LAUSR

In order to investigate the effect of notoginsenoside Rg1 on cognitive function in 5∗FAD mice and the mechanism of Cx43 in improving cognitive function in mice, the methods 5∗FAD mice are selected as experimental animals and normal mice as healthy control. They were divided into three groups: healthy control group (n = 10), disease group (n = 10), and treatment group (n = 10, Panax notoginsenoside Rg 1150 mg/kg/d) for 2 months. Two months later, three groups of mice were subjected to classical water maze and Y-maze to test the cognitive ability of mice, and the correct response times and total response time were recorded. At the end of the cognitive function test, the mice were executed, and the brain tissues were taken. The expression of Cx43 protein and the changes of glial cells and neurons in the brain of the mice were analyzed at the cellular level. After treatment with Panax notoginseng saponin Rg 1150 mg/kg/d, it was found that the escape latency of mice in the treatment group was significantly lower than that in the disease group from the third day of training (P < 0.05); the time spent on the platform quadrant and the number of times crossing the platform in the treated mice were significantly increased, and the difference was statistically significant (P < 0.05); the expression of Cx43 protein in the brain of mice after treatment was significantly higher than that of mice in the disease group (P < 0.05). Conclusion. Panax notoginseng saponin Rg1 can effectively improve the cognitive function of 5∗FAD mice by increasing the secretion of Cx43 protein, thus increasing the reactivity of glial cells and neurons.