Ben Amara Ibtissem, Fetoui Hamadi, Guermazi Fadhel, Zeghal Najiba
Animal Physiology Laboratory, Sfax Faculty of Science, 3000 Sfax, Tunisia.
Int J Dev Neurosci. 2009 Nov;27(7):719-26. doi: 10.1016/j.ijdevneu.2009.07.002. Epub 2009 Jul 15.
The aim of this study is to investigate the improving effects of selenium (Se) on cerebrum and cerebellum impairments induced by methimazole (MMI) in suckling rats. Animals were randomly divided into four groups of six each: group I served as control which received standard diet; group II received only MMI (250 mg L(-1)(,) orally); group III received both MMI (250 mg L(-1), orally) and Se (0.5 mg kg(-1) of diet); group IV served as a positive control and received Se (0.5 mg kg(-1) of diet) as sodium selenite (Na(2)SeO(3)). Treatments were started from the 14th day of pregnancy until day 14 after delivery. In the MMI-treated group, plasma-free thyroid hormone levels (FT(3) and FT(4)), protein, DNA and RNA contents in cerebrum and cerebellum decreased when compared to control. Co-treatment with Se ameliorated these parameters. In the MMI-treated group, antioxidant enzyme activities (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) significantly decreased, while malonaldialdehyde (MDA) levels in cerebrum and cerebellum increased. Co-administration of Se through the diet restored these parameters to near normal values. The biochemical modifications are correlated histologically with the abnormal development of an external granular layer, indicating a delay of granular cells migration towards the molecular layer in the MMI-treated group. Our results showed that Se improved cerebrum and cerebellum MMI-induced damages in suckling rats. Moreover, we concluded that Se is an important neuroprotective element that may be used as a dietary supplement against brain impairments.
本研究旨在探讨硒(Se)对甲巯咪唑(MMI)诱导的乳鼠大脑和小脑损伤的改善作用。将动物随机分为四组,每组六只:第一组作为对照组,给予标准饮食;第二组仅接受MMI(250 mg L⁻¹,口服);第三组接受MMI(250 mg L⁻¹,口服)和Se(0.5 mg kg⁻¹饮食);第四组作为阳性对照组,接受亚硒酸钠(Na₂SeO₃)形式的Se(0.5 mg kg⁻¹饮食)。从怀孕第14天开始治疗,直至分娩后第14天。与对照组相比,MMI治疗组的血浆游离甲状腺激素水平(FT₃和FT₄)、大脑和小脑中的蛋白质、DNA和RNA含量降低。Se联合治疗改善了这些参数。在MMI治疗组中,抗氧化酶活性(超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px))显著降低,而大脑和小脑中的丙二醛(MDA)水平升高。通过饮食共同给予Se可将这些参数恢复到接近正常水平。这些生化改变在组织学上与外颗粒层的异常发育相关,表明MMI治疗组颗粒细胞向分子层迁移延迟。我们的结果表明,Se改善了MMI诱导的乳鼠大脑和小脑损伤。此外,我们得出结论,Se是一种重要的神经保护元素,可作为预防脑损伤的膳食补充剂。