Establishment of high-fat and high-glucose and low dose of Streptozocin induced rat models of diabetic nephropathy
YAO Lan1 ZHANG Yujie2,3 WANG Jian3 LIU Jing3 LI Linlin3 WANG Ye3 LAN Yi4 MAO Xinmin5
1.Staff Room of Chinese Medicinal Resources, College of Traditional Chinese Medicine, Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi 830011, China;
2.Department of Pharmacy, the First Affiliated Hospital of Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi 830011, China;
3.Staff Room of Pharmacology, College of Basic Medicine, Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi 830011, China;
4.The Second Department of Cadres, Affiliated Hospital of Traditional Chinese Medicine, Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi 830000, China;
5.College of Traditional Chinese Medicine, Xinjiang Medical University, Xinjiang Uygur Autonomous Region, Urumqi 830011, China
Abstract：Objective To establish the early diabetic nephropathy (DN) rat model induced by high-fat and high-glucose and low dose of Streptozocin (STZ), so as to simulate the pathologic and renal function changes of early DN. Methods Thirty SPF level of normal male SD rats were divided into normal group and model group by weight. Normal group was fed with normal diet, model group was fed with high-fat and high-glucose diet for 8 weeks continuously, then 35 mg/kg of STZ was injected intraperitoneally to establish diabetic rats model, after that, high-fat and high-glucose diet was fed for 4 weeks continuously. Renal pathological changes, biochemical and renal function indexes of two groups were observed. Results The body weight of rats in the model group was significantly lower than that of normal group (P ＜ 0.01), while the random blood glucose level was higher than that of normal group (P ＜ 0.01), which had reached to standard of diabetes mellitus. The level of serum insulin in the model group was lower than that of normal group, the values of relative kidney weight, 24 h microalbuminuria, α1-microglobulin, β2-macroglobulin were higher than those of normal group, the differences were highly statistically significant (P ＜ 0.01). The pathological characteristics of model group presented the thickening of glomerular basement membrane, mesangial broadening, accumulation of glycogen and collagen fiber in both glomerulus and kidney tubules. Conclusion This molding method can imitate the basic characteristics of early DN.
姚蓝1 张雨洁2,3 王健3 刘菁3 李琳琳3 王烨3 兰怡4 毛新民5. 高脂高糖与低剂量链脲佐菌素诱导的糖尿病肾病大鼠模型的建立[J]. 中国医药导报, 2017, 14(17): 12-15.
YAO Lan1 ZHANG Yujie2,3 WANG Jian3 LIU Jing3 LI Linlin3 WANG Ye3 LAN Yi4 MAO Xinmin5. Establishment of high-fat and high-glucose and low dose of Streptozocin induced rat models of diabetic nephropathy. 中国医药导报, 2017, 14(17): 12-15.
[1] Furukawa M，Gohda T，Tanimoto M，et al. Pathogenesis and novel treatment from the mouse model of type 2 diabetic nephropathy [J]. Sci World J，2013，2013：928197.
[2] Packham DK，Alves TP，Dwyer JP，et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy：results from the DIAMETRIC（Diabetes Mellitus Treatment for Renal Insufficiency Consortium）database [J]. Am J Kidney Dis，2012，59（1）：75-83.
[3] Yang W，Lu J，Weng J，et al. Prevalence of diabetes among men and women in China [J]. N Engl J Med，2010，362（12）：1090-1101.
[4] Coll-de-Tuero G，Mata-Cases M，Rodriguez-Poncelas A，et al. Chronic kidney disease in the type 2 diabetic patients：prevalence and associated variables in a random sample of 2642 patients of a Mediterranean area [J]. BMC Nephrol，2013，13：87-96.
[5] Ichinose K，Kawasaki E，Eguchi K. Recent advancement of understanding pathogenesis of type 1 diabetes and potential relevance to diabetic nephropathy [J]. Am J Nephrol，2007，27（6）：554-564.
[6] 刘丹丹，仇春健，吴亮，等.中国汉族人群TGF-β1 T869C基因多态性与糖尿病肾病易感性的Meta分析[J].中外医学研究，2015，13（34）：5-8.
[7] Alpers CE，Hudkins KL. Mouse models of diabetic nephropathy [J]. Curr Opin Nephrol Hypertens，2011，20（3）：278-284.
[8] Vashistha H，Meggs L. Diabetic nephropathy：lessons from the mouse [J]. Ochsner J，2013，13（1）：140-146.
[9] 朱以良，杨李，文晔.链尿佐菌素1次和2次注射在2型糖尿病肾病大鼠模型制作中的比较[J]实用医学杂志，2009，25（16）：2649-2650.
[10] 闫永恒，李渐鹏，刘战伟，等.不同2型糖尿病肾病模型建立方法及成模特点比较[J].中国食物与营养，2016，2（1）：65-69.
[11] Piret SE，Olinger E，Reed AA，et al. Mouse model for inherited renal fibrosis associated with endoplasmic reticulum stress [J]. Dis Model Mech，2017. doi: 10.1242/dmm.029488. [Epub ahead of print]
[12] 付黎明，李铁，吕佳，等.糖尿病动物模型复制方法研究概况[J].中国医药科学，2016，6（3）：41-45.
[13] 冯晓轩，于梅，包海鹏.糖尿病肾病动物模型的研究[J].黑龙江中医药，2016，45（1）：60-61.
[14] 张丽芬，吕仁和，黄文政.链脲佐菌素糖尿病肾病大鼠模型的建立及稳定性评价[J].中国比较医学杂志，2014， 24（4）：8-18.
[15] Murea M，Freedman BI，Parks JS，et al. Lipotoxicity in diabetic nephropathy：the potential role of fatty acid oxidation [J]. Clin J Am Soc Nephrol，2010，5（12）：2373-2379.
[16] 朱聪，黄芝瑛，周晓冰，等.肾毒性标志物临床研究及应用进展[J].中国新药杂志，2014，23（4）：319-396.
[17] 方朝晖，赵进东.苁归益肾胶囊对糖尿病大鼠肾小球及肾小管功能的影响[J].中药材，2013，36（3）：447-451.
[18] 沈漪萍，昌涛.HbA1c联合血清α1-MG、β2-MG检测在糖尿病早期肾功能损害诊断中的价值探讨[J].中国实验诊断学，2016，20（11）：1875-1877.
[19] 邢东杰，宿世震，陈桂玉，等.糖尿病肾病大鼠模型建立的比较[J]辽宁中医药大学学报，2014，16（9）：102-104.
[20] 李娇阳，高彦彬，周盛楠，等.通心络对2型糖尿病大鼠肾脏血管紧张素Ⅱ表达的影响[J].世界中医药，2015， 10（8）：1222-1226.
[21] 杨亦彬，张翥，苏克亮，等.链脲佐菌素诱导大鼠糖尿病肾病模型的方法学探讨[J].华西医学，2005，20（2）：299-300.
2017, Vol. 14 
京公网安备 11010502046598号