Pharmacological Modulation of Aldehyde Dehydrogenase 2 in N-Methyl-N-Nitrosourea-Induced Damage in 661W Retinal Photoreceptor Cells

N-Methyl-N-nitrosourea (MNU)-induced damage in 661W retinal photoreceptor cells was used to examine the effects of pharmacological modulation of aldehyde dehydrogenase 2 (ALDH2) on cell morphology, viability, migration ability, and sirtuin 1 (SIRT1) and ALDH2 protein expression. Cells were divided into four treatment groups: control, MNU, MNU plus the ALDH2 agonist Alda-1, and MNU plus the ALDH2 inhibitor daidzin. Most quantitative assessments included three biological replicates per group; for Western blot analysis, the control group included two biological replicates and the remaining groups included three. Treatments were administered for 24 h after cells reached 80%-90% confluence. Cell morphology and floating cell area were assessed by phase-contrast microscopy; cell viability was evaluated using the Cell Counting Kit-8 (CCK-8) assay; migration ability was analyzed using a wound healing assay; and SIRT1 and ALDH2 protein expression was assessed by Western blotting. Group differences were evaluated using bootstrap analysis. After 24 h, floating cell area followed the order control > MNU > ALDH2 agonist > ALDH2 inhibitor. The CCK-8 assay showed a significant difference between the MNU and control groups, whereas differences between the MNU and ALDH2-modulated groups were not statistically significant. No significant differences in migration ability were observed among the groups. SIRT1 and ALDH2 expression was numerically lower in the MNU group than in the control group, while the inhibitor group showed significantly higher expression than the MNU and agonist groups. These preliminary findings indicate that ALDH2 inhibition with daidzin was associated with altered cell morphology and increased SIRT1 and ALDH2 protein expression under MNU-treated conditions; however, its effects on cell viability and the underlying mechanisms required further investigation.