Objective To investigate the effects ofWenyujinessential oil on tau protein phosphorylation in mice with Alzheimer Disease (AD); To discuss the relevant mechanism of action.MethodsSixty Kunming mice were divided into six groups randomly: sham-operation group, model group,Wenyujin essential oil low- and high-dose group, donepezil group andShenzhiling group.β-Amyloid protein (Aβ25-35) was infused into the hippocampal of mice. Mice in each group were given relevant medicine for gavage for 15 d. After the last administration, immunohistochemistry was used to detect the expressions of tau protein phosphorylation points (Ser 404 and Thr 231). Western blot was used to detect tau protein phosphorylation points and the expression of PI3K/Akt protein. Results Compared with sham-operation group, tau protein phosphorylation points in the model group increased (P<0.05), but the phosphorylation levels of PI3K and Akt decreased significantly (P<0.05). Compared with the model group, tau protein phosphorylation (Thr231 and Ser404) inWenyujin essential oil high-dose group decreased significantly (P<0.05), and the phosphorylation levels of PI3K and Akt increased(P<0.01). ConclusionWenyujinessential oil can inhibit tau protein phosphorylation in mice. The possible mechanism may be related to the PI3K/Akt signal pathway.%目的：观察温郁金挥发油对阿尔茨海默病（AD）模型小鼠 tau 蛋白磷酸化的影响，探讨其相关作用机制。方法60只昆明种小鼠随机分为假手术组、模型组、温郁金挥发油低剂量组、温郁金挥发油高剂量组、盐酸多奈哌齐组和参枝苓组，海马组织注射 Aβ25-35制作 AD 小鼠模型，各给药组给予相应药物灌胃，连续15 d。末次给药后，免疫组化检测小鼠tau蛋白磷酸化位点（Ser 404和Thr 231）的蛋白表达，Western blot检测tau蛋白磷酸化位点及磷脂酰肌醇-3-激酶信号/蛋白激酶B（PI3K/Akt）的蛋白表达。结果与假手术组比较，模型组tau蛋白磷酸化位点蛋白表达增加（P＜0.05），PI3K及Akt磷酸化水平明显降低（P＜0.05）；与模型组比较，温郁金挥发油高剂量组tau蛋白（Thr231和Ser404）磷酸化水平明显降低（P＜0.05），PI3K及Akt磷酸化水平明显增加（P＜0.05，P＜0.01）。结论温郁金挥发油可降低模型小鼠tau蛋白磷酸化水平，其作用机制可能与PI3K/Akt信号途径有关。
展开▼
