Abstract

The aim of this study was to evaluate the neuroprotective effects of kinetin (Kn) on oxidative damage induced by D-galactose (D-gal). In vitro, cultured astrocytes were distributed equally in different culture flasks to serve as control, model, and test groups. They were incubated respectively with 0 μM (model group), 50, 100 or 200 μM Kn along with 15 mM D-gal for 24 and 72 h, but cells in the control group received only normal medium. Activities of total-superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and malondialdehyde (MDA) levels were measured by biochemical analysis. In vivo, mice were also randomly divided into control, model, and test groups. They were subcutaneously injected with D-gal (125 mg/kg), and administered with 0 (model group), and 10, 20 and 40 mg/kg Kn (test groups) per day simultaneously by gastric perfusion, but mice in the control group only received 0.4 ml physiologic saline solution per day by gastric perfusion. After 6 weeks, T- SOD and GSH-Px activities, and MDA levels in the brain tissue were assessed by biochemical analysis. Results show that both D-gal-treated astrocytes and mice brains displayed impaired antioxidant systems, an increase in MDA levels, and a decrease in T-SOD and GSH-Px activities. After Kn treatment, the changes of antioxidant enzymes activities and MDA levels were reversed both in vitro and in vivo. In conclusion, results of this study indicate that supplementation of Kn protects cultured astrocytes in vitro and mouse brain from D-gal-induced oxidative damage.

Key words: Kinetin, D-galactose, oxidative stress, astrocytes, brain aging.

Abbreviation

Kn, Kinetin; D-gal, D-galactose; T-SOD, total-superoxide dismutase; GSH-Px, glutathione peroxidase; MDA, malondialdehyde; ROS,reactive oxygen species.