Neuroprotective Activity of Beetroot (Beta vulgaris) Extract on H2O2-Induced Damage in IMR32 and SHSY5Y Cell Lines

Abstract

In several ailments, oxidative stress intercedes cell damage, including neuro-degenerative conditions. This study aims to ascertain the protective ability of methanol extract of beetroot (Beta vulgaris) as a neuroprotective agent, through the biochemical perspective of neuroprotection. Oxidative stress was induced using hydrogen peroxide (H2O2) in neuroblastoma IMR32 and SHSY5Y cell line. MTT assay was performed to assess cell viability. IMR32 and SHSY5Y cell-line were pre and post-treated with four doses of beetroot extract. It was observed that cells recovered in a dose-dependent manner. This indicated that beetroot treatment facilitate the cells to recover from hydrogen peroxide insult. The result for LDH indicated that with increase in time at higher concentration SHSY5Y cell gets stressed and releases the LDH. Catalase activity in IMR32 and SHSY5Y cells decreases at higher concentrations and increases with a decrease in concentration. IMR32 and SHSY5Y cell lysate showed no activity of acetylcholinesterase. However, the media in which the cells were grown showed the activity of acetylcholinesterase. The biochemical assay showed that beetroot extract mitigates the cells from oxidative insult. Our study suggests that beetroot extract helps in the proliferation and neuroprotection of IMR 32 and SHSY5Y cells. IMR32 and SHSY5Y neuroblastoma cell lines were used to assess neuroprotective efficacy of beetroot extract when the cells were subjected to oxidative insult. In the current study, MTT assay was used to determine the cell viability after the treatments. Biochemical assays viz. LDH, Catalase and specific activity acetylcholine esterase were performed to define neuroprotective property of beetroot extract. Results from cell viability assay confirmed the ability of beetroot extract to enable cell proliferation. Biochemical assays also showed a striking result that beetroot extract protected the cells from oxidative insult.