Rosuvastatin Calcium Affects Alzheimer's Disease Through Regulating Defensive Transduction Pathways of Oxidative and Chemical Stress Signaling Pathway

Abstract

Alzheimer's disease (AD) treatment is not effective. Statins are lipid-lowering drugs. However, the role and mechanism of statins for treating AD remains unclear. SD rats were separated into sham operation group; AD group and rosuvastatin calcium group followed by analysis of cognitive function and neuronal morphology. ELISA was to measure the level of TNF-α and IL-1; SOD activity and ROS levels were measured,. Real-time quantitative PCR was to analyze Bcl-2 and Bax level. The expression of Nuclear Erythroid 2-Related Factor 2/Antioxidant Responsive Element (NRF2/ARE) signaling pathway was analyzed by Western blot. Compared with sham operation group, the cognitive ability of the AD group was significantly decreased; with elevated secretion of TNF-α and IL-1, decreased SOD activity, increased ROS generation, decreased Bcl-2 expression as well as increased Bax expression (P < 0.05). In addition, AD group rats showed neuronal damage in the hippocampus and decreased expression of NRF2 and ARE. However, rosuvastatin calcium treatment improved cognitive ability, decreased TNF-α and IL-1 secretion, increased SOD activity, decreased ROS content, increased Bcl-2 expression and decreased Bax expression as well as ameliorated neuronal damage, increased number of nerve cells, and increased expression of NRF2 and ARE. Rosuvastatin calcium can inhibit the oxidative stress and inflammation, inhibit the apoptosis of hippocampus cells and improve the cognitive ability of AD rats by regulating NRF2/ARE signaling pathway.