Lycopene protects neuroblastoma cells against oxidative damage via depression of ER stress

Abstract

Lycopene is a pigment derived from tomatoes and other red fruits, and has potent antioxidant and antitumor effects. However, its potential role in alleviating oxidative damage in neuronal cells is not well defined. In this study, we investigated the effects of lycopene on H 2 O 2-induced damage in neuroblastoma cells, as well as the underlying mechanisms. Exposure to H 2 O 2 markedly decreased the viability of SH-SY5Y cells and increased LDH release, both of which were reversed by lycopene pretreatment. Lycopene also ameliorated H 2 O 2-induced damage and reduced the expression of apoptotic markers, such as Bcl-2, Bax, and cleaved caspase 3. In addition, the H 2 O 2-induced oxidative markers, including MDA, 8-OHdG, and protein carbonyls, were also downregulated by lycopene. Exogenous H 2 O 2 activated the GRP78/PERK/eIF2α signaling pathway, which was inhibited by pretreatment with lycopene. Finally, lycopene significantly ameliorated ER stress-induced activation and nuclear translocation of CHOP. Overexpression of CHOP markedly reversed the antiapoptotic effects of lycopene, indicating that it is essential for the latter's protective effects. Taken together, lycopene protects neuroblastoma cells from oxidative stress and ER stress-induced damage by inhibiting the PERK-CHOP signaling pathway, which is a potential therapeutic target in neurodegenerative diseases.

Palmitic acid induces intestinal lipid metabolism disorder, endoplasmic reticulum stress and inflammation by affecting phosphatidylethanolamine content in large yellow croaker Larimichthys crocea

“…We also found that addition of PE down-regulated gene expression related to UPR pathway, leading to relieve ER stress. The result was consistence with the previous study that inhibiting the PERK-CHOP signaling pathway to protect cells from ER stress-induced damage (48). Moreover, PE supplementation could inhibit inflammation induced by PA treatment.…”

Lycopene Treatment Ameliorates Amyloid Plaque Deposition and Memory Impairment in the APP/PS1 Mice

“…For example, several experimental models have demonstrated the anti-oxidative effects of lycopene in both the peripheral and central nervous systems [8][9][10] . Our previous studies proved that lycopene shielded SH-SY5Y cells against oxidative toxicity through decreased endoplasmic reticulum stress [11] . The antineuroin ammatory effect of lycopene has been demonstrated in primary cultured rodent microglia [12,13] .…”

Apocynin exerts neuroprotective effects in fumonisin b1–induced neurotoxicity via attenuation of oxidative stress and apoptosis in an animal model

“…Cell viability is quantitative colorimetric assay to measure the mitochondrial activity of living cells (Ou et al, 2020). Briefly, the cells are observed to reach the 70% confluency, and cells were treated with various concentration (25, 50, 100, 150, 200, and 250 µM) of Fb1 for 24 h at 37 • C. On the other hand, to examine the protective effect of AP against Fb1, the cells were pretreated with AP at different concentrations (25, 50, and 100 µg).…”