Protective effect of lutein supplementation on oxidative stress and inflammatory progression in cerebral cortex of streptozotocin-induced diabetes in rats

Abstract

Oxidative stress and inflammation are deemed to play a vital role in diabetic cerebral and neurological dysfunction. The present study was designed to investigate the protective effect of the naturally occurring antioxidant, lutein, against oxidative injury and inflammation in cerebral cortex (CCT) of diabetic animals. Using single IP injection of streptozotocin (STZ, 65 mg/kg) diabetes was induced in rats. Lutein dietary supplement was provided to diabetic animals for 5 consecutive weeks in three different doses. The extent of lipid peroxidation and cellular damage were estimated in CCT. Endogenous antioxidants molecules such as non-protein sulfhydryl groups (NP-SH) and enzymes including superoxide dismutase (SOD) and catalase (CAT) were also estimated in CCT. Levels of neurotrophic factors such as brain derived nerve factor (BDNF), nerve growth factor (NGF) and insulin growth factor (IGF) and pro-inflammatory cytokines, as markers for neural inflammation, were assessed in CCT. Lutein dietary supplement, significantly inhibited the diabetes induced increased in CCT levels of thiobarbituric acid reactive substances (TBARS), caspase-3, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6. Diabetes caused inhibition in the levels of NP-SH, DNA and RNA was significantly increased following lutein dietary supplementation to diabetic group compared to normal diet fed animals in dose dependent manner. Diabetes induced down regulation of BDNF, NGF and IGF was also attenuated by lutein dietary supplementation to diabetic model for 5 weeks. These findings suggest that lutein has the potential to ameliorate diabetes-induced oxidative and inflammatory damage and neural degeneration in the CCT.