Yoshinori Okada and Mizue Okada
Objective: Alzheimer’s disease (AD) is receiving attention as “Type 3 diabetes” and it is evident that this neurodegenerative disease has multiple shared pathologies with diabetes mellitus. Progressive dementia, increased deposition of amyloid β (Aβ) protein in the brain is the hallmark of AD. Aβ leads to Aβ associated Reactive Oxygen Species (ROS) production and cell death. In this study, we investigated the effects of Komatsuna Seed Extracts (KSE) on Aβ (1-42)-induced neurotoxicity and on the regulation of cell death processing in hippocampus neurons (HN).
Methods: We selected sixteen plants. We investigated the effects of plant seeds’ aqueous extractson (PSAE) on Aβ structure modification using SDS gel electrophoresis. The neuroprotective effects of KSE were evaluated by measuring the cell viability with a CCK-8 assay. Furthermore, we carried out an anti-glycation experiment of KSE and an anti-aggregation experiment of KSE to confirm the modification mechanism of KSE. To find the effects of KSE on Aβ-induced oxidative stress, we examined KSE using a 2’, 7’-dichlorofluorescein diacetate assay. To further unravel the effects of KSE on Aβ-induced cell death, we examined the influence of KSE on glucose uptake.
Results: No bands of Aβ were recognized in Komatsuna, Common bean or Qing gengcai. KSE showed enhancement of cell survival amounting to a 100% blockade of Aβ-induced cell death. KSE caused the decrease in BSA and lactalbumin glycation. Furthermore, intracellular ROS accumulation resulting from Aβ treatment was reduced when cells were treated with KSE. KSE improves glucose uptake by Aβ in HN.
Conclusion: KSE inhibits Aβ-induced cell death. KSE reduces the toxicity of Aβ by modifying Aβ. KSE improves the inhibition of Aβ glucose uptake thereby modifying Aβ. KSE inhibits ROS in cells produced by Aβ. The possibility that KSE protects cells was suggested by these results.