The effects of nitric oxide production blockage by aminoguanidine on passive avoidance memory and expression of Bcl-2 family genes in diabetic rats

Memory impairment is one of the complications of diabetes which may accompany with changes in expression of apoptotic and antiapoptotic genes. The aim of the present study was the evaluation of intra-hippocampal injection of aminoguanidine (AG), as an antioxidant and inducible nitric oxide synthase inhibitor, on passive avoidance memory and Bcl-2 family genes expression in diabetic rats. Diabetes was induced in male rats using streptozotocin (STZ) (50 mg/kg, i.p). AG (10 and 90 μg/rat) was injected by intra-hippocampal implanted cannulae. Passive avoidance memory was assessed 7 weeks later. Then, animals were killed and hippocampus was removed. The expressions of Bcl-2, Bcl-xLand Bax mRNA were measured using semi-quantitative RT-PCR technique. Diabetes caused significant impairment in passive avoidance memory. None of the AG doses improved the memory impairment. In diabetic rats, the levels of Bcl–2 and Bcl-xL were decreased in hippocampus while the expression of Bax, Bax/Bcl-2 and Bax/Bcl-xL was increased. In comparison to diabetic control group, AG treatment increased the levels of Bcl–2 and Bcl-xL but decreased Bax/Bcl–2 and Bax/Bcl-xL. Although AG was not associated with the significant improvement of memory but it modified the expression of the apoptosis involved genes in hippocampus of STZ-induced diabetic rats.