Aminoguanidine exhibits an inhibitory effect on β‑amyloid‑induced damage in F98 glioma cells.

The present study investigated the role of aminoguanidine in the prevention of harmful effects in astroglioma F98 cells induced by β‑amyloid treatment. MTT assay was used to analyze cell viability. Expression of inducible nitric oxide synthase (iNOS) was analyzed using western blot analysis. Treatment of the F98 cells with a 15 µM concentration of β‑amyloid for 12 h reduced cell viability to 18% compared with the control cells. However, pretreatment with a 30 µM concentration of aminoguanidine for 12 h completely prevented the β‑amyloid‑induced reduction in cell viability. The production of ROS and the expression of iNOS were significantly (P<0.005) higher in the β‑amyloid‑treated F98 cells. Aminoguanidine pre‑treatment inhibited the β‑amyloid‑induced increase in the expression of ROS, with increased mRNA and proteins levels of iNOS12 h following treatment at a 30 µM concentration. The β‑amyloid treatment also resulted in a marked increase in the expression of cyclooxygenase‑2 (COX‑2) in F98 cells. By contrast, pre‑treatment with aminoguanidine for 12 h led to reduction in the mRNA and protein expression levels of COX‑2. Pre‑treatment of the F98 cells with aminoguanidine at a 30 µM concentration for 12 h prior to incubation with β‑amyloid significantly (P<0.002) reduced the expression of prostaglandin E2 (PGE2). Aminoguanidine pre‑treatment also caused the inhibition of β‑amyloid‑induced translocation of nuclear factor (NF)‑κB p65 into the cytosol. Thus, aminoguanidine prevented β‑amyloid‑induced Alzheimer's disease through reductions in the expression levels of NO, iNOS, PGE2 and COX‑2, and the inactivation of NF‑κB. Therefore, aminoguanidine offers potential for use in the treatment of neurological disorders, including Alzheimer's disease.