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首页> 外文期刊>Cellular and Molecular Neurobiology >Protective role of lithium in ameliorating the aluminium-induced oxidative stress and histological changes in rat brain.
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Protective role of lithium in ameliorating the aluminium-induced oxidative stress and histological changes in rat brain.

机译:锂在减轻铝诱导的大鼠脑组织氧化应激和组织学变化中的保护作用。

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This study was carried out to investigate the effects of lithium (Li) supplementation on aluminium (Al) induced changes in antioxidant defence system and histoarchitecture of cerebrum and cerebellum in rats. Al was administered in the form of aluminium chloride (100 mg/kg b.wt./day, orally) and Li was given in the form of Li carbonate through diet (1.1 g/kg diet, daily) for a period of 2 months. Al treatment significantly enhanced the levels of lipid peroxidation and reactive oxygen species in both the cerebrum and cerebellum, which however were decreased following Li supplementation. The enzyme activities of catalase, superoxide dismutase (SOD) and glutathione reductase (GR) were significantly increased in both the regions following Al treatment. Li administration to Al-fed rats decreased the SOD, catalase and GR enzyme activities in both the regions; however, in cerebellum the enzyme activities were decreased in comparison to normal controls also. Further, the specific activity of glutathione-s-transferase and the levels of total and oxidized glutathione were significantly decreased in cerebrum and cerebellum following Al treatment, which however showed elevation upon Li supplementation. The levels of reduced glutathione were significantly decreased in cerebrum but increased in cerebellum following Al treatment, which however were normalized upon Li supplementation but in cerebellum only. Apart from the biochemical changes, disorganization in the layers of cerebrum and vacuolar spaces were also observed following Al treatment indicating the structural damage. Similarly, the loss of purkinje cells was also evident in cerebellum. Li supplementation resulted in an appreciable improvement in the histoarchitecture of both the regions. Therefore, the study shows that Li has a potential to exhibit neuroprotective role in conditions of Al-induced oxidative stress and be explored further to be treated as a promising drug against neurotoxicity.
机译:进行了这项研究,以研究补充锂(Li)对铝(Al)诱导的大鼠抗氧化防御系统的变化以及大脑和小脑的组织结构的影响。铝以氯化铝的形式(100 mg / kg体重/天,口服)给药,锂以碳酸锂的形式通过饮食(1.1 g / kg体重,每天)给药,持续2个月。铝处理显着提高了大脑和小脑中脂质过氧化和活性氧的水平,但是在补充锂后降低了。在铝处理后的两个区域中,过氧化氢酶,超氧化物歧化酶(SOD)和谷胱甘肽还原酶(GR)的酶活性均显着增加。锂对铝喂养的大鼠的给药降低了这两个区域的SOD,过氧化氢酶和GR酶活性。然而,与正常对照组相比,小脑中的酶活性也降低了。此外,Al处理后,大脑和小脑中谷胱甘肽-s-转移酶的比活性以及总谷胱甘肽和氧化谷胱甘肽的水平显着降低,但是在补充Li后其水平升高。铝处理后,还原型谷胱甘肽的水平在大脑中显着降低,但在小脑中升高,但是在补充Li后仅在小脑中恢复正常。除生化变化外,Al处理后还观察到大脑和液泡空间层的混乱,表明结构受损。同样,小脑中浦肯野细胞的损失也很明显。补充锂使两个地区的组织结构都有明显改善。因此,该研究表明,Li具有在Al诱导的氧化应激条件下发挥神经保护作用的潜力,并被进一步探索作为抗神经毒性的有前途的药物。

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