D-limonene protects PC12 cells against corticosterone-induced neurotoxicity by activating the AMPK pathway

Publication date: Available online 2 May 2019Source: Environmental Toxicology and PharmacologyAuthor(s): Xue-ping Tang, Xiao-hua Guo, Di Geng, Lian-Jin WengAbstractThe stress-induced hormone corticosterone initiates oxidative stress and inflammatory responses, culminating in cell apoptosis and neurological changes. We assessed the effects of d-limonene on a PC12 cellular model of corticosterone-induced neurotoxicity, and whether these effects involved the AMP-activated protein kinase (AMPKα) pathway. PC12 cells were treated with corticosterone with or without d-limonene for 24 h. Western blots were performed to measure activation of AMPK pathway members [Silent mating type information regulation 2 homolog-1 (SIRT1), AMPKα, and nuclear factor (NFκB)], reactive oxygen species, inflammatory cytokines, and markers of apoptosis. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) was used to measure cell death after treatment. d-limonene reversed the effects of corticosterone on PC12 cells: it decreased the levels of malondialdehyde (MDA) and nitric oxide (NO), activities of NADPH oxidase (p67-phox and p47-phox), expression of pro-inflammatory markers [inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin 6 (IL-6), interleukin 1β (IL-1β), and tumor necrosis factor α (TNF-α)], and expression of pro-apoptotic proteins [Bcl2 associated with X protein (Bax) and cleaved caspase-3)]. d-limonene also increased levels of th...
Source: Environmental Toxicology and Pharmacology - Category: Environmental Health Source Type: research