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Evidence suggests that brain tissues of patients with Alzheimer's disease (AD) are easily attacked by oxidative stress, and numerous studies indicate that heme oxygenase (HO) is a major cell adaptive responder to stress. However, whether HO‑1 and HO‑2 play different roles in this process has not yet been studied. In the present study, it was shown in an AD model that HO‑1 and HO‑2 have different roles in the early stages of AD. Learning and memory ability was tested in APPswe/PS1ΔE9 (APP/PS1) transgenic and wild‑type mice using the Morris water maze. β‑amyloid plaques were measured using immunofluorescence staining. Changes in reactive oxygen species (ROS) levels in the hippocampi were measured using a fluorescence technique. The results indicated that the escape latency, amyloid plaque deposition and ROS production increased in the hippocampi of APP/PS1 transgenic mice compared with wild‑type mice. Furthermore, using double‑immunofluorescence staining and western blot analysis, it was found that the expression of HO‑1 and HO‑2 increased in the hippocampi of APP/PS1 mice and, notably, HO‑2 was also found to be overexpressed in astrocytes. Little difference was observed in the plasma HO‑1 concentrations between the two groups, while the plasma HO‑2 concentration of the APP/PS1 mice was lower than that of the wild‑type mice, shown by ELISA. In conclusion, HO‑2 overexpression is an early event and plays a more critical role in the progression of AD.

Early induction of oxidative stress in a mouse model of Alzheimer’s disease with heme oxygenase activity