Tanshinone IIA Alleviates Amyloid β‑Induced Neurotoxicity of SH‑SY5Y Cells through GSK‑3β Pathway

Background: The deposition of amyloid β (Aβ) proteins and hyperphosphorylation of tau proteins are the two notable features of Alzheimer’s disease. During the past decades, novel drug candidates have been found from natural herbs and its derived compounds due to their broad spectra of therapeutic effects with low toxicity. Among the different compounds studied, tanshinone IIA, which is derived from Salvia miltiorrhiza, has been reported to attenuate Aβ‑induced neurotoxicity. Materials and Methods: In this study, we studied the effects of tanshinone IIA on the neurotoxicity, proliferation, and apoptosis of Aβ25–35‑induced SH‑SY5Y cells. We applied various methods such as Western blot, fluorescence staining, and flow cytometry. We analyzed the tau phosphorylation and inflammatory response of SH‑SY5Y cells, and we further discuss the relationship between phosphorylated tau and GSK‑3β pathway. Results: Tanshinone IIA promoted proliferation and inhibited neurotoxicity of Aβ25–35‑induced SH‑SY5Y cells. In addition, it downregulated the level of phosphorylation of tau protein, leading to the inhibition of inflammatory response. The Y216 phosphorylation level of GSK‑3β was downregulated by tanshinone IIA, whereas the S9 phosphorylation level was upregulated. Conclusion: The results of this study provide evidence that tanshinone IIA exerts its beneficial effects by attenuating the neurotoxicity induced by Aβ25–35 through the GSK‑3β pathway.