| Autor: |
Zhang Y; Research Institute for Marine Drugs and Nutrition, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang 524088, China. zhangyp2015@163.com.; Department of Psychology and Neuroscience, Dalhousie University, Halifax, NS B3H 4R2, Canada. zhangyp2015@163.com., Jiao G; Coastal Zones Research Institute Inc., 232B, avenue de l'Église, Shippagan, NB E8S 1J2, Canada. sebrina2006@gmail.com.; Aquatic and Crop Resource Development, National Research Council of Canada, 1411 Oxford Street, Halifax, NS B3H 3Z1, Canada. sebrina2006@gmail.com., Song C; Research Institute for Marine Drugs and Nutrition, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang 524088, China. cai.song@dal.ca.; Department of Psychology and Neuroscience, Dalhousie University, Halifax, NS B3H 4R2, Canada. cai.song@dal.ca.; Graduate Institute of Neural and Cognitive Sciences, China Medical University Hospital, Taichung 40402, Taiwan. cai.song@dal.ca., Gu S; Department of Psychology and Neuroscience, Dalhousie University, Halifax, NS B3H 4R2, Canada. xiaomei.gu@dal.ca., Brown RE; Department of Psychology and Neuroscience, Dalhousie University, Halifax, NS B3H 4R2, Canada. Richard.Brown@dal.ca., Zhang J; Aquatic and Crop Resource Development, National Research Council of Canada, 1411 Oxford Street, Halifax, NS B3H 3Z1, Canada. Junzeng.Zhang@nrc-cnrc.gc.ca., Zhang P; Department of Psychology and Neuroscience, Dalhousie University, Halifax, NS B3H 4R2, Canada. pczhang2000@yahoo.com., Gagnon J; Coastal Zones Research Institute Inc., 232B, avenue de l'Église, Shippagan, NB E8S 1J2, Canada. jacques.gagnon@umoncton.ca., Locke S; Aquatic and Crop Resource Development, National Research Council of Canada, 550 University Avenue, Charlottetown, PE C1A 4P3, Canada. Steven.Locke@nrc-cnrc.gc.ca., Stefanova R; Aquatic and Crop Resource Development, National Research Council of Canada, 1411 Oxford Street, Halifax, NS B3H 3Z1, Canada. Roumiana.Stefanova@nrc-cnrc.gc.ca., Pelletier C; Coastal Zones Research Institute Inc., 232B, avenue de l'Église, Shippagan, NB E8S 1J2, Canada. Claude.pelletier@umoncton.ca., Zhang Y; Research Institute for Marine Drugs and Nutrition, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang 524088, China. hubeizhangyi@163.com., Lu H; Research Institute for Marine Drugs and Nutrition, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang 524088, China. irislhy@126.com. |
| Abstrakt: |
Increased evidence suggests that marine unsaturated fatty acids (FAs) can protect neurons from amyloid-β (Aβ)-induced neurodegeneration. Nuclear magnetic resonance (NMR), high performance liquid chromatography (HPLC) and gas chromatography (GC) assays showed that the acetone extract 4-2A obtained from shrimp Pandalus borealis industry processing wastes contained 67.19% monounsaturated FAs and 16.84% polyunsaturated FAs. The present study evaluated the anti-oxidative and anti-inflammatory effects of 4-2A in Aβ 25-35 -insulted differentiated SH-SY5Y cells. Cell viability and cytotoxicity were measured by using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and lactate dehydrogenase (LDH) assays. Quantitative PCR and Western blotting were used to study the expression of neurotrophins, pro-inflammatory cytokines and apoptosis-related genes. Administration of 20 μM Aβ 25-35 significantly reduced SH-SY5Y cell viability, the expression of nerve growth factor (NGF) and its tyrosine kinase TrkA receptor, as well as the level of glutathione, while increased reactive oxygen species (ROS), nitric oxide, tumor necrosis factor (TNF)-α, brain derived neurotrophic factor (BDNF) and its TrkB receptor. Aβ 25-35 also increased the Bax/Bcl-2 ratio and Caspase-3 expression. Treatment with 4-2A significantly attenuated the Aβ 25-35 -induced changes in cell viability, ROS, GSH, NGF, TrkA, TNF-α, the Bax/Bcl-2 ratio and Caspase-3, except for nitric oxide, BDNF and TrKB. In conclusion, 4-2A effectively protected SH-SY5Y cells against Aβ-induced neuronal apoptosis/death by suppressing inflammation and oxidative stress and up-regulating NGF and TrKA expression. |
