Neurons in the hippocampal and cortical functional regions are more susceptible to damage induced by
hyperglycemia, which can result in severe spatial learning and memory impairment. Neuroprotection ameliorates
cognitive impairment induced by
hyperglycemia in
diabetic encephalopathy (DE).
Astaxanthin has been widely studied in
diabetes mellitus and
diabetic complications due to its
hypoglycemic,
antioxidant and anti-apoptotic effects. However, whether
astaxanthin can alleviate cognition deficits induced by DE and its precise mechanisms remain undetermined. In this study, DE was induced by
streptozotocin (STZ, 150 mg/kg) in ICR mice. We observed the effect of
astaxanthin on cognition and investigated its potential mechanisms in DE mice. Results showed that
astaxanthin treatment significantly decreased the latency and enhanced the distance and time spent in the target quadrant in the Morris water maze test. Furthermore, neuronal survival was significantly increased in the hippocampal CA3 region and the frontal cortex following treatment with
astaxanthin. Meanwhile, immunoblotting was used to observe the nuclear translocation of
nuclear factor-kappaB (NF-κB) p65 and the expression of
tumor necrosis factor-α (TNF-α) in the hippocampus and frontal cortex. The results indicated that
astaxanthin could inhibit NF-κB nuclear translocation and downregulate TNF-α expression in the hippocampus and frontal cortex. Overall, the present study implied that
astaxanthin could improve cognition by protecting neurons against
inflammation injury potentially through inhibiting the nuclear translocation of NF-κB and down-regulating TNF-α.