体内木酚素水平影响糖尿病肾病患者病程的机制研究

目的：观察糖尿病肾病患者体内木酚素代谢物尿肠内酯及血浆中丙二醛（MDA）、血清超氧化物歧化酶（SOD）、血清过氧化氢酶（GSH-Px）的变化，探寻木酚素影响糖尿病肾病患者病程的可能机制。方法采用病例对照研究的方法，选择出82例糖尿病患者。根据尿微量白蛋白排泄率值分为：糖尿病肾病组（尿微量白蛋白排泄率≥20μg/min，n＝41）；糖尿病无肾病组（尿微量白蛋白排泄率＜20μg/min， n＝41）；另外选择正常对照组30例（尿微量白蛋白排泄率＜20μg/min，n＝30）。比较各组人群尿肠内酯的水平、尿微量白蛋白排泄率、血浆MDA、血清SOD及血清GSH-Px的水平。结果与正常对照组相比，糖尿病患者的尿肠内酯水平和血清SOD、GSH-Px活性明显降低（P＜0.05），且糖尿病肾病患者的尿肠内酯水平和血清SOD、GSH-Px活性显著低于糖尿病无肾病组（P＜0.05）；糖尿病患者的尿肠内酯水平与尿微量白蛋白排泄率及血浆 MDA 含量等呈负相关，相关系数分别-0.763和-0.708（P＜0.05），与血清超氧化物歧化酶、过氧化氢酶活性等指标呈正相关，相关系数分别为0.695和0.776（P＜0.05）。结论糖尿病肾病患者尿肠内酯水平低下，反映出体内木酚素水平低与糖尿病肾脏病变的发生发展相关，其机制涉及氧化应激过程。

Levels of lignan affects the process of patients with diabetic nephropathy

Objective To investigate the changes of urinary enterolactone which are metabolites of lignan. Methods Eighty-two diabetes patients were chosed by means of case-control study and divided into two groups by urinary albumin excretion rate（UAER）, such as diabetic nephropathy group（UAER≥20μg/min,n=41） and diabetic non-nephropathy group（UAER〈20μg/min,n=41）; 30 normal adult as Control group（UAER〈20μg/min,n=30）. Levels of urinary enterolactone, UAER, the content of plasma MDA and the activities of plasma SOD, GSH-Px were measured.Results Levels of urinary enterolactone and the activities of plasma SOD, GSH-Px of diabetes patients were significantly lower than those of Control group（P〈0.05）, the levels of urinary enterolactone and the activities of plasma SOD, GSH-Px in patients of diabetic nephropathy were also lower than those of diabetic non-nephropathy group（P〈0.05）; Levels of urinary enterolactone of diabetes patients were negative correlated with UAER and the content of plasm MDA（P〈0.05） and were positive correlated with the activities of plasm SOD, GSH-Px（P〈0.05）. The correlation coefficient were-0.763,-0.708, 0.695 and 0.776, respectively. Conclusion There are lower levels of urinary enterolactone which are metabolites of Lignan in patients with diabetic nephropathy. Above data show that the content of Lignan of body is associated with the development of diabetic nephropathy and the mechanism may be related to oxidative stress.