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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：用氨基胍阻断AGE形成并不能改善慢性同种异体肾病。

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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：高级糖基化终产物（AGEs）是通过糖氧化和脂质过氧化产生的。 AGEs诱导氧化应激和炎症，并在肾移植后积累在肾小管细胞中。我们假设AGE形成阻滞剂氨基胍（AG）减少AGE形成并改善肾移植功能。主要方法：将Fisher 344个肾脏原位移植到Lewis受体中。接受者接受AG（100 mg / kg /天），坎地沙坦（CAND; 5mg / kg /天）或赋形剂（VEH）治疗24周。移植后使用气相色谱-串联质谱或免疫组织化学方法检测主要的非交联AGE N（ε）-羧甲基赖氨酸（CML）。作为全身性脂质过氧化的标志物，通过ELISA测量了8-异前列腺素。我们通过超声心动图确定了动脉内血压，心脏重量/体重比，心肌细胞大小和心脏肥大。为了进行心脏和肾脏纤维化的生化评估，我们测量了羟脯氨酸的含量。主要发现：AG可显着降低血清CML和8-异前列腺素，但不能降低慢性同种异体肾病（CAN）或血压的迹象。 AG没有改变肾小管的AGE积累。 AG降低心脏重量/体重比（AG：2.7 +/- 0.1g / kg; CAND：2.2 +/- 0.1，VEH：3.0 +/- 0.4 g / kg），心肌细胞大小（P <0.05）一种减少心脏肥大的趋势（壁体积平均径向AG 7.072 +/- 0.83 cm（3）与CAND 6.841 +/- 0.66 cm（3）与VEH 7.839 +/- 0.74 cm（3））。意义：尽管有效降低了血清CML和8-异前列腺素，但AG并没有改善CAN或减少肾脏AGE的积累。另一方面，AG减小了心脏的大小，表明其支持性心脏保护作用与血压无关。

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