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首页> 外文期刊>Renal failure. >The protective effects of taurine against early renal injury in STZ-induced diabetic rats, correlated with inhibition of renal LOX-1-mediated ICAM-1 expression.
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The protective effects of taurine against early renal injury in STZ-induced diabetic rats, correlated with inhibition of renal LOX-1-mediated ICAM-1 expression.

机译：牛磺酸对STZ诱导的糖尿病大鼠早期肾脏损伤的保护作用，与抑制肾脏LOX-1介导的ICAM-1表达有关。

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摘要

Oxidative stress is a key cause in the development of diabetic nephropathy (DN). As a main receptor of oxidized low-density lipoprotein (oxLDL), LOX-1 plays an important role in the induction of leukocyte adhesion molecules, such as intercellular cell adhesion molecule-1 (ICAM-1). Taurine (TAU), a potent endogenous antioxidant, showed renoprotective effects in several model animals. This study was designed to determine the renoprotective effect and possible mechanism involved LOX-1 and ICAM-1 expression of taurine in early DN. Six-week-old male Wistar rats were divided into three groups: normal control (NC), diabetes mellitus (DM), and taurine-treated DM (DM+TAU). Diabetes was induced by streptozotocin (STZ, 60 mg/kg, i.p.). After the onset of diabetes, drinking water containing 1% taurine was given to rats in the DM+TAU group. After six weeks of treatment, blood glucose (BG), serum levels of creatinine (sCr) and BUN, and LOX-1 and ICAM-1 expression (protein and gene) in kidney cortices were estimated. Meanwhile, renal malondialdehyde (MDA) levels and glutathione peroxidase (GSH-Px) activities were examined as parameters of oxidative stress in diabetic rats. For DM+TAU rats, when compared with DM rats, the levels of serum BUN, sCr, and renal MDA were reduced, and the activities of renal GSH-Px were increased, but the BG levels were not influenced. Simultaneously, taurine attenuated histopathologic evidence of renal damages and reduced the overexpression of LOX-1 and ICAM-1 in kidney cortices of diabetic rats. In conclusion, taurine showed protective effects against early renal injury in diabetic rats. These renoprotective effects may be partly caused by suppression of oxLDL/LOX-1 system and subsequently ICAM-1 overexpression on renal cortex via its antioxidative property.
机译：氧化应激是糖尿病性肾病（DN）发展的关键原因。作为氧化的低密度脂蛋白（oxLDL）的主要受体，LOX-1在诱导白细胞粘附分子（例如细胞间细胞粘附分子1（ICAM-1））中起重要作用。牛磺酸（TAU）是一种有效的内源性抗氧化剂，在几种模型动物中均显示出肾脏保护作用。这项研究旨在确定牛磺酸在早期DN中的肾脏保护作用和可能的机制与LOX-1和ICAM-1表达有关。六周大的雄性Wistar大鼠分为三组：正常对照组（NC），糖尿病（DM）和牛磺酸治疗的DM（DM + TAU）。链脲佐菌素（STZ，60 mg / kg，腹腔注射）可诱发糖尿病。糖尿病发作后，给DM + TAU组的大鼠喝含1％牛磺酸的饮用水。治疗六周后，评估了肾皮质中的血糖（BG），肌酐（sCr）和BUN的血清水平以及LOX-1和ICAM-1的表达（蛋白质和基因）。同时，将肾丙二醛（MDA）水平和谷胱甘肽过氧化物酶（GSH-Px）活性作为糖尿病大鼠氧化应激的参数。对于DM + TAU大鼠，与DM大鼠相比，其血清BUN，sCr和肾MDA水平降低，肾GSH-Px活性升高，但BG水平未受影响。同时，牛磺酸减弱了肾脏损伤的组织病理学证据，并降低了糖尿病大鼠肾皮质中LOX-1和ICAM-1的过表达。总之，牛磺酸对糖尿病大鼠的早期肾脏损伤具有保护作用。这些肾脏保护作用可能部分由oxLDL / LOX-1系统的抑制以及随后通过其抗氧化特性在肾皮质上ICAM-1的过表达引起。

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