Budni Josiane, Pacheco Robson, da Silva Sabrina, Garcez Michelle Lima, Mina Francielle, Bellettini-Santos Tatiani, de Medeiros Jesiel, Voss Bruna Constantino, Steckert Amanda Valnier, Valvassori Samira da Silva, Quevedo João
Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil; Laboratório de Doenças Neurodegenerativas, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
Laboratório de Neurociências, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil; Laboratório de Doenças Neurodegenerativas, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
Behav Brain Res. 2016 Apr 1;302:35-43. doi: 10.1016/j.bbr.2015.12.041. Epub 2015 Dec 31.
d-Galactose (d-gal) is a reducing sugar that can be used to mimic the characteristics of aging in rodents; however, the effects of d-gal administration by oral route are not clear. Therefore, the aim of this study was to elucidate if the oral administration of d-gal induces cognitive impairments, neuronal loss, and oxidative damage, mimicking an animal model of aging. Male adult Wistar rats (4 months old) received d-gal (100mg/kg) via the oral route for a period of 1, 2, 4, 6 or 8 weeks. The results showed cognitive impairments in the open-field test in the 4th and 6th weeks after d-gal administration, as well as an impairment in spatial memory in the radial maze test after the 6th week of d-gal administration. The results indicated increase of levels of thiobarbituric acid reactive species-TBARS-and carbonyl group content in the prefrontal cortex from the 4th week, and in all weeks of d-gal administration, respectively. An increase in the levels of TBARS and carbonyl group content was observed in the hippocampus over the entire period of d-gal treatment. In the 8th week of d-gal administration, we also observed reductions in synaptophysin and TAU protein levels in the prefrontal cortex. Thus, d-gal given by oral route caused cognitive impairments which were accompanied by oxidative damage. Therefore, these results indicate that orally administered d-gal can induce the behavioral and neurochemical alterations that are observed in the natural aging process. However, oral d-gal effect in rats deserve further studies to be better described.
D-半乳糖（d-gal）是一种还原糖，可用于模拟啮齿动物的衰老特征；然而，口服给予D-半乳糖的效果尚不清楚。因此，本研究的目的是阐明口服D-半乳糖是否会诱发认知障碍、神经元丢失和氧化损伤，从而模拟衰老动物模型。成年雄性Wistar大鼠（4个月大）通过口服途径接受D-半乳糖（100mg/kg），持续1、2、4、6或8周。结果显示，给予D-半乳糖后第4周和第6周的旷场试验中出现认知障碍，给予D-半乳糖第6周后的放射状迷宫试验中出现空间记忆障碍。结果表明，从第4周开始，前额叶皮质中硫代巴比妥酸反应性物质（TBARS）水平和羰基含量增加，在给予D-半乳糖的所有周数中均如此。在整个D-半乳糖治疗期间，海马体中TBARS水平和羰基含量均增加。在给予D-半乳糖的第8周，我们还观察到前额叶皮质中突触素和TAU蛋白水平降低。因此，口服给予D-半乳糖会导致认知障碍，并伴有氧化损伤。因此，这些结果表明，口服D-半乳糖可诱发在自然衰老过程中观察到的行为和神经化学改变。然而，大鼠口服D-半乳糖的作用值得进一步研究以更好地描述。
