Soy isoflavone attenuates brain mitochondrial oxidative stress induced by beta‐amyloid peptides 1–42 injection in lateral cerebral ventricle

Abstract

The aim of this study is to investigate whether soy isoflavone (SIF) reduces oxidative stress and improves the antioxidant ability in mitochondria of rat brain damaged by injection of beta-amyloid peptides 1-42 (Aβ1-42). Forty Wistar rats were randomly divided into control, Aβ1-42, SIF + Aβ1-42, and SIF groups according to body weight. The rats in the SIF + Aβ1-42 group and SIF group were intragastrically administered SIF suspension in 0.5% CMC-Na for 28 days, whereas the rats in control group and Aβ1-42 group were administered the same volume of 0.5% CMC-Na. On day 14, the rats in the Aβ1-42 group and SIF + Aβ1-42 group were injected with Aβ1-42 into the lateral cerebral ventricle with physiological saline. The rat brains were then sampled, and brain mitochondria were isolated. After this, the mitochondrial membrane potential (MMP) and mitochondrial redox state were measured. The contents of brain nuclear factor E2-related factor (Nrf2) and heme oxygenase-1 (HO-1) protein in brain tissue were quantitated by Western blot. The results showed that SIF maintained the MMP, elevated the reduced glutathione/oxidized glutathione (GSH/GSSG) ratio, and increased glutathione peroxidase (GPx) and manganese superoxide dismutase (MnSOD) protein expression in brain mitochondria. Additionally, SIF reversed the Aβ1-42-induced downregulation of the protein expression of Nrf2 and HO-1 in brain tissue. These results indicated that SIF could alleviate the oxidative damage and maintain the redox imbalance in brain mitochondria damaged by Aβ1-42. This might result from regulation of the Nrf2/HO-1 pathway.