of rats was detected by ELISA.The insulin resistance index and insulin sensitivity index were calculated.HE staining was used to observe the morphological changes of pancreatic tissue.The expression of IRS-1/Akt signaling pathway related proteins in skeletal muscle and NF-κB protein in adipose tissue were detected by Western blot.Results In diabetic rats,tectochrysin decreased fasting glucose and serum insulin levels,improved oral glucose tolerance,decreased insulin resistance index,increased insulin sensitivity index,increased IRS-1/Akt signaling pathway related protein expression in skeletal muscle,decreased NF-κB expression in adipose tissue of diabetic rats,and had no significant effect on pancreatic histopathological injury.Conclusion Tectochrysin can increase insulin sensitivity in diabetic rats,which may be related to inhibition of NF-κB signaling pathway.
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