Jin Ai, Shi Xiao-Chen, Deng Wei, Sun Jian, Ji Hong
College of Animal Science and Technology, Northwest A&F University, Yangling, 712100, People's Republic of China.
Fish Physiol Biochem. 2019 Jun;45(3):1091-1099. doi: 10.1007/s10695-019-00623-8. Epub 2019 Mar 21.
Our previous study has shown that overload of lipid accumulation results in cell apoptosis and inflammation in grass carp (Ctenopharyngodon idella). In this study, we investigated the potential protective effects of docosahexaenoic acid (DHA) on inhibiting oleic acid (OA)-induced apoptosis and inflammation in grass carp hepatocytes. Firstly, the hepatocyte of grass carp were treated with OA (800 μM) and different concentration (0, 50, 100 and 200 μM) of DHA for 24 h, the apoptotic ratio, gene expression levels of apoptosis such as caspase 3, caspase 8, and caspase 9, protein levels of Caspase3, and mRNA levels of inflammation genes such as nf-kb, tnf-α, and il-8 were detected. Furthermore, the mRNA levels of lipogenesis genes srebp1c, fas, acc, and scd and a key enzyme of lipolysis Atgl were also detected. These results showed that the cell apoptosis and the inflammation increased by OA were significantly attenuated by DHA (P < 0.05). Furthermore, DHA could significantly decrease fatty acid synthesis gene expression levels which were induced by OA (P < 0.05). However, the hepatocytes exposed with DHA had no significant influence on the expression of Atgl. Taken together, the study indicated that DHA protects the hepatocytes against apoptosis and inflammation induced by OA might via inhibiting fatty acid synthesis, instead of promoting lipolysis. These results call for further studies to assess the effectiveness of DHA.
我们之前的研究表明,脂质积累过载会导致草鱼(Ctenopharyngodon idella)细胞凋亡和炎症。在本研究中,我们调查了二十二碳六烯酸(DHA)对抑制油酸(OA)诱导的草鱼肝细胞凋亡和炎症的潜在保护作用。首先,用OA(800 μM)和不同浓度(0、50、100和200 μM)的DHA处理草鱼肝细胞24小时,检测凋亡率、凋亡相关基因如caspase 3、caspase 8和caspase 9的基因表达水平、Caspase3的蛋白水平以及炎症基因如nf-kb、tnf-α和il-8的mRNA水平。此外,还检测了脂肪生成基因srebp1c、fas、acc和scd以及脂解关键酶Atgl的mRNA水平。这些结果表明,DHA显著减轻了OA诱导的细胞凋亡和炎症(P < 0.05)。此外,DHA可显著降低OA诱导的脂肪酸合成基因表达水平(P < 0.05)。然而,DHA处理的肝细胞对Atgl的表达没有显著影响。综上所述,该研究表明DHA可能通过抑制脂肪酸合成,而非促进脂解,来保护肝细胞免受OA诱导的凋亡和炎症。这些结果需要进一步研究来评估DHA的有效性。