Mercury is a widespread pollutant. Mercuric ions uptake into tubular cells is supported by the Organic anion transporter 1 (Oat1) and 3 (Oat3) and its elimination into urine is through the Multidrug resistance-associated protein 2 (Mrp2). We investigated the effect of recombinant human erythropoietin (Epo) on renal function and on renal expression of Oat1, Oat3, and Mrp2 in a model of mercuric chloride (HgCl₂)-induced renal damage. Four experimental groups of adult male Wistar rats were used: Control, Epo, HgCl₂, and Epo + HgCl₂. Epo (3000 IU/kg, b.w., i.p.) was administered 24 h before HgCl₂ (4 mg/kg, b.w., i.p.). Experiments were performed 18 h after the HgCl₂ dose. Parameters of renal function and structure were evaluated. The protein expression of Oat1, Oat3 and Mrp2 in renal tissue was assessed by immunoblotting techniques. Mercury levels were determined by cold vapor atomic absorption spectrometry. Pretreatment with Epo ameliorated the HgCl₂-induced tubular injury as assessed by histopathology and urinary biomarkers. Immunoblotting showed that pretreatment with Epo regulated the renal expression of mercury transporters in a way to decrease mercury content in the kidney. Epo pretreatment ameliorates HgCl₂-induced renal tubular injury by modulation of mercury transporters expression in the kidneys.

汞是一种广泛存在的污染物。汞离子摄入肾小管细胞由有机阴离子转运蛋白 1 (Oat1) 和 3 (Oat3) 支持，并通过多药耐药相关蛋白 2 (Mrp2) 排入尿液。我们在氯化汞 (HgCl ₂ ) 诱导的肾损伤模型中研究了重组人促红细胞生成素 (Epo) 对肾功能以及 Oat1、Oat3 和 Mrp2 肾脏表达的影响。使用成年雄性Wistar大鼠的四个实验组：对照、Epo、HgCl ₂和Epo+HgCl ₂ 。 Epo (3000 IU/kg, bw, ip) 在 HgCl ₂ (4 mg/kg, bw, ip) 之前 24 小时施用。实验在HgCl ₂剂量后18小时进行。评估肾功能和结构参数。通过免疫印迹技术评估肾组织中 Oat1、Oat3 和 Mrp2 的蛋白表达。汞含量通过冷蒸气原子吸收光谱法测定。根据组织病理学和尿液生物标志物的评估，Epo 预处理改善了 HgCl ₂诱导的肾小管损伤。免疫印迹表明，Epo 预处理可调节汞转运蛋白的肾脏表达，从而降低肾脏中的汞含量。 Epo 预处理通过调节肾脏中汞转运蛋白的表达来改善 HgCl ₂诱导的肾小管损伤。