文献类型：期刊文献

中文题名：红芪多糖对糖尿病肾病db/db小鼠肾脏保护作用及其对肾组织PKCα与VEGF表达的影响

英文题名：Protective effect of hedysarum polybotrys polysacchcaide on kidney in db /db mice with diabetic nephropathy and its influence on expressions of renal PKCα and VEGF

作者：魏玉娇[1];金智生[1];朱真灵[1];郑丽红[2];林海龙[1];关雁[1];齐雪艳[1];楚慧媛[1]

第一作者：魏玉娇

机构：[1]甘肃中医学院,甘肃730000;[2]黑龙江中医药大学第二附属医院

第一机构：甘肃中医药大学

年份：2014

卷号：37

期号：2

起止页码：116

中文期刊名：北京中医药大学学报

外文期刊名：Journal of Beijing University of Traditional Chinese Medicine

收录：CSTPCD;;北大核心:【北大核心2011】；CSCD:【CSCD2013_2014】；

基金：国家自然科学基金地区科学基金项目资助(No.81160427)

语种：中文

中文关键词：糖尿病肾病;红芪多糖;蛋白激酶Cα;血管内皮生长因子;db;db小鼠

外文关键词：diabetic nephropathy; hedysarum polybotrys polysacchcaide; protein kinase Cα; vascular endothelial growth fattor db/db mice

摘要：目的通过研究红芪多糖(HPS)对糖尿病肾病(DN)db/db小鼠肾组织中蛋白激酶Cα(PKCα)与血管内皮生长因子(VEGF)表达的影响,初步探讨HPS对DN小鼠肾脏的保护机制。方法将50只12周龄的雄性db/db小鼠随机分为5组:HPS高、中、低剂量组,依那普利阳性对照组,模型对照组;正常组为10只同周龄的db/m小鼠。给药8周。于给药前及给药后第2、4、6、8周末检测小鼠血糖浓度,第8周末收集小鼠24 h尿,检测24 h尿蛋白排泄量后处死小鼠,眼球取血并分离血清,检测血清肌酐(Scr)、尿素氮(BUN)等,并采用反转录聚合酶链式反应(RT-PCR)、蛋白质印迹(Western blotting)检测肾组织PKCα及其下游因子VEGF mRNA和蛋白的表达。结果经HPS治疗8周后,db/db小鼠的血糖较模型组偏低,但无统计学差异(P>0.05);Scr、BUN和24 h蛋白尿排泄量与模型组相比均明显降低(P<0.05)。HPS低剂量组PKCα蛋白及VEGF蛋白的表达与模型组无显著差异(P>0.05),其余各治疗组较模型组均有显著下降(P<0.05),且HPS高剂量治疗组改善更明显(P<0.01)。结论 HPS具有治疗db/db小鼠2型糖尿病肾病的作用,其治疗作用不依赖于降血糖,可能是通过抑制PCKα及其下游因子VEGF的过度表达,进而减缓糖尿病肾病的病程进展。
Objective To discuss the protective mechanism of hedysarum polybotrys polysacchcaide （HPS） on kidney in mice with diabetic nephropathy （DN） through studying the influences of HPS on renal protein kinase Cot （PKCot） and vascular endothelial growth factor （VEGF） in db/db mice with DN. Methods Male db/db mice （n =50, 12 weeks old） were randomly divided into five groups： low- dose, mid-dose and high-dose HPS groups （low-dose group, mid-dose group and high-dose group）, enalapril group, model group. The mice in normal group （ n = 10） were db/m mice of the same age. The mice in all groups were given intervention respectively for 8 w. The concentration of blood glucose wasdetected before intervention and at the end of the 2nd w, 4th w, 6th w and 8th W after intervention. The mice were killed at the end of 8th w after 24th urine was collected and 2d-h urine protein excretion quantity was detected. The levels of serum creatinine （Scr） and blood urea nitrogen （BUN） were detected. The mRNA and protein expressions of renal PKCoL and VEGF were detected by using reverse transcription polymerase chain reaction （RT-PCR） and Western blotting. Results The level of blood glucose decreased in HPS groups after 8 w compared with model group （ P 〉 0.05 ）, and Scr, BUN and 24-h urine protein excretion quantity decreased significantly compared with model group i P 〈 0.05 ）. There was no significant difference in protein expression between low-dose group and model group （P 〉 0.05 ）. The protein expression in all intervention groups decreased compared with model group （P 〈 0. 05 ）, which was more significant in high-dose group （P 〈 0.01 ）. Conclusion HPS has a therapeutic effect on DN in db/db mice with type 2 diabetes, while the effect dose not dependent on hyperglycemic. HPS may slow down DN progression by inhibiting the excessive expression of PKCα and VEGF.