Oxymatrine attenuates amyloid beta 42 (Aβ1-42)-induced neurotoxicity in primary neuronal cells and memory impairment in rats

Amyloid beta 42 (A beta(1-42))-induced oxidative stress causes the death of neuronal cells and is involved in the development of Alzheimer's disease. Oxymatrine (OMT) inhibits oxidative stress. In this study, we investigated the effect of OMT on A beta(1-42)-induced neurotoxicity in vivo and in vitro. In the Morris water maze test, OMT significantly decreased escape latency and increased the number of platform crossings. In vitro, OMT markedly increased cell viability and superoxide dismutase activity. Moreover, OMT decreased lactate dehydrogenase leakage, malondialdehyde content, and reactive oxygen species in a dosedependent manner. OMT upregulated the ratio of Bcl-2/Bax and downregulated the level of caspase-3. Furthermore, OMT inhibited the activation of MAP kinase (ERK 1/2, JNK) and nuclear factor kappa B. In summary, OMT may potentially be used in the treatment of Alzheimer's disease.