Achin Nurul A, Kit Tan J, Ngah Wan Z W, Makpol Suzana, Mazlan Musalmah, Hamezah Hamizah S, Damanhuri Hanafi A
Department of Biochemistry, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia.
Faculty of Medicine, Universiti Teknologi MARA, Kuala Lumpur, Malaysia.
Curr Aging Sci. 2018;11(3):182-194. doi: 10.2174/1874609811666181019141217.
Cognitive frailty emerges as one of the threats to healthy aging. It is in continuum with advancing of age with uncertain indicator between pathological and physiological changes. Alterations in pathways associated with the aging process have been observed including oxidative stress, lipid metabolism, and inflammation. However, the exact mechanisms leading to cognitive decline are still unclear.
This study was sought to assess the level of cognitive functions and linked with blood oxidative status during normal aging in rats.
A longitudinal study using male Sprague Dawley rats was performed starting from the age of 14 months old to 27 months old. Cognitive functions tests such as open field, Morris water maze and object recognition were determined at the age of 14, 18, 23, and 27 months old and were compared with group 3 months old. Blood was collected from the orbital venous sinus and oxidative status was determined by measuring the level of DNA damage, lipid peroxidation, protein oxidation and antioxidant enzymes activity.
Aged rats showed declining exploratory behavior and increased in the level of anxiety as compared to the young rats. The level of DNA damage increased with increasing age. Interestingly, our study found that both levels of malondialdehyde and plasma carbonyl content decreased with age. In addition, the level of superoxide dismutase activity was significantly decreased with age whereas catalase activity was significantly increased from 18 months of age. However, no significant difference was found in glutathione peroxidase activity among all age groups.
The progressions of cognitive impairment in normal aging rats are linked to the increment in the level of DNA damage.
认知衰弱已成为健康老龄化的威胁之一。它随着年龄的增长而连续变化,病理和生理变化之间的指标尚不确定。已观察到与衰老过程相关的途径发生改变,包括氧化应激、脂质代谢和炎症。然而,导致认知衰退的确切机制仍不清楚。
本研究旨在评估正常衰老大鼠认知功能水平及其与血液氧化状态的关系。
采用雄性Sprague Dawley大鼠进行纵向研究,从14月龄开始至27月龄。在14、18、23和27月龄时进行认知功能测试,如旷场试验、莫里斯水迷宫试验和物体识别试验,并与3月龄组进行比较。从眶静脉窦采集血液,通过测量DNA损伤水平、脂质过氧化、蛋白质氧化和抗氧化酶活性来确定氧化状态。
与年轻大鼠相比,老年大鼠的探索行为减少,焦虑水平增加。DNA损伤水平随年龄增长而增加。有趣的是,我们研究发现丙二醛水平和血浆羰基含量均随年龄下降。此外,超氧化物歧化酶活性水平随年龄显著降低,而过氧化氢酶活性从18月龄起显著增加。然而,各年龄组间谷胱甘肽过氧化物酶活性未发现显著差异。
正常衰老大鼠认知障碍的进展与DNA损伤水平的增加有关。