Luo Wenli, Li Li, Xu Weina, Zhang Jing, Xu Jianxiong
Shanghai Key Laboratory of Veterinary Biotechnology, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, China.
Toxics. 2021 May 20;9(5):112. doi: 10.3390/toxics9050112.
The cytotoxicity of docosahexaenoic acid (DHA) on normal cells is still unclear. This study investigated the effects of DHA on the cytotoxicity and possible mechanism in the BRL-3A cell. The cultured rat liver BRL-3A cell line was treated with 50, 100 and 200 μM DHA for 24 h. The cell viability was increased in the 50 and 100 μM DHA treatments, but decreased in the 200 μM DHA treatment. The 50, 100 and 200 μM DHA treatments increased the proportion of the apoptotic cells, the levels of lactate dehydrogenase (LDH), alkaline phosphatase (AKP) and IL-6 in the supernatant, and the ratio of the phosphonated p38MAPK to the p38MAPK (p-p38/p38) protein in the cells. The expression of TGF beta-activated kinase 1 (TAK1), nuclear transcription factor-κB p65 (NF-κB p65) and the inhibitor of NF-κB alpha (IκBα) mRNA, and the ratio of the phosphonated IκBα (p-IκBα) to IκBα protein were increased in the 200 μM DHA treatment, while the ratio of phosphonated extracellular regulated protein kinases (p-ERK) to ERK protein was decreased in the 200 μM DHA treatment. These results indicate that DHA-treated (50, 100 and 200 μM) BRL-3A cells for 24 h promotes cell apoptosis and inflammatory response, and the p38 MAPK, ERK and NF-κB signal pathways were involved in mediating the apoptosis and inflammatory response.
二十二碳六烯酸(DHA)对正常细胞的细胞毒性仍不明确。本研究调查了DHA对BRL-3A细胞的细胞毒性影响及可能机制。将培养的大鼠肝脏BRL-3A细胞系用50、100和200μM DHA处理24小时。50和100μM DHA处理组细胞活力增加,但200μM DHA处理组细胞活力降低。50、100和200μM DHA处理均增加了凋亡细胞比例、上清液中乳酸脱氢酶(LDH)、碱性磷酸酶(AKP)和IL-6水平以及细胞中磷酸化p38丝裂原活化蛋白激酶(p38MAPK)与p38MAPK(p-p38/p38)蛋白的比值。200μM DHA处理组中,转化生长因子β激活激酶1(TAK1)、核转录因子-κB p65(NF-κB p65)和NF-κBα抑制剂(IκBα)mRNA的表达以及磷酸化IκBα(p-IκBα)与IκBα蛋白的比值增加,而200μM DHA处理组中磷酸化细胞外调节蛋白激酶(p-ERK)与ERK蛋白的比值降低。这些结果表明,24小时用DHA(50、100和200μM)处理BRL-3A细胞可促进细胞凋亡和炎症反应,且p38丝裂原活化蛋白激酶、ERK和NF-κB信号通路参与介导细胞凋亡和炎症反应。