Chronic
inflammation appears to play a critical role in sickness behavior caused by
diabetes mellitus.
Astaxanthin has been used in treating
diabetes mellitus and
diabetic complications because of its neuroprotective and anti-inflammatory actions. However, whether
astaxanthin can improve sickness behavior induced by diabetes and its potential mechanisms are still unknown. The aim of this study was to investigate the effects of
astaxanthin on diabetes-elicited abnormal behavior in mice and its corresponding mechanisms. An experimental diabetic model was induced by
streptozotocin (150 mg/kg) and
astaxanthin (25 mg/kg/day) was provided orally for 10 weeks.
Body weight and water consumption were measured, and the sickness behavior was evaluated by the open field test (OFT) and closed field test (CFT). The expression of
glial fibrillary acidic protein (GFAP) was measured, and the frontal cortical cleaved
caspase-3 positive cells,
interleukin-6 (IL-6), and interleukin-1β (IL-1β) expression levels were also investigated. Furthermore,
cystathionine β-synthase (CBS) in the frontal cortex was detected to determine whether the protective effect of
astaxanthin on sickness behavior in diabetic mice is closely related to CBS. As expected, we observed that
astaxanthin improved general symptoms and significantly increase horizontal distance and the number of crossings in the OFT and CFT. Furthermore, data showed that
astaxanthin could decrease GFAP-positive cells in the brain and down-regulate the cleaved
caspase-3,
IL-6, and IL-1β, and up-regulate CBS in the frontal cortex. These results suggest that
astaxanthin provides neuroprotection against diabetes-induced sickness behavior through inhibiting
inflammation, and the protective effects may involve CBS expression in the brain.