Special Issue Article
Swapnil Pandey and Puneet Sing
Abstract
Betula utilis (BU), an important medicinal plant that grows in high altitudes of the Himalayan region, has been utilized traditionally due to its antibacterial, hepatoprotective, and anti-tumor properties. Here, we demonstrated the lifespan promoting and amyloid-β-induced toxicity attenuating activity of B. utilis ethanolic extract (BUE) in a multicellular model organism, i.e., Caenorhabditis elegans. Our results showed that BUE (50µg/ml) extended the mean lifespan of C. elegans by 35.99% and increased its survival under both oxidative and thermal stress conditions. The BUE (50µg/ml) also reduced the levels of intracellular reactive oxygen species (ROS) by 22.47%. The BUE treatment significantly improved the survival of human amyloid-β (Aβ) expressing CL4176 worms in response to proteotoxic stress induced by Aβ protein aggregation. Interestingly, the BUE (50 μg/ml) supplementation was also able to reduce the aggregation of Parkinson’s related protein, α-synuclein in the transgenic strain NL5901 and improved chemotactic behavior in wild-type C. elegans. Moreover, the BUE-mediated lifespan extension was found to be dependent on mev-1, daf-16, hsf-1, and skn-1 but not on sir-2.1 gene. Transgenic reporter gene expression assay showed that BUE (50µg/ml) treatment enhanced the expression of stress protective genes such as sod-3 and gst-4. The present findings suggested that ROS scavenging activity together with multiple longevity mechanisms were involved in BUE-mediated lifespan extension. Thus, BUE might have a potential to increase lifespan and to attenuate neuro-related disease progression.