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首页> 外文期刊>American Journal of Physiology >Treatment with pyrrolidine dithiocarbamate improves proteinuria, oxidative stress, and glomerular hypertension in overload proteinuria
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Treatment with pyrrolidine dithiocarbamate improves proteinuria, oxidative stress, and glomerular hypertension in overload proteinuria

机译：吡咯烷二硫代氨基甲酸酯治疗可改善蛋白尿过多，氧化应激和肾小球高血压

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We evaluated whether the blockade of the proinflammatory transcription factor NF-KB would modify the oxidative stress, inflammation, and structural and hemodynamic alterations found in the kidney as a result of massive proteinuria. Twenty male Sprague-Dawley rats were injected with 2 g of BSA intraperitoneally daily for 2 wk. Ten of them received in addition the inhibitor of NF-KB activation pyrrolidine dithiocarbamate (PDTC$a200 mg-kg~(-1)day~(-1) sc) and the rest received vehicle. Seven rats that received intraperitoneal saline were used as controls. Glomerular hemodynamics were studied after 14 days. Markers of oxidative stress (NF-KB subunit p65+ cells, 3-ni-trotyrosine, and 4-hydroxynonenal), inflammation (cortical CD68+ cells and NOS-II), and afferent arteriole damage were assessed by immunohistochemistry and morphometry. Activity of antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase was evaluated in renal cortex and medulla. Albumin overload induced massive proteinuria, oxidative stress with reduced activity of antioxidant enzymes, NF-KB activation, inflammatory cell infiltration, a significant presence of proteinaceous casts, systemic and glomerular hypertension, as well as arteriolar remodeling. Treatment with PDTC prevented or improved all of these findings. In this model of nephrotic syndrome, we demonstrate a key role for oxidative stress and inflammation in causing systemic and glomerular hypertension and proteinuria. Oxidative stress and inflammation may have a key role in accelerating renal injury associated with intense proteinuria.
机译：我们评估了促炎性转录因子NF-κB的阻断是否会由于大量蛋白尿而改变肾脏中的氧化应激，炎症以及结构和血液动力学改变。每天腹膜内向20只雄性Sprague-Dawley大鼠注射2 g BSA，连续2周。他们中的十人另外接受了NF-κB活化吡咯烷二硫代氨基甲酸酯的抑制剂（PDTC $ a200 mg-kg〜（-1）day〜（-1）sc），其余接受了赋形剂。接受腹膜内盐水的七只大鼠用作对照。 14天后研究肾小球的血流动力学。通过免疫组织化学和形态计量学评估了氧化应激（NF-KB亚基p65 +细胞，3-硝基酪氨酸和4-羟基壬烯醛），炎症（皮质CD68 +细胞和NOS-II）和传入小动脉损伤的标记。在肾皮质和髓质中评估了抗氧化酶超氧化物歧化酶，过氧化氢酶，谷胱甘肽过氧化物酶和谷胱甘肽还原酶的活性。白蛋白超负荷引起大量蛋白尿，氧化应激，抗氧化酶活性降低，NF-κB活化，炎性细胞浸润，大量蛋白基团，全身性和肾小球性高血压以及小动脉重构。用PDTC治疗可以预防或改善所有这些发现。在这种肾病综合征模型中，我们证明了氧化应激和炎症在引起全身性和肾小球性高血压以及蛋白尿中的关键作用。氧化应激和炎症可能在加速与强烈蛋白尿有关的肾损伤中起关键作用。

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