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目的观察甲钴胺对2型糖尿病(type 2 diabetes mellitus,T2DM)患者血同型半胱氨酸(serum homocysteine,s Hcy)和尿单核细胞趋化蛋白-1(monocyte chemoattractant protein-1,MCP-1)、转化生长因子-β1(transforming growth factor-β1,TGF-β1)排泄的影响,探讨其肾脏保护的可能机制。方法 33例T2DM患者在原糖尿病治疗方案的基础上联合甲钴胺(甲钴胺治疗组,DE组),观察6个月,比较治疗前后空腹血糖(fasting plasma glucose,FPG)、糖化血红蛋白(haemoglobin A1c,Hb A1c)、s Hcy水平及尿MCP-1、TGF-β1及尿白蛋白(albumin,ALB)排泄的变化。结果基础状态时,DE组FPG、Hb A1c、s Hcy及尿白蛋白肌酐逼(urinary albumin to creatinine ratio,UACR)、尿单核细胞趋化蛋白-1肌酐比(urine MCP-1 to creatinine ratio,UMCR)、尿转化生长因子-β1肌酐比(urine TGF-β1 to creatinine ratio,UTCR)水平均高于NC组(均有P<0.05);与治疗前比较,DE组治疗后FPG、Hb A1c无明显变化,s Hcy、UMCR、UTCR及UACR下降(均有P<0.05);T2DM患者UMCR,UTCR分别与UACR的呈正相关(r1=0.611,P1<0.001;r2=0.635,P2<0.001);s Hcy与UACR、UTCR和UMCR呈正相关(r1=0.634,P1<0.001;r2=0.507,P2<0.001;r3=0.433,P3<0.001)。结论甲钴胺可以降低T2DM患者体内增强的炎症反应,该作用可能与其肾脏保护有关。
Objective To observe the effects of mecobalamin on serum homocysteine (sHcy) and monocyte chemoattractant protein-1 (MCP-1) in type 2 diabetes mellitus (T2DM) 1), transforming growth factor-β1 (TGF-β1) excretion, to explore its possible mechanism of renal protection. Methods 33 cases of T2DM patients were treated with mecobalamin (mecobalamin, DE group) on the basis of the original diabetes mellitus treatment program for 6 months. The fasting plasma glucose (FPG), hemoglobin A1c , Hb A1c), s Hcy levels and excretion of urinary MCP-1, TGF-β1 and albumin (ALB). Results In the basal state, the levels of FPG, Hb A1c, sHcy and urinary albumin to creatinine (UACR), urine MCP-1 to creatinine ratio UMCR) and urine TGF-β1 creatinine ratio (UTCR) were higher than those in NC group (all P <0.05). Compared with those before treatment, FPG, Hb A1c, UMCR, UTCR and UACR decreased (all P <0.05). There was a positive correlation between UMCR and URCR in T2DM patients (r1 = 0.611, P1.001; r2 = 0.635, P2.001) Hcy was positively correlated with UACR, UTCR and UMCR (r1 = 0.634, P1 <0.001; r2 = 0.507, P2 <0.001; r3 = 0.433, P3 <0.001). Conclusion Mecobalamin can reduce the enhanced inflammatory response in T2DM patients, which may be related to its renal protection.