continuously exposed to NaNO2 from different sources especially vegetables and cured meat. Many cases of toxicities or even death in humans and animals from nitrate and nitrite were reported.
Aim of the Work: The aim of the present study was to analyze the role of metformin in reduction of toxicity induced by NaNO2 administration in rat cerebellar cortex.
Materials and Methods: Forty adult male albino rats were used and were classified into four groups (10 rats in every group).
Group I control. Group II: the animals were given metformin (200 mg/kg/day). Group III: the animals were given sodium nitrite (80 mg/kg/day) orally for 7 days. Finally, group IV was given sodium nitrite and metformin with same doses and duration. At end of the experiment cerebellar specimens were subjected to light microscopic, morphometric and immunohistochemical studies for expression of caspase-3, GFAP, iNOS, MAP2 and HIF-1α.
Results: Cerebellar cortex sections from sodium nitrite treated rats showed neurodegenerative changes in the three layers of rat cerebellar cortex particularly Purkinje cell layer. There was disturbed monolayer arrangement of Purkinje cells as well as patchy loss of some of them with significant decrease in their number (P<0.01), deformed and pyknotic Purkinje cells with empty spaces around them. Vacuolations in the neuropil of all layers of cerebellar cortex. The granular cells were dispersed and pyknotic. Significant increase in caspase-3, GFAP, iNOS, HIF-1α and significant decrease in MAP2 immunoreactivity were detected. However, administration of metformin improved the cerebellar cortex architecture.
Conclusion: The results revealed the neurological protective role of metformin therapy on hazardous effect of sodium nitrite of adult rat cerebellar cortex.