Upregulation effects of Tanshinone IIA on the expressions of NeuN, Nissl body, and IκB and downregulation effects on the expressions of GFAP and NF-κB in the brain tissues of rat models of Alzheimer's disease.

This study aimed to observe the effects of Tanshinone IIA(Tan IIA) treatment on the expression levels of brain tissue NeuN, Nissl body, IκB, GFAP and NF-κB in Alzheimer's disease (AD) rats to explore the possible anti-inflammatory and neuroprotective mechanisms of Tan IIA. Thirty healthy male Sprague-Dawley rats were randomized into three groups: Sham group, AD+vehicle control group, and AD+Tan IIA group. The models of AD were established by injecting Aβ1-42 into the hippocampus of rats. Tagged position and the expression levels of Aβ1-42 were observed by immunohistochemistry staining to prove the success of the model of AD. Brain tissues of all groups were collected after Tan IIA treatment and paraffin sections were prepared to assess pathological changes and expression levels of GFAP, IκB and NF-κB by both immunohistochemistry and western blotting. After Aβ1-42 injection, the expression levels of GFAP and NF-κB were significantly stronger in the AD+vehicle control group than those in the AD+Tan IIA group and the sham group (P<0.05), the IκB expression level and the number of neurons and Nissl bodies of AD+vehicle control group was reduced compared with the sham or the AD+Tan IIA group (P<0.05). In conclusion, Aβ induces a cerebral tissue inflammation reaction. Tan IIA treatment can suppress the proliferation of astrocytes in an AD model, lower the level of NF-κB, and increase the level of NeuN, Nissl body, IκB, thus exerting anti-inflammatory and neuroprotective effects.