2Ataturk University, Faculty of Medicine, Department of Pharmacology, Erzurum, Turkey DOI : 10.5137/1019-5149.JTN.4313-11.0 AIM: Glutamate is known to be neurotoxic at concentrations of 10-6M and 10-7M. Angiotensin converting enzyme (ACE) inhibitors can be assumed to be neuroprotective as they open the mitochondrial adenosine triphosphate-sensitive potassium channels by inhibiting the degradation of bradykinin. In this study, we investigated whether the ACE inhibitors captopril, ramipril and perindopril have protective effects in glutamate-induced neurotoxicity in newborn rat cerebral cortex cell cultures.
MATERIAL and METHODS: Viability tests were performed among ACE inhibitors by constituting groups of control and 10-7M and 10-6M glutamate doses in newborn rat cortex cultures.
RESULTS: While the mean viable cell number was 0.47±0.06 in the control group, it was 0.37±0.03 in the group exposed to 10-7M glutamate (p<0.05) and 0.37±0.01 in the group exposed to 10-6M glutamate (p<0.05). Captopril was used at a dose of 10 μM, perindopril was used at a dose of 1 μM, and ramipril was used at a dose of 30 μM against 10-7M and 10-6M glutamate. Ramipril and perindopril reversed the toxicity against 10-6M glutamate (p<0.05). The neuroprotective properties of captopril, perindopril and ramipril were not found to be statistically significant against 10-7M glutamate at the doses mentioned above.
CONCLUSION: Data obtained from this study indicate that ramipril and perindopril can prevent 10-6M glutamate-induced neurotoxicity.
Keywords : ACE inhibitors, Glutamate, Neuroprotection, Neurotoxicity