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首页> 外文期刊>Life sciences >AGE formation blockade with aminoguanidine does not ameliorate chronic allograft nephropathy.
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AGE formation blockade with aminoguanidine does not ameliorate chronic allograft nephropathy.

机译：用氨基胍的年龄形成阻滞不改善慢性同种异体移植肾病。

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AIMS: Advanced glycation end products (AGEs) are produced by glycoxidation and lipid peroxidation. AGEs induce oxidative stress and inflammation, and accumulate in tubular cells after kidney transplantation. We hypothesize that the AGE formation blocker aminoguanidine (AG) reduces AGE formation and improves renal transplant function. MAIN METHODS: Fisher 344 kidneys were orthotopically transplanted into Lewis recipients. Recipients were treated with AG (100 mg/kg/day), candesartan (CAND; 5mg/kg/day), or vehicle (VEH) for 24 weeks. The major non-cross linking AGE N(epsilon)-carboxymethyllysine (CML) was measured post-transplantation with gas chromatography-tandem mass spectrometry or immunohistochemistry. As a marker of systemic lipid peroxidation 8-isoprostane was measured by ELISA. We determined intra-arterial blood pressure, heart weight/body weight ratio, size of cardiomyocytes and cardiac hypertrophy as assessed by echocardiography. For biochemical evaluation of cardiac and renal fibrosis we measured hydroxyproline content. KEY FINDINGS: AG significantly reduced serum CML and 8-isoprostane, but did not reduce signs of chronic allograft nephropathy (CAN) or blood pressure. AG did not alter tubular AGE accumulation. AG reduced heart weight/body weight ratio (AG: 2.7 +/- 0.1g/kg; CAND: 2.2 +/- 0.1, VEH: 3.0 +/- 0.4 g/kg), size of cardiomyocytes (P < 0.05) and showed a tendency to reduce cardiac hypertrophy (wall volume average radial AG 7.072 +/- 0.83 cm(3) vs. CAND 6.841 +/- 0.66 cm(3) vs. VEH 7.839 +/- 0.74 cm(3)). SIGNIFICANCE: Despite effective reduction of serum CML and 8-isoprostane, AG did not ameliorate CAN or reduce renal AGE accumulation. On the other hand AG reduced cardiac size suggesting a supportive cardio-protective action which is blood pressure independent.
机译：目的：先进的糖化末端产品（年龄）由甘醇氧化和脂质过氧化产生。年龄诱导氧化应激和炎症，并在肾移植后在管状细胞中积聚。我们假设年龄形成阻滞剂氨基胍（Ag）降低年龄形成并改善肾移植功能。主要方法：Fisher 344肾脏正向移植到Lewis受体中。接受者用Ag（100mg / kg /天）治疗，坎糖（Cand; 5mg / kg /天），或车辆（veh）24周。通过气相色谱 - 串联质谱或免疫组化进行移植后，将主要的非交联龄N（ε） - 羧甲基氰基（CML）进行测定。作为全身脂质过氧化的标记，通过ELISA测量8-异前烷烃。通过超声心动图评估，我们确定动脉内血压，心脏重量/体重比，心肌细胞和心脏肥大的大小。对于心脏和肾纤维化的生化评估，我们测量了羟脯氨酸含量。主要发现：AG显着降低血清CML和8异己烷，但没有减少慢性同种异体移植肾病（罐）或血压的迹象。 AG没有改变管状时代积累。 AG减少心脏重量/体重比（AG：2.7 +/- 0.1g / kg; Cand：2.2 +/- 0.1，Veh：3.0 +/- 0.4g / kg），心肌细胞的大小（P <0.05）并显示减少心肌肥大的趋势（壁体积平均径向Ag 7.072 +/- 0.83cm（3）与Cand 6.841 +/- 0.66cm（3）与VAV 7.839 +/- 0.74 cm（3））。意义：尽管有效地减少了血清CML和8-异前烷烃，但AG没有改善可以或减少肾年龄积累。另一方面，AG减少心脏尺寸，表明血压无关的支持性心脏保护作用。

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