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首页> 外文期刊>Cell biology international. >Renal damage following Alloxan-induced diabetes is associated with generation of reactive oxygen species, alterations of p53, TGF-beta 1, and extracellular matrix metalloproteinases in rats
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Renal damage following Alloxan-induced diabetes is associated with generation of reactive oxygen species, alterations of p53, TGF-beta 1, and extracellular matrix metalloproteinases in rats

机译：阿洛昔班诱导的糖尿病后肾损伤与大鼠的反应性氧物质的产生，改变p53，TGF-β1和细胞外基质金属蛋白酶的产生相关

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Renal damage is a common problem in diabetes. Alloxan, a potent hyperglycemic and diabetogenic molecule, can induce diabetes through oxidative stress-related mechanisms. Here, we hypothesize that Alloxan-induced renal damage is associated with alterations of p53, TGF-1, and extracellular matrix metalloproteinases. To test our hypothesis, we established an animal model (male abino rats) and induced diabetes by intraperitoneal injection of Alloxan monohydrate. Rats with fasting blood glucose level200mg/dL were considered diabetic and were sacrificed after 14, 28, and 42 day intervals. Tissue levels of malondialdehyde and glutathione levels (markers of oxidative stress), and serum MMP-1 were measured. The expression patterns of p53, TGF-1were evaluated using Western blot and immunohistochemical methods. TIMP-1 expression pattern was determined using RT-PCR and immunohistochemical methods. Alloxan treatment induced histological features of renal damage (inflammation and fibrosis) and was associated with deterioration of the renal functions (elevated blood urea nitrogen and creatinin levels), hyperglycemia, and oxidative stresss (increased malondialdehyde and decreased glutathione levels). There was over-expression of the TGF-1 protein (profibrogenic protein), p53 (proapoptotic protein), and alterations of extracellular matrix proteins (low level of serum MMP-1 and over-expression of TIMP-1). Alterations of TGF-, p53, and extracellular matrix metalloproteinases contribute to the pathogenesis of Alloxan-induced renal damage.
机译：肾损伤是糖尿病的常见问题。艾三烷，有效的高血糖和糖苷分子，可以通过氧化应激相关机制诱导糖尿病。在这里，我们假设Alloxan诱导的肾损伤与P53，TGF-1和细胞外基质金属蛋白酶的改变相关。为了测试我们的假设，我们建立了一种动物模型（男性亚藻毒大鼠），并通过腹膜内注射阿仑胍一水合物诱导糖尿病。具有禁食血糖含量的大鼠200mg / dl被认为是糖尿病患者，但在14,28和42天间隔后处死。测定丙二醛和谷胱甘肽水平的组织水平（氧化应激的标志物）和血清MMP-1。使用蛋白质印迹和免疫组化方法评估P53，TGF-1的表达模式。使用RT-PCR和免疫组化方法测定TIMP-1表达模式。血酮治疗诱导肾功能损伤（炎症和纤维化）的组织学特征，与肾功能的恶化（血尿尿素氮和肉桂瘤水平升高），高血糖和氧化胁迫（丙二醛含量增加，谷胱甘肽水平降低）。 TGF-1蛋白（Procibronic蛋白），P53（促液酵母蛋白）和细胞外基质蛋白的改变（血清MMP-1的低水平和TIMP-1的过表达）的改变。 TGF-，P53和细胞外基质金属蛋白酶的改变有助于血酮诱导的肾损伤的发病机制。

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