动物造模,阿尔茨海默症模型 z-bio 2022-09-28 454

　　Objective To investigate the neuroprotective effect of tanshinone IIA (Tan IIA) on Alzheimer's disease (AD) model mice and its effect on phosphatidylinositol-3-kinase/protein kinase B (PI3K/AKT) pathway.

　　Methods AD mice models were established by intracerebroventricular injection of lipopolysaccharide (LPS). They were randomly divided into model group, Tan IIA low, medium and high dose groups; Tan IIA treatment group was administered intraperitoneally at doses of 1, 5 and 10 mg/kg once a day for 7 consecutive weeks. The behavioral ability of mice in each group was tested (Morris water maze test, Y maze test and autonomic activity test), the pathological changes of brain tissue were observed by HE staining, the contents of brain-derived neurotrophic factor (BDNF), choline system and inflammatory factors in brain tissue homogenate were detected by ELISA, the expression of ionic calcium connector protein (IBA-1) and glial fibrillary acidic protein (GFAP) in brain tissue was detected by immunohistochemistry, and nuclear factor was detected by Western Blot κ B(NF- κ B) The expression of Toll like receptor 4 (TLR4), PI3K and AKT.

　　Results Compared with the blank group, the escape latency, AchE, IL-6, TNF in brain homogenate of model group mice- α, IBA-1, GFAP, p-NF in brain tissue- κ B/ NF- κ B. The level of TLR4 increased significantly (P<0.05), while the free alternative reaction rate, BDNF, Ach, p-PI3K/PI3K, p-AKT/AKT levels decreased significantly (P<0.05); Compared with the model group, Tan IIA treatment group escaped latency, AchE, IL-6, TNF in brain tissue homogenate- α, IBA-1, GFAP, p-NF in brain tissue- κ B/ NF- κ B. The level of TLR4 decreased significantly (P<0.05), and the free alternative reaction rate, BDNF, Ach, p-PI3K/PI3K, p-AKT/AKT levels increased significantly (P<0.05), especially in the high-dose group (P<0.05); there="" was="" no="" significant="" difference="" in="" the="" distance="" of="" autonomous="" activities="" among="" groups="" p="">0.05).

　　Conclusion Tan IIA can protect the nerve damage of AD mice and improve the learning and memory ability, which may be related to activating PI3K/AKT pathway, reducing the inflammatory reaction in the brain, and inhibiting the over activation of microglia and astrocytes.