摘要
[目的]探讨水飞蓟宾-磷脂酰胆碱复合物(silybin-phosphatidylcholine compound,SPC)对糖尿病小鼠肾非酶糖基化终产物(advanced glycation end products,AGEs)的抑制作用。[方法]小鼠70只,随机选10只作为正常对照组,其余60只尾静脉注射80 mg.kg-1四氧嘧啶(Alloxan)造模,72 h后测空腹血糖,将血糖值﹥16.7 mmol.L-1的小鼠41只随机分为模型组、SPC高剂量组、SPC中剂量组、SPC低剂量组,正常对照组和模型组每日灌胃给予0.5%羧甲基纤维素钠(CMC-Na)混悬液,SPC高、中、低剂量组分别给予SPC(用0.5%CMC-Na配成一定浓度的混悬液)400、200、100 mg.kg-1灌胃,连续12周,并于第4、8、12周剪尾采血测血糖。12周末摘眼球取血,分离血清检测血清中肌酐、尿素氮、糖化血清蛋白,同时取肾组织匀浆测SOD与MDA、取肾皮质测AGEs。[结果]SPC对糖尿病小鼠血糖浓度无明显影响(P﹥0.05),但能明显降低糖尿病小鼠血清中肌酐(Crea)、尿素氮(BUN)、糖化血清蛋白(果糖胺,Fmn)及肾皮质中AGEs的含量,抑制肾组织中SOD活性的降低和MDA值的升高(与模型组比较,P﹤0.05)。[结论]高、中剂量SPC(400、200 mg.kg-1)对糖尿病小鼠肾非酶糖基化产物的形成有抑制作用。
[Objective]To investigate the depressant effect of silybin-phosphatidylcholine compound（SPC）on the formation of advanced glycation end products（AGEs）in alloxan-induced diabetic mice.[Methods]Among seventy mice,ten mice were randomly selected as normal controls,the others were injected with 80 mg·kg-1 alloxan through vena caudalis respectively.The level of blood-fasting sugar of the mice were measured after 72 hours,and 41 diabetic mice whose blood glucose was higher than 16.7 mmol·L-1 were randomly divided into four groups：model group,high dose of SPC group,medium dose of SPC group and low dose of SPC group.Mice in normal control group and model group were administered with 0.5% CMC-Na suspension for 12 weeks,while mice in three SPC groups were respectively administered with 400 mg·kg-1,200 mg·kg-1 and 100 mg·kg-1 SPC mixed with 0.5% CMC-Na suspension for 12 weeks.The blood glucose level of vena caudalis were detected at the fourth,eighth and twelfth week,and at the end of the twelfth week,the serum levels of creatinine（Crea）,urea nitrogen（BUN）and fructosamine（Fmn）were detected,the levels of MDA and SOD in nephridial tissue and the level of AGEs in cortex renis were detected.[Results]SPC had no significant effect on the blood glucose level of diabetic mice（P﹤0.05）,but could obviously decrease the serum levels of Crea,BUN and Fmn,as well as the content of AGEs in cortex renis;besides,SPC had obvious depressant effect on the decrease of SOD activity and the increase of MDA value in nephridial tissue compared with model group（P﹤0.05）.[Conclusions]High and medium dose of SPC can inhibit the formation of advanced glycation end products in alloxan-induced diabetic mice.
出处
《现代预防医学》
CAS
北大核心
2007年第22期4204-4206,共3页
Modern Preventive Medicine
基金
河南省科技攻关项目(001180203)
