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Avocado oil (Persea americana) protects SH‐SY5Y cells against cytotoxicity triggered by cortisol by the modulation of BDNF, oxidative stress, and apoptosis molecules
Journal of Food Biochemistry ( IF 4 ) Pub Date : 2021-01-22 , DOI: 10.1111/jfbc.13596
Jéssica Rosso Motta 1 , Ivo Emilio da Cruz Jung 2 , Verônica Farina Azzolin 1 , Cibele Ferreira Teixeira 2 , Luiza Elizabete Braun 3 , Daniel Augusto De Oliveira Nerys 3 , Marco Aurélio Echart Motano 4 , Marta Maria Medeiros Frescura Duarte 2, 5 , Ednea Aguiar Maia-Ribeiro 6 , Ivana Beatrice Mânica da Cruz 1 , Fernanda Barbisan 1, 2
Affiliation  

Chronic psycho‐environmental stress can induce neurological dysfunction due to an increase in cortisol levels. It is possible that some food supplements could attenuate its negative impact, such as avocado oil (AO), which is rich in fatty acids with beneficial effects on the brain. This hypothesis was tested by an in vitro model using undifferentiated neuroblastoma cells (SH‐SY5Y) exposed to hydrocortisone (HC), an active cortisol molecule with and without AO‐supplementation. Cortisol can induce oxidative stress, apoptosis events, and a lowering effect on brain‐derived neurotrophic factor (BDNF), a neurogenic molecule. As AO protective effects on HC‐exposed cells could involve these routes, some markers of these routes were compared among neuroblastoma cultures. In the first assay, the range concentrations of HC exposure that trigger cell mortality and range AO‐concentrations that could revert the HC effect. AO at all concentrations tested (2–30 µg/ml) did not present a cytotoxic effect on SH‐SY5Y cells, whereas HC at 0.3–10 ng/ml had a dose‐dependent cytotoxic effect on these cells. From these results, HC at 10 ng/ml and AO at 5 µg/ml were chosen for mechanistic analysis. AO was able to decrease the oxidative molecules; however, both AO‐ and HC‐induced differential and varied gene expression modulation of these enzymes. AO partially reverted the protein and gene expression of apoptotic markers that were higher in HC‐exposed cells. AO also increases the BDNF levels, which are lower HC‐exposed cultures. The results indicate that AO could be a beneficial supplement in situations where cortisol levels are elevated, including chronic psycho‐environmental stress.

中文翻译:

鳄梨油(Persea americana)通过调节BDNF,氧化应激和凋亡分子来保护SH‐SY5Y细胞免受皮质醇触发的细胞毒性

长期的心理环境压力会由于皮质醇水平的升高而诱发神经功能障碍。某些食品补充剂可能会减轻其负面影响,例如鳄梨油(AO),富含脂肪酸,对大脑有益。通过使用暴露于氢化可的松(HC)的未分化神经母细胞瘤细胞(SH‐SY5Y)的体外模型验证了这一假设,氢化可的松是一种有或没有AO补充的活性皮质醇分子。皮质醇可以诱导氧化应激,细胞凋亡事件,并降低对脑源性神经营养因子(BDNF)的作用。由于AO对暴露于HC的细胞的保护作用可能涉及这些途径,因此在神经母细胞瘤培养物中比较了这些途径的一些标记。在第一个分析中 触发细胞死亡的HC暴露浓度范围和可以逆转HC效应的AO浓度范围。在所有测试浓度(2–30 µg / ml)下,AO对SH‐SY5Y细胞均无细胞毒性作用,而0.3–10 ng / ml HC对这些细胞具有剂量依赖性细胞毒性作用。从这些结果中,选择10 ng / ml的HC和5 µg / ml的AO进行机理分析。AO能够还原氧化分子。但是,AO和HC均可诱导这些酶的差异表达和变异基因表达调控。AO部分还原了暴露于HC的细胞中凋亡标记物的蛋白质和基因表达。AO还增加了BDNF含量,这是较低的HC暴露培养物。结果表明,在皮质醇水平升高的情况下,AO可能是有益的补充,
更新日期:2021-02-22
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