Abstract
Background Ginkgo biloba extract is widely studied for antiaging activities, but little is known about its antiaging mechanism of protein carbonylation. In order to verify carbonyl toxification (stress) hypothesis of aging, we have investigated the effects of EGb761 on hippocampal neuronal injury and carbonyl stress of aging rats. Methods Seventy-two Wister male rats were randomly assigned into six groups (n = 12), normal control (NC), model control (MC), vitamin E (VE, 60 mg/kg) group, EGb761 low doses (GBEL, 8.75 mg/kg), EGb761 moderate doses (GBEM, 17.5 mg/kg), and EGb761 high doses (GBEH, 35 mg/kg). Except the NC, the other groups were subject to subcutaneous administration of 0.5% D-gal (10 ml/kg/day) for 6 weeks to induce aging model. The study detected cognitive impairment in rats by Morris water maze test and the contents of superoxidase dismutase (SOD), malondialdehyde (MDA), total antioxidant capacity (T-AOC) by the related kits. The level of 4-hydroxy-2-nonenal (4-HNE) protein adducts in rat brain was detected, and the ultrastructure of hippocampus was observed. Results The EGb761 treatment groups significantly improved the spatial learning and memory of rats. Moreover, EGb761 treatment could reduce hippocampal neuronal damage based on histopathological and ultrastructural observation. Further studies have proved that these activities are remarkably related with the reducing level of MDA, protein carbonyl and lipofuscin, and 4-HNE protein expression, as well as the increasing of SOD and T-AOC content. Furthermore, EGb761 improves telomerase activity by detecting telomerase activity in the brain of aging rats. Conclusion Our data indicate that EGb761 is an effective agent against D-gal-induced hippocampal neuronal loss owing to its antioxidative as well as carbonyl stress properties. Meanwhile, the carbonylation hypothesis is confirmed that the high level of 4-HNE may cause age-related neurodegenerative disorders.
Highlights
BackgroundGinkgo biloba extract is widely studied for antiaging activities, but little is known about its antiaging mechanism of protein carbonylation
Aging, occurring in the later stage of life, refers to a process of functional deterioration that affects normal homeostasis [1]
Protein aggregation is a common pathological hallmark due to amino acid mutation and changes in the primary structure of the proteins in many degenerative diseases of the central nervous system, such as Alzheimer’s, Parkinson’s, and Huntington’s disease [21]. us, the present study investigated the effect of EGb761 on hippocampal neuronal injury and protein carbonylation and discusses the relationship between aging and protein carbonylation
Summary
Ginkgo biloba extract is widely studied for antiaging activities, but little is known about its antiaging mechanism of protein carbonylation. E level of 4-hydroxy-2-nonenal (4-HNE) protein adducts in rat brain was detected, and the ultrastructure of hippocampus was observed. EGb761 treatment could reduce hippocampal neuronal damage based on histopathological and ultrastructural observation. Further studies have proved that these activities are remarkably related with the reducing level of MDA, protein carbonyl and lipofuscin, and 4-HNE protein expression, as well as the increasing of SOD and T-AOC content. EGb761 improves telomerase activity by detecting telomerase activity in the brain of aging rats. Our data indicate that EGb761 is an effective agent against D-gal-induced hippocampal neuronal loss owing to its antioxidative as well as carbonyl stress properties. The carbonylation hypothesis is confirmed that the high level of 4-HNE may cause age-related neurodegenerative disorders
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