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. 2006 Jun;31(6):777-83.
doi: 10.1007/s11064-006-9076-0. Epub 2006 Jun 21.

Neuroprotective effect of etomidate in the central nervous system of streptozotocin-induced diabetic rats

Ozkan Ates  1 , Neslihan Yucel, Suleyman R Cayli, Eyup Altinoz, Saim Yologlu, Ayhan Kocak, Celal Ozbek Cakir, Yusuf Turkoz
Affiliations

Neuroprotective effect of etomidate in the central nervous system of streptozotocin-induced diabetic rats

Ozkan Ates et al. Neurochem Res. 2006 Jun.

Abstract

It is well known that hyperglycaemia due to diabetes mellitus leads to oxidative stress in the central nervous system. Oxidative stress plays important role in the pathogenesis of neurodegenerative changes. In the present study we investigated the possible neuroprotective effect of etomidate against streptozotocin-induced (STZ-induced) hyperglycaemia in the rat brain and spinal cord. A total of 40 rats were used in this study. Rats were divided into four groups: sham-control, diabetic, diabetic-etomidate treated and vehicle for etomidate treatment group. Diabetes mellitus was induced by a single injection of streptozotocin (60 mg/kg body weight). Three days after streptozotocin injection, etomidate (2 mg/kg) was injected intraperitoneally for etomidate group and lipid emulsion (10%) for vehicle group was injected with corresponding amount intraperitoneally every day for 6 weeks. Six weeks after streptozotocin injection, seven rats from each group were killed and brain, brain stem and cervical spinal cord were removed. The hippocampus, cortex, cerebellum, brain stem and spinal cord were dissected for the biochemical analysis (the level of malondialdehyde [MDA], total nitrite, reduced glutathione [GSH], and xanthine oxidase [XO] activity). STZ-induced diabetes resulted in significantly elevation of MDA, XO and nitrite levels in the hippocampus, cortex, cerebellum, brain stem and spinal cord of the rats (P < 0.05) while etomidate treatment provided significantly lower values (P < 0.05). This study demonstrated that etomidate have neuroprotective effect on the neuronal tissue against the diabetic oxidative damage.

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