Neuroprotective Effect of Fucoidan on H2O2-Induced Apoptosis in PC12 Cells Via Activation of PI3K/Akt Pathway

Abstract

One of the plausible ways to prevent the reactive oxygen species (ROS)-mediated cellular injury is dietary or pharmaceutical augmentation of endogenous antioxidant defense capacity. In this study, we investigated the neuroprotective effect of fucoidan on H(2)O(2)-induced apoptosis in PC12 cells and the possible signaling pathways involved. The results showed that fucoidan inhibited the decrease of cell viability, scavenged ROS formation and reduced lactate dehydrogenase release in H(2)O(2)-induced PC12 cells. These changes were associated with an increase in superoxide dismutase and glutathione peroxidase activity, and reduction in malondialdehyde. In addition, fucoidan treatment inhibited apoptosis in H(2)O(2)-induced PC12 cells by increasing the Bcl-2/Bax ratio and decreasing active caspase-3 expression, as well as enhancing Akt phosphorylation (p-Akt). However, the protection of fucoidan on cell survival, p-Akt, the Bcl-2/Bax ratio and caspase-3 activity were abolished by pretreating with phosphatidylinositol-3-kinase (PI3K) inhibitor LY294002. In consequence, fucoidan might protect the neurocytes against H(2)O(2)-induced apoptosis via reducing ROS levels and activating PI3K/Akt signaling pathway.

Lycium Barbarum Polysaccharides Alleviates Oxidative Damage Induced by H2O2 Through Down-Regulating MicroRNA-194 in PC-12 and SH-SY5Y Cells

“…Additionally, it can halt excessive autophagy [39]. The PI3K/AKT pathway was activated by H 2 O 2 , and was further activated by LBPs stimulation in our study, which was consistent with a previous literature [40]. Moreover, the activation was abrogated by miR-194 overexpression while was enhanced by miR-194 inhibition, indicating that LBPs might affect H 2 O 2 -induced PC-12 and SH-SY5Y cells through miR-194-mediated activation of the PI3K/AKT pathway.…”

Insulin Receptor Signaling in Cones

“…In addition, the huge oxygen consumption by the mitochondria in light and dark generates abundant free radicals and reactive oxygen species. Several studies have shown that protection against reactive oxygen species-induced cell death can be mediated via phosphoinositide 3-kinase (PI3K), a downstream effector of the insulin receptor (2)(3)(4)(5).…”

Fucoidan attenuates 6-hydroxydopamine-induced neurotoxicity by exerting anti-oxidative and anti-apoptotic actions in SH-SY5Y cells

“…Similarly, we now show that fucoidan inhibits the elevation of caspase 3/7 activity evoked by 6-OHDA and consequent apoptotic death. An earlier report showed that fucoidan inhibited the elevation of caspase-3 activity in a model of H 2 O 2 -induced neurotoxicity [7], and protected against MPTP-induced lipid peroxidation of, and 1-methyl-4-phenylpyridinium (MPP + )-induced neuronal injury to, MN9D cells [11]. Thus, fucoidan acts a neuroprotectant in experimental models of PD, such as MPTP or 6-OHDA.…”