κ-carrageenan-derived pentasaccharide attenuates Aβ25-35-induced apoptosis in SH-SY5Y cells via suppression of the JNK signaling pathway

beta-amyloid (A beta)-mediated neuronal apoptosis is an important pathological feature of Alzheimer's disease (AD). Inhibiting apoptosis induced by A beta may lead to the development of a potential therapeutic target for AD treatment. K-carrageenan-derived pentasaccharide (KCP) extracted from marine red algae is involved in a variety of biological activities and may be an effective in the treatment of AD. The present study aimed to investigate the neuroprotective effect of KCP against A beta(25-35)-induced neurotoxicity in SH-SY5Y cells, and to examine the potential underlying mechanisms. The results of the present study revealed that pretreatment with KCP significantly attenuated A beta(25-35)-induced loss of cell viability and apoptosis, as evaluated by MTT assays and annexin V/propidium iodide staining, respectively, in a dose-dependent manner. Furthermore, KCP downregulated the protein expression levels of A beta(25-35)-induced cleavage caspase 3 by inhibiting the overactivation of the JNK signaling pathway. The results of the present study indicated that KCP attenuated A beta(25-35)-induced neuroblastoma cell cytotoxicity, suggesting that KCP may be a potential therapeutic agent for the treatment of AD.