Gelidium jelly was traditionally made by boiling processed Gelidium seaweed and allowing the filtrate to congeal into jelly. The processing of Gelidium seaweed was very complicate involved the repeated procedures of water washing and sun drying for 7 times, and the seaweed was originally purple-red in color turned into yellow after the repeated wash and sun drying. This study aimed to evaluate the effects of halogen lamp drying methods in replace of sun drying on the physical-chemical qualities of Gelidium jellies. Properties included the agar yield, gelling temperature, hardness, springiness, rheological parameters, sensory attributes, color, and volatile compounds were investigated. The results demonstrated halogen lamp drying method required 12 times of washing and drying processes to achieve the similar jelly properties compared to sun drying for 7 times in the experimental conditions. Volatiles including heptanal, β-ionone, and (E)-2-decenal could be used as indicators to monitor the washing and drying processing. Halogen lamp was found could be an alternative processing method for seaweed drying, especially at rainy days.

Oxidative stress is known to be critically implicated in the pathophysiology of several neurological disorders, including Alzheimer’s disease and ischemic stroke. The remarkable neurotrophic activity of Gelidium amansii, has been reported consistently in a series of our previous studies, inspired us to investigate whether this popular agarophyte could protect against hypoxia/reoxygenation (H/R)-induced oxidative injury in hippocampal neurons. The primary culture of hippocampal neurons challenged with H/R suffered from a significant loss of cell survival, accompanied by apoptosis and necrosis, DNA damage, generation of reactive oxygen species (ROS), and dissipation of mitochondrial membrane potential (MMP) which were successfully attenuated when the neuronal cultures were preconditioned with GAE, an optimized ethanolic extract of G. amansii. Moreover, the expression of N-methyl-D-acetate receptor subunit 2B (GluN2B), an extrasynaptic glutamate receptor, was significantly repressed in GAE-treated neurons as compared to those without GAE intervention. Together, this study demonstrates that GAE attenuated H/R-induced oxidative injury in hippocampal neurons through, at least in part, a potential neuroprotective mechanism that involves inhibition of GluN2B-mediated excitotoxicity and suppression of ROS production, and suggest that this edible seaweed could be a potential source of bioactive metabolites having therapeutic significance against oxidative stress-related neurodegeneration, including ischemic stroke and neurodegenerative diseases.