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Nephroprotective potential of selenium and taurine against mercuric chloride induced nephropathy in rats

机译:硒和牛磺酸对氯化汞致大鼠肾病的肾保护作用

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摘要

The study was aimed to estimate whether pre-treatment with sodium selenite or taurine would reverse kidney damage induced by intraperitoneal injection of mercuric chloride in rats. Animals were divided into six groups: (1) control group; (2) sodium selenite group; (3) taurine group; (4) HgCl2 group; (5) sodium selenite pretreated group; (6) taurine pretreated group. The results demonstrated that HgCl2 causes significant enhancement in serum malondialdehyde (MDA), creatinine, N-acetyl-beta-D-glucosaminidase (NAG), cystatin C, nephrin and interleukin 6 (IL-6) levels accompanied with significant reduction in serum nitric oxide (NO) level. Pretreatment with sodium selenite or taurine produces significant depletion in MDA, NAG, cystatin C, nephrin and IL-6 levels in concomitant with significant elevation in serum NO level as compared to HgCl2 group. HgCl2 induced pathological alterations in the kidney. The ultrastructural investigation of renal cortex of HgCl2-administered group revealed that the glomerular basement membrane is uniform, the fenestrations of endothelial cells are swollen, and the secondary foot processes appear also swollen even fused at some points. The proximal convoluted tubules showed apical short and few microvilli, while, some tubular cells showed relatively normal microvilli. In contrast, sodium selenite or taurine pretreatment could significantly reduce the pathological alterations in the kidney caused by HgCl2 intoxication. The current results suggested that selenium and taurine possess nephroprotective efficacy due to their antioxidative capacity and anti-inflammatory activity.
机译:该研究旨在评估亚硒酸钠或牛磺酸预处理是否可以逆转大鼠腹膜内注射氯化汞诱导的肾脏损害。将动物分为六组:(1)对照组; (2)亚硒酸钠基团; (3)牛磺酸基团; (4)HgCl2基团; (5)亚硒酸钠预处理组; (6)牛磺酸预处理组。结果表明,HgCl2导致血清丙二醛(MDA),肌酐,N-乙酰基-β-D-氨基葡萄糖苷酶(NAG),胱抑素C,肾素和白介素6(IL-6)水平显着提高,同时血清硝酸水平显着降低氧化物(NO)水平。与HgCl2组相比,用亚硒酸钠或牛磺酸预处理可导致MDA,NAG,半胱氨酸蛋白酶抑制剂C,nephrin和IL-6水平显着降低,同时血清NO水平显着升高。 HgCl2引起肾脏的病理改变。 HgCl2给药组肾皮质的超微结构研究表明,肾小球基底膜是均匀的,内皮细胞的窗孔是肿胀的,继发性足突在某些点甚至也被融合了。近曲小管显示顶端短而微绒毛少,而一些肾小管细胞显示相对正常的微绒毛。相比之下,亚硒酸钠或牛磺酸预处理可以显着减少HgCl2中毒引起的肾脏病理改变。目前的结果表明,硒和牛磺酸由于具有抗氧化能力和抗炎活性,因此具有肾脏保护作用。

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