Edaravone Ameliorates Memory, Hippocampal Morphology, and Inflammation in a Rat Model of Alzheimer’s Disease

Abstract

Oxidative stress and neural inflammation play a role in the pathogenesis of Alzheimer's
disease (AD). Edaravone (EDA) has an antioxidant-free radical scavenger property. The
purpose of this study to evaluate the effect of EDA on memory, hippocampal
morphology, and inflammation in a streptozocin (STZ)-induced AD model. This study
used 18 Wistar albino adult rats, weighing 200-220 g. Following general anesthesia, 3
mg/kg STZ was dissolved in 0.9% NaCl and administered intracerebroventricularly
(ICV) in both lateral ventricles to 12 rats in a total of 5 µl. The animals were allowed to
recover for two weeks and then divided into two groups. Six rats were given 0.9% NaCl
i.p. for 15 days, and the other six were administered EDA 40 mg/kg i.p. for 15 days,
once a day. The control group of six rats did not undergo any surgical procedures or
medications. After treatment, a passive avoidance learning (PAL) test was used,
followed by the removal of the brain tissue in all animals. Nissl staining was used to
count neurons in the hippocampal CA1 and CA3 regions, and TNF-α and IL-6 levels in
the brain were measured. In the STZ group, significantly shorter latency time, and
decreased number of neurons in the CA1 and CA3 hippocampal regions compared to
the control group were observed. EDA significantly prolonged the latency time and
increased hippocampal CA1 and CA3 neuron counts compared to the STZ group. TNFα and IL-6 levels were higher in the STZ+saline group than in the control group.
Similarly, EDA treatment reduced TNF-α and IL-6 levels when compared to the
STZ+saline and control groups. For the first time, we demonstrated the neuroprotective
and anti-inflammatory potential of EDA in an experimental AD model. Our results may
provide evidence for EDA therapy in addition to the standard regimen in patients with
cognitive decline.