Abstract

We examined the biological effect of krill phosphatidylserine (K-PS) on brain ageing and investigated the mechanisms that how K-PS works on the brain using senescence-accelerated mouse (SAM) model with age-associated neurodegeneration. SAMP10 mice with 5 months of age were treated orally once a day for 75 days with 10 or 100 mg kg^?1 d^?1 K-PS (low and high dose). The effect of K-PS treatment on the cross-sectional area and Nissl body number of the neocortex at point C, an area prone to atrophy in SAMP10 mice, behavior and oxidative stress were evaluated by Image-Pro Plus software, step-down testing, and malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) assays. Ionized calcium binding adaptor molecule 1 (Iba-1) and insulin-like growth factor 1 (IGF-1) expression was evaluated using immunohistochemistry. Low or high doses of K-PS significantly increased the cross-sectional area and Nissl body number at point C, partly reversed memory impairment, increased the activity of GSH-Px and reduced MDA levels. Moreover, immunohistochemistry indicated that K-PS suppressed Iba-1 expression and upregulate the expression of IGF-1. These findings suggest that K-PS could prevent or slow the progression of brain atrophy and neuronal damage associated with aging by the inhibition of Iba-1 and the upregulation of IGF-1 expression.

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