Beta-Asarone Reduces Autophagy in a Dose-Dependent Manner and Interferes with Beclin 1 Function

Beta-asarone, extracted from Acorus tatarinowii Schott, has significant pharmacological effects on the central nervous system (CNS). Beta-asarone can pass through the blood–brain barrier and then enter into the brain. The absorption, distribution, and elimination of beta-asarone are rapid and it is found in low accumulations in the body. Brain is an important organ of distribution. Beta-asarone is quickly excreted in urine, feces, and bile, but the excretion efficiency in urine is the highest. Beta-asarone could attenuate neuronal autophagy. We examined effects of gradient concentrations of beta-asarone on autophagy and found that a high dose has a stronger effect than that of a low dose. Beta-asarone reduces autophagy in a dose-dependent manner. In view of the close relationship between Beclin 1 and autophagy, we found that beta-asarone interfered with Beclin 1 function. Our studies on the mechanism by which beta-asarone attenuates autophagy indicate that it is likely that beta-asarone can modulate JNK, p-JNK, Bcl-2, and Beclin 1. Also, autophagy induced by increased intracellular free calcium concentration ([Ca 2+ ] i ) and decreased mitochondrial membrane potential (MMP) in oxygen-glucose deprivation and reperfusion (OGD/R)-treated PC12 cells was detected. Beta-asarone significantly increased cell viability and MMP, and improved cellular morphology but decreased Beclin 1 and [Ca 2+ ] i . Along with the development of research, more and more mechanisms of beta-asarone are being found in relation to the regulation of autophagy. This helps us to understand more deeply the significance of beta-asarone in treatment of disease.