Amyloidosis is a group of diseases characterized by
protein misfolding and aggregation to form
amyloid fibrils and subsequent deposition within various tissues. Previous studies have indicated that
amyloidosis is often associated with oxidative stress. However, it is not clear whether oxidative stress is involved in the progression of
amyloidosis. We administered the oxidative stress inhibitors
tempol and
apocynin via
drinking water to the R1.P1-Apoa2c mouse strain induced to develop mouse
apolipoprotein A-II (AApoAII)
amyloidosis and found that treatment with oxidative stress inhibitors led to reduction in AApoAII
amyloidosis progression compared to an untreated group after 12 weeks, especially in the skin, stomach, and liver. There was no effect on
ApoA-II plasma levels or expression of Apoa2
mRNA. Detection of the lipid peroxidation markers
4-hydroxynonenal (4-HNE) and
malondialdehyde (MDA) revealed that the antioxidative effects of the treatments were most obvious in the skin, stomach, and liver, which contained higher levels of basal oxidative stress. Moreover, the unfolded protein response was reduced in the liver and was associated with a decrease in oxidative stress and
amyloid deposition. These results suggest that
antioxidants can suppress the progression of AApoAII
amyloid deposition in the improved microenvironment of tissues and that the effect may be related to the levels of oxidative stress in local tissues. This finding provides insights for antioxidative stress treatment strategies for
amyloidosis.