The protective mechanism of Lycium ruthenicum Murr. polyphenols (LRP) on acrylamide (ACR)-induced oxidative stress injury in SH-SY5Y cells were investigated.The oxidative stress injury model of SH-SY5Y cells was established by ACR, cells were pretreated with LRP.SH-SY5Y cells were divided into control group, ACR group (2.5 mmol/L) and LRP groups (500, 1 000, and 1 500 μg/mL).The cell viability was measured by CCK-8, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) activity were evaluated by biochemical kits, the expression levels of the nuclear factor E2-related factor 2 (Nrf2), glutamate-cysteine ligase catalytic subunit (GCLC), glutamate-cysteine ligase (GCLM), heme oxygenase-1(HO-1), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38), cysteinyl aspartate-specific proteinase-3 (Caspase-3) protein were measured by Western blot.The effects of expression of the above proteins were also observed after small interfering RNA (siRNA) blocking Nrf2 expression.The results showed that after the treatment of LRP, cell viability was increased, the levels of ROS and MDA reduced, SOD and GSH content increased, the expression levels of Nrf2, GCLC, GCLM, and HO-1 protein increased, while the expression levels of JNK, p38, and Caspase-3 protein decreased, the SH-SY5Y cells treated with 1 500 μg/mL LRP had the highest activity and the strongest ability to resist acrylamide-induced oxidative stress injury.After silencing Nrf2 gene expression with siRNA, the expression of Nrf2, GCLC, GCLM, and HO-1 protein decreased, the expression of JNK, p38, and Caspase-3 protein increased.In addition, there were significant differences between LRP group and LRP group with siRNA treated (P<0.05).Our research proved that LRP showed antioxidant and anti-apoptosis biological activities.And LRP can attenuate the toxicity of ACR to SH-SY5Y cells by activating Nrf2 signaling pathway and inhibiting apoptotic proteins JNK, p38, and Caspase-3.
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