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

Liu,Yang; Jiang,Liumi; Li,Xiaofeng

doi:10.3892/mmr.2016.6006

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

Authors:
- Yang Liu
- Liumi Jiang
- Xiaofeng Li
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Affiliations: Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 40016, P.R. China
Published online on: December 7, 2016 https://doi.org/10.3892/mmr.2016.6006
Pages: 285-290

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Abstract

β-amyloid (Aβ)-mediated neuronal apoptosis is an important pathological feature of Alzheimer's disease (AD). Inhibiting apoptosis induced by Aβ may lead to the development of a potential therapeutic target for AD treatment. κ‑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 Aβ25‑35‑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 Aβ25‑35‑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 Aβ25‑35‑induced cleavage caspase 3 by inhibiting the overactivation of the JNK signaling pathway. The results of the present study indicated that KCP attenuated Aβ25‑35‑induced neuroblastoma cell cytotoxicity, suggesting that KCP may be a potential therapeutic agent for the treatment of AD.

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