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首页> 外文期刊>Life sciences >Silymarin induces recovery of pancreatic function after alloxan damage in rats
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Silymarin induces recovery of pancreatic function after alloxan damage in rats

机译：水飞蓟素诱导大鼠四氧嘧啶损伤后胰腺功能的恢复

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Alloxan has been widely used to produce experimental diabetes mellitus syndrome. This compound causes necrosis of pancreatic beta-cells and, as is well known, induces oxidant free radicals which play a relevant role in the etiology and pathogenesis of both experimental and human diabetes mellitus. Previously we have reported hypoglycemic and antilipoperoxidative actions of silymarin in serum and pancreatic tissue respectively. The aim of this study was to test whether silymarin could reduce the hyperglycemia and revert the pancreatic damage in alloxan treated rats, tested with silymarin in two protocols: using both compounds simultaneously for four or eight doses, or using the compound 20 days after alloxan administration for 9 weeks. Serum glucose and insulin were determined, and pancreatic fragments were used for histology and insulin immunohistochemistry. Pancreatic islets were isolated to assess insulin and Pdx1 mRNA expression by RT-PCR.Our results showed that 72 hours after alloxan administration, serum glucose increased and serum insulin decreased significantly, whereas pancreatic tissue presented morphological abnormalities such as islet shrinkage, necrotic areas, loss of cell organization, widespread lipoid deposits throughout the exocrine tissue, and loss of beta cells, but insulin and glucagon immunoreactivity was scattered if any. In contrast the pancreatic tissue and both insulin and glucose serum levels of rats treated with silymarin were similar to those of control animals. In addition, insulin and glucagon immunoreactive cells patterns in Langerhans islets were also normal, and normal insulin and Pdx1 mRNA expression patterns were detected during pancreatic recovery in Langerhans islets. The overall results suggest that silymarin induces pancreatic function recovery demonstrated by insulin and glucagon expression protein and normoglycemia after alloxan pancreatic damage in rats. (C) 2004 Elsevier Inc. All rights reserved.
机译：四氧嘧啶已被广泛用于产生实验性糖尿病综合征。该化合物引起胰腺β细胞坏死，并且众所周知，其诱导氧化性自由基，其在实验性和人类糖尿病的病因和发病机理中起着重要作用。先前我们已经报道了水飞蓟素在血清和胰腺组织中的降血糖和抗脂过氧化作用。这项研究的目的是测试水飞蓟素是否可以降低四氧嘧啶治疗的大鼠的高血糖症和恢复胰腺损伤，通过水飞蓟素在两种方案中进行了测试：两种化合物同时使用四或八次剂量，或者在四氧嘧啶给药后20天使用该化合物持续9周。测定血清葡萄糖和胰岛素，并使用胰腺片段进行组织学和胰岛素免疫组化。胰岛分离通过RT-PCR评估胰岛素和Pdx1 mRNA的表达。我们的研究结果显示，在四氧嘧啶给药72小时后，血糖升高，血清胰岛素显着降低，而胰腺组织表现出形态异常，如胰岛缩小，坏死区域，丢失细胞组织的分布，整个外分泌组织中广泛的类脂沉积以及β细胞的丢失，但胰岛素和胰高血糖素的免疫反应性（如果有的话）会分散。相反，水飞蓟素治疗的大鼠的胰腺组织以及胰岛素和葡萄糖血清水平均与对照动物相似。此外，朗格汉斯胰岛中的胰岛素和胰高血糖素免疫反应细胞模式也正常，并且在朗格汉斯胰岛的胰腺恢复期间检测到正常的胰岛素和Pdx1 mRNA表达模式。总体结果表明，水飞蓟素可在大鼠四氧嘧啶胰腺损伤后通过胰岛素和胰高血糖素表达蛋白以及正常血糖来诱导胰腺功能恢复。 （C）2004 Elsevier Inc.保留所有权利。

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