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首页> 外文期刊>American Journal of Physiology >Kidney expression of glutathione peroxidase-1 is not protective against streptozotocin-induced diabetic nephropathy.
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Kidney expression of glutathione peroxidase-1 is not protective against streptozotocin-induced diabetic nephropathy.

机译：谷胱甘肽过氧化物酶-1的肾脏表达对链脲佐菌素诱导的糖尿病性肾病没有保护作用。

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摘要

In many diseases, including progressive renal disorders, tissue injury and pathological intracellular signaling events are dependent on oxidative stress. Glutathione peroxidase-1 (Gpx1) is an antioxidant enzyme that is highly expressed in the kidney and removes peroxides and peroxynitrite that can cause renal damage. Therefore, we examined whether this abundant renal antioxidant enzyme limits renal damage during the development of type 1 diabetic nephropathy. Wild-type (Gpx1+/+) and deficient (Gpx1-/-) mice were made diabetic by intraperitoneal injection of streptozotocin (100 mg/kg) on 2 consecutive days. Diabetic Gpx1+/+ and -/- mice with equivalent blood glucose levels (23 +/- 4 mM) were selected and examined after 4 mo of diabetes. Compared with normal mice, diabetic Gpx1+/+ and -/- mice had a two- to threefold increase in urine albumin excretion at 2 and 4 mo of diabetes. At 4 mo, diabetic Gpx1+/+ and -/- mice had equivalent levels of oxidative renal injury (increased kidney reactive oxygen species, kidney lipid peroxidation, urine isoprostanes, kidney deposition of advanced glycoxidation, and nitrosylation end products) and a similar degree of glomerular damage (hypertrophy, hypercellularity, sclerosis), tubular injury (apoptosis and vimentin expression), and renal fibrosis (myofibroblasts, collagen, TGF-beta excretion). A lack of Gpx1 was not compensated for by increased levels of catalase or other Gpx isoforms in diabetic kidneys. Contrary to expectations, this study showed that the high level of Gpx1 expressed in the kidney is not protective against the development of renal oxidative stress and nephropathy in a model of type 1 diabetes.
机译：在许多疾病中，包括进行性肾脏疾病，组织损伤和病理性细胞内信号转导事件均取决于氧化应激。谷胱甘肽过氧化物酶-1（Gpx1）是一种在肾脏中高度表达的抗氧化酶，可去除可能引起肾脏损害的过氧化物和过氧亚硝酸盐。因此，我们检查了这种丰富的肾脏抗氧化酶是否在1型糖尿病肾病的发展过程中限制了肾脏的损害。通过连续2天腹膜内注射链脲佐菌素（100 mg / kg），使野生型（Gpx1 + / +）和缺陷型（Gpx1-/-）患糖尿病。糖尿病4个月后，选择具有同等血糖水平（23 +/- 4 mM）的糖尿病Gpx1 + / +和-/-小鼠进行检查。与正常小鼠相比，糖尿病Gpx1 + / +和-/-小鼠在糖尿病2个月和4个月时尿白蛋白排泄增加了2到3倍。在4 mo时，糖尿病Gpx1 + / +和-/-小鼠具有同等程度的氧化性肾损伤（增加的肾脏活性氧种类，肾脏脂质过氧化，尿异前列腺素，晚期糖氧化的肾脏沉积和亚硝基化终产物）和相似程度的肾小球损伤（肥大，细胞肥大，硬化），肾小管损伤（细胞凋亡和波形蛋白表达）和肾纤维化（成肌纤维细胞，胶原蛋白，TGF-β排泄）。糖尿病肾脏中过氧化氢酶或其他Gpx亚型水平的升高无法弥补Gpx1的缺乏。与预期相反，这项研究表明，在1型糖尿病模型中，肾脏中高水平表达的Gpx1不能抵抗肾脏氧化应激和肾病的发展。

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