NANJING, China—Ginsenoside Rb1 may protect the brain from autophagy induced by certain neurotoxins (Neurosci Lett. ePub 26 July 2010. DOI: 10.1016/j.neulet.2010.07.052). Researchers from the Nanjing University School of Medicine aimed to determine the mechanism of action behind ginsenoside Rb1’s demonstrated neuroprotective effects. In particular, the focus was on the activation of autophagy in injured neurons; this catabolic process involves the lysosomal degradation of certain intracellular components.
Different concentrations of ginsenoside Rb1 (1.2, 12 or 120 μM) or the autophagy inhibitor 3-methyladenine (5 mM) were added to culture medium for cortical neurons after they were treated with glutamate. Glutamate alone activated autophagy in the cells and increased levels of beclin-1, an autophagy-related gene. The research team found ginsenoside Rb1 not only protected the neurons from glutamate-induced cell injury, but also attenuated the formation of autophagosome and decreased the levels of beclin-1 compared to cells treated with glutamate alone.
