@article{APS3581,
author = {Giyasettin BAYDAS and Ertugrul SONKAYA and Mehmet TUZCU and Abdullah YASAR and Emir DONDER},
title = {Novel role for gabapentin in neuroprotection of central nervous system in streptozotocine-induced diabetic rats},
journal = {Acta Pharmacologica Sinica},
volume = {26},
number = {4},
year = {2016},
keywords = {},
abstract = {Aim: To investigate the effect of gabapentin on neural [neuron-specific enolase
(NSE)] and glial markers [glial fibrillary acidic protein (GFAP) and S100B] in different
brain regions of diabetic rats. Methods: Diabetes was induced by a single
intraperitoneal injection of streptozotocine (50 mg/kg body weight). Rats in one
diabetic group received gabapentin (50 mg•kg-1•d-1) and rats in the other diabetic
group received vehicle only for 6 weeks. The levels of GFAP, S100B, and NSE were
determined by immunoblotting in the hippocampus, cortex, and cerebellum. Lipid
peroxidation (LPO as malondialdehyde+ 4-hydroxyalkenals) and glutathione (GSH)
levels were also determined in the same brain parts. Results: Total and degraded
GFAP content and S100B protein expression in different areas of brain tissues
significantly increased in diabetic rats compared to control rats. Similarly, NSE
levels were also significantly elevated in hyperglycemic rats. In addition, there
was a significant increase in LPO levels in the diabetic rat brain compared to
control rat brains. Pretreatment with gabapentin prevented the upregulation of
GFAP, S100B, and NSE in all brain regions of diabetic rats. The level of LPO was
reduced, but not completely halted, by treatment with gabapentin. Conclusion:
These results suggest that diabetes causes glial and neuronal injury, possibly as
a result of elevated oxidative stress, and that gabapentin protects neurons and
glial cells. Thus, we predict that gabapentin treatment will attenuate the hippocampal
and cortical neurodegeneration observed during diabetes mellitus in rats.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/3581}
}