Effects of Tanshinone IIA on Cognitive Impairment in Alzheimer’s Disease Rats Via Oxidative Stress, Inflammatory Responses and Apoptosis

Abstract

The rationale for the pathogenesis of Alzheimer’s disease (AD) is the production of amyloid-beta (Aβ) and its resultant toxic effects. In this work, rats with AD were used as models to assess the modulatory effects of tanshinone IIA (tan IIA) in alleviating cognitive impairment, oxidative damage, inflammation and apoptosis. Aβ1–42 was injected bilaterally in the hippocampus to establish an AD rat model. The effects of tan II A on the learning and memory capacities of AD rats were detected by ethological experiments. Tan IIA’s anti-inflammatory and antioxidant capacities were examined in this study using biochemical and immunohistochemical methods on rat hippocampus tissues. The experimental data showed that the cognitive ability of rats could be significantly improved by tan IIA. Furthermore, fewer injured neuron apoptosis was demonstrated in the tan IIA rats than in the AD group. More importantly, on the one hand, we discovered that the tan IIA group had considerably lower levels of interleukin 1 beta, tumour necrosis factor-alpha and inducible nitric oxide synthase. On the other hand, tan IIA was discovered to prevent oxidative stress by raising glutathione and superoxide dismutase activity and lowering malondialdehyde, protein carbonyl and 8-hydroxy-2′-deoxyguanosine levels. Tan IIA can alleviate cognitive impairment and neuronal cell damage by inhibiting oxidative stress and inflammatory responses during AD.