Lotus seedpod proanthocyanidins protect against neurotoxicity after methyl-mercuric chloride injury.

In the present study, to investigate the prevention mechanism of proanthocyanidins from lotus seedpod (LSPCs) on methyl mercuric chloride (MMC) induced neurotoxicity, neuron/astrocyte cells were co-cultured to simulate the microenvironment in vivo to the greatest extent. The results showed that, compared with MMC group, pretreatment with LSPCs not only improved cell survival rate, decreased the release of lactate dehydrogenase (LDH), decreased the intracellular reactive oxygen species (ROS) level, and prevented the increase of intracellular [Ca2+]i, but also significantly increased the total anti-oxidation capacity (T-AOC) (p＜0.05), the levels of glutathione peroxidase (GSH-Px) (p＜0.05), glutathione (GSH) (p＜0.05), and mitochondrial membrane potential (MMP) (p＜0.01). Besides, LSPCs up-regulated the expression of transcriptional factor Nrf2/HO-1 in a concentration-dependent manner. Moreover, LSPCs reduced the expression of Bax protein, significantly increased the expression of Bcl-xl, Bcl-2, β-Ⅲ-Tubulin, SYN, and Arc proteins. The expression of these proteins is mainly regulated by genes and reflects the changes of genes functions. Taken together, these results suggested that LSPCs could enhance cellular antioxidant defense capacity through regulating the activation of Nrf2/HO-1, and involving the inhibition of mitochondria-mediated apoptotic signaling pathway.