Laminarin is a
polysaccharide isolated from brown algae that has various biological and pharmacological activities, such as
antioxidant and anti-inflammatory properties. We recently reported that pretreated
laminarin exerted neuroprotection against transient forebrain
ischemia/reperfusion (IR) injury when we pretreated with 50 mg/kg of
laminarin once a day for seven days in adult gerbils. However, there have been no studies regarding a
neuroprotective effect of pretreated
laminarin against IR injury in aged animals and its related mechanisms. Therefore, in this study, we intraperitoneally inject
laminarin (50 mg/kg) once a day to aged gerbils for seven days before IR (5-min transient
ischemia) surgery and examine the
neuroprotective effect of
laminarin treatment and the mechanisms in the gerbil hippocampus. IR injury in vehicle-treated gerbils causes loss (death) of pyramidal neurons in the hippocampal CA1 field at five days post-IR. Pretreatment with
laminarin effectively protects the CA1 pyramidal neurons from IR injury. Regarding the
laminarin-treated gerbils, production of
superoxide anions,
4-hydroxy-2-nonenal expression and pro-inflammatory
cytokines [
interleukin(IL)-1β and
tumor necrosis factor-α] expressions are significantly decreased in the CA1 pyramidal neurons after IR. Additionally,
laminarin treatment significantly increases expressions of
superoxide dismutase and anti-inflammatory
cytokines (IL-4 and IL-13) in the CA1 pyramidal neurons before and after IR. Taken together, these findings indicate that
laminarin can protect neurons from ischemic
brain injury in an aged population by attenuating IR-induced oxidative stress and
neuroinflammation.