The aqueous extract of Curcuma wenyujin rescues learning and memory deficits through PI3k/Akt/GSK-3β pathway in Aβ-induced AD mice

Clinical studies have demonstrated that a prescription with the Curcuma wenyujin as the main component is favourable for Alzheimer's disease (AD) treatment. Our previous study had shown that the aqueous extract of Curcuma wenyujin has neuroprotective effects in the AD mouse model. However, the exact mechanism through which the aqueous extract of Curcuma wenyujin improves Amyloidal beta (A beta)-induced memory impairment by inhibiting the production of hyperphosphorylated tau protein is unknown. We used Intracerebroventricular (ICV) injection of amyloid25-35 (A beta 25-35) mice model to test the effects of Curcuma wenyujin on A beta-induced tau protein expression. Levels of tau protein on the serine (ser) 404 sites and threonine (thr) 231 sites were determined with immunohistochemistry assay, and western blot was used to detect the expressions of tau protein on ser404, thr231, and thr181 sites, as well as the changes in the phosphorylation level in the PI3K/Akt/GSk-3 beta signaling pathways. The results demonstrated that the aqueous extract of Curcuma wenyujin significantly reduced the phosphorylation level of tau protein in the hippocampus (Thr-181, Thr-231, and Ser-404), and elevated phosphorylation level of PI3K, Akt, and GSK-3 beta. These results suggest that aqueous extract of Curcuma wenyujin improves learning and memory function, and reduce the phosphorylation of the tau protein, and the possible mechanism is mediated through the PI3K/Akt/GSK-3 beta signaling pathway.