摘要
目的:观察祛胰抵方对2型糖尿病胰岛素抵抗大鼠糖脂代谢和胰岛的影响,并探讨其可能的分子机制。方法:清洁级大鼠80只,适应性喂养1周后,随机分为模型组70只与对照组10只,模型组大鼠予高脂饲料、对照组予基础饲料喂养4周后,模型组给予链脲佐菌素诱导2型糖尿病模型,造模成功大鼠测定各项基础指标,并评估胰岛素抵抗程度。将60只2型糖尿病胰岛素抵抗模型大鼠随机分为生理盐水组,中药低、中、高浓度组,西药组,各12只。灌胃治疗12周后,测定大鼠空腹血糖(FPG)、空腹胰岛素(FINS)、血脂,检测胰岛病理及免疫组化。结果:治疗后,中药高、中浓度组、西药组大鼠FPG、FINS、甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL-C)与治疗前比较均明显降低(P<0.05),胰岛素敏感性(ISI)、高密度脂蛋白(HDL-C)上升(P<0.01);与生理盐水组比较,胰岛萎缩得到改善。结论:本研究表明祛胰抵方可有效控制空腹血糖,改善血脂紊乱,并有保护胰岛β细胞及恢复胰岛β细胞分泌功能的作用。
Objective : Observation of Quyidi Prescription on the liver of rats with type 2 diabetes islet and metabolism of glucose and lipid was carried on to explore the possible mechanism of action. Methods- 10 out of 80 male Wistar rats, were randomly selected out as the control group with normal feeding, and the rest experimental group was fed by high fat forage. Four weeks later, the experimental group used STZ ( 30 mg/kg ) one-tinae intraperitoneal injection method to establish insulin resistance of type 2 diabetes rat model. 60 model rats, according to random number table were divided into low,medium and high concentration groups of traditional Chinese medicine, Western medicine group, model group. Each group was treated for 12 weeks. Before and after treatment, FPG, FINS, lipids, islet pathology and immunohistochemistry were tested. Insulin sensitivity index ( ISI ) was used to evaluate the degree of insulin resistance. Results: Compared with those before treatment, FPG, FINS, TG, TC and LDL-C levels of medium and high groups of traditional Chinese medicine and Western medicine group were significantly decreased, ISI and HDL-C were escalated. Compared with the saline group, islet atrophy improved. Conclusion: Quyidi Prescription can effectively control FPG, improve dyslipidemia, and protect pancreatic islet beta cell and restore islet function.
出处
《辽宁中医药大学学报》
CAS
2013年第8期5-9,共5页
Journal of Liaoning University of Traditional Chinese Medicine
基金
黑龙江省自然科学基金项目(D201072)
关键词
祛胰抵方
2型糖尿病
胰岛素抵抗
糖脂代谢
胰岛
Quyidi Prescription
type 2 diabetes
IR
metabolism of glucose and lipid pancreatic isletbeta cell