Oxymatrine mediated prevention of amyloid β-peptide induced apoptosis on Alzheimer's model PC12 cells an in vitro cell culture studies and in vivo cognitive assessment in rats

Abstract

Abstract Alzheimer’s disease (AD) is a major neurological disease affecting elder people worldwide. Existing drugs only reduce the symptoms of the disease. Commonly, Aβ25–35 peptide aggregation is the main reason for AD development. Recently, the discovery of multiple protein-targeting molecules is a new strategy for AD treatment. This study demonstrates the neuroprotective potential of oxymatrine against multiple mechanisms like acetylcholinesterase, mitochondrial damage, and β-amyloid induced cell toxicity. The in vitro cell culture studies showed that oxymatrine possesses significant potential in the inhibition of the Acetylcholine esterase enzyme. Treatment of oxymatrine enhanced the antioxidant, antiapoptotic, and Aβ25–35 peptide aggregation prevention mechanism in PC12 cells. Furthermore, oxymatrine has the competence to protect the PC12 cells against Aβ25–35 induced cytotoxicity and down-regulates the ROS generation. The in vivo acute toxicological studies confirmed that the oxymatrine did not induce any organ damage or death in test animal groups. Overall, the study evidenced that, oxymatrine as an efficient neuroprotective agent, might be a multifunctional drug for Alzheimer’s disease treatment. We believed that this is a reliable and synergistic approach to Alzheimer’s treatment strategy.