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The antioxidant and anti-inflammatory properties of the marine red alga Neorhodomela aculeate (N. aculeata) MASUDA were investigated with neuronal and microglial cells. Extracts of N. aculeata had potent neuroprotective effects on glutamate-induced neurotoxicity and inhibited reactive oxygen species (ROS) generation in the murine hippocampal HT22 cell line. Also, extracts of N. aculeata inhibited H 2 O 2 -induced lipid peroxidation in rat brain homogenates. The properties of the extract as an anti-inflammatory agent were investigated in microglial activation by interferon-gamma (IFN-g g): it reduced the inducible nitric oxide synthase that consequently resulted in the reduction of nitric oxide. These results suggest that the marine red alga N. aculeata could be considered as a potential source for reducing reactive oxygen species and inflammation related to neurological diseases.

The activation of cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) via phosphorylation in the hippocampus is an important signaling mechanism for enhancing memory processing. Although melatonin is known to increase CREB expression in various animal models, the signaling mechanism between melatonin and CREB has been unknown in vitro. Thus, we confirmed the signaling pathway between the melatonin receptor 1 (MT1) and CREB using melatonin in HT-22 cells. Melatonin increased MT1 and gradually induced signals associated with long-term memory processing through phosphorylation of Raf, ERK, p90RSK, CREB, and BDNF expression. We also confirmed that the calcium, JNK, and AKT pathways were not involved in this signaling pathway by melatonin in HT-22 cells. Furthermore, we investigated whether melatonin regulated the expressions of CREB-BDNF associated with long-term memory processing in aged HT-22 cells. In conclusion, melatonin mediated the MT1-ERK-p90RSK-CREB-BDNF signaling pathway in the in vitro long-term memory processing model and increased the levels of p-CREB and BDNF expression in melatonin-treated cells compared to untreated HT-22 cells in the cellular aged state. Therefore, this paper suggests that melatonin induces CREB signaling pathways associated with long-term memory processing in vitro.