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KMID : 1161520140180020119
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Animal Cells and Systems
2014 Volume.18 No. 2 p.119 ~ p.134
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Neuroprotective effects of Eriobotrya japonica and Salvia miltiorrhiza Bunge in in vitro and in vivo models
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Bae Dong-Hyuck
Kim Yong-jae
Kim Ji-Hye
Kim Yu-Jin
Oh Kyo-Nyeo
Jun Woo-Jin
Kim Sun-Oh
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Abstract
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We previously reported that Eriobotrya japonica (EJ) improves the cognitive dysfunction caused by amyloid-β (Aβ) peptide injection. Here, we further examined the possible neuroprotective effects and the combined ameliorating effects of EJ and Salvia miltiorrhiza Bunge (SM) in various in vitro and in vivo models. We confirmed the combined effects of a mixture of 5% ethanol extract from EJ leaves (EJE) and water extract from SM roots (SMW) on Aβ1?42-induced toxicity in an in vitro model. Treatment with the mixture (1:1) of EJ and SM (Mix) produced significantly better protection of cells from Aβ-induced toxicity and more strongly suppressed caspase-3 activity compared to treatment with EJE or SMW alone. Additionally, EJE, SMW, and Mix attenuated CoCl2-induced hypoxic damage and corticosterone-induced impairment in SH-SY5Y cells. To examine the combined effects of EJE and SMW in in vivo models, behavioral performance in the Morris water maze was tested two days after injection of Aβ1?42. Administration of Mix provided significantly more protection of spatial learning and memory against the impairments induced by Aβ1?42 injection than did administration of EJE or SMW alone. Additionally, the behavioral deficits that accompanied Aβ-induced memory impairment were attenuated to a greater extent by the administration of the mixture. Furthermore, acetylcholinesterase (AChE) activity and neuronal apoptosis were significantly more inhibited in rats treated with Aβ and the mixture than in rats treated with Aβ1?42 alone. Thus, the results of this study indicate that the mixture of EJ and SM has combined effects that are neuroprotective against Aβ1?42-induced neuronal toxicity.
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KEYWORD
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Eriobotrya japonica, Salvia miltiorrhiza Bunge, Alzheimer’s disease, amyloid-β, memory, cognition
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