Abstract: Objective To explore the mechanism of notoginsenoside Rg1 in preventing and treating Alzheimer′s disease (AD). Methods Rat model of AD was established by injecting amyloid beta peptide 1-42(Aβ1-42) into the lateral ventricle of SD rats. Then the animals were randomly divided into three groups: sham-operated group, model group and Rg1 treatment group. The treatment group was treated with Rg1 gavage and the sham-operated group was treated with saline gavage. Learning and memory capacity of rats were examined by Morris water maze experiment (MWM). Moreover, the contents of MDA and SOD in cerebral cortex were detected by chemical colorimetry; immuno-histochemistry was used to detect caspase-3 protein in the cerebral cortex and Western blot was employed to detect the expression of p38 and p-p38 proteins. Results Compared with the sham-operated group, the model group had a prolonged escape latency, reduced stay time in the target quadrant and reduced frequency of leaping over platform; increased MDA and decreased SOD in cerebral cortex; increased caspase-3 protein-positive neurons. The difference of p38 expression was not statistically significant and the phosphorylation of p38 was upregulated(P＜0.05). The rats in Rg1 treatment group had a shorter escape latency, increased stay time in quadrant Ⅲ, increased frequency of leaping over platform, decreased caspase-3 positive neurons and the phosphorylation level of p38,decreased MDA and increased SOD compared with the model group(P＜0.05). Conclusions Rg1 significantly improves learning and memory capacities, increases antioxidant capacity and plays neuro-protective effect in AD rat model by inhibition of p38 activation.

Key words: notoginsenoside Rg1, p38, cell apoptosis, nervous system