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首页> 外文期刊>Bulletin of experimental biology and medicine >Neuroprotective Dipeptide Noopept Prevents DNA Damage in Mice with Modeled Prediabetes
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Neuroprotective Dipeptide Noopept Prevents DNA Damage in Mice with Modeled Prediabetes

机译:NeuroPropotective Dipeptide noopept防止小鼠的DNA损伤与模拟的前奶酪

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In experiments on BALB/c mice, prediabetes was modeled by administration of streptozotocin in a dose of 130 mg/kg. DNA damage was assessed by the method of DNA comets. Noopept (0.5 mg/kg intraperitoneally) was administered for 14 days before and for 6, 13, or 14 days after streptozotocin administration. Despite moderate hyperglycemia and increased malondialdehyde level, the intensity of DNA damage in cells of the pancreas, liver, and kidneys significantly surpassed the control values. Noopept normalized these parameters due to its pronounced antigenotoxic effect. For both the damaging effect of streptozotocin and the normalizing effect of Noopept, DNA changes manifested mainly in terms of atypical DNA comets. Our findings confirm the role of DNA damage in the pathogenesis of diabetes. They indicate the possibility of pharmacological protection of pancreatic beta cells with the neuroprotective drug and provide an important argument in favor of the hypothesis about the similarity of the mechanisms of formation of the resistance of neurons and beta cells to the cytotoxic influences.
机译:在BALB / C小鼠的实验中,预先通过施用链脲佐菌素以130mg / kg的剂量进行建模。通过DNA彗星的方法评估DNA损伤。在链脲佐菌素给药后,在13,13,13或14天之前施用Nopept(0.5mg / kg腹膜内)。尽管高血糖和丙二醛水平增加,但胰腺,肝脏和肾脏细胞中DNA损伤的强度显着超越了对照值。由于其明显的抗原毒性效应,Noopept标准化这些参数。对于链脲佐菌素的破坏性效果和Nopept的正常化效果,DNA变化主要是在非典型DNA彗星方面表现出。我们的研究结果证实了DNA损伤在糖尿病发病机制中的作用。它们表明胰腺β细胞与神经保护药物的药理保护的可能性,并提供了一个重要的论据,有利于关于形成神经元和β细胞抗性的形成机制对细胞毒性影响的方法的重要性。

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