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首页> 外文期刊>Comparative Medicine >Dietary Repletion with omega 3 Fatty Acid or with COX Inhibition Reverses Cognitive Effects in F3 omega 3 Fatty-Acid Deficient Mice
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Dietary Repletion with omega 3 Fatty Acid or with COX Inhibition Reverses Cognitive Effects in F3 omega 3 Fatty-Acid Deficient Mice

机译：饮食补充ω3脂肪酸或COX抑制可逆转F3ω3脂肪酸缺乏型小鼠的认知作用。

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Dietary deficiency of omega 3 fatty acid during development leads to impaired cognitive function. However, the effects of multiple generations of omega 3 fatty-acid deficiency on cognitive impairment remain unclear. In addition, we sought to test the hypothesis that the cognitive impairments of omega 3 fatty-acid-deficient mice are mediated through the arachidonic acid cyclooxygenase (COX) pathway. To address these issues, C57BL/6J mice were bred for 3 generations and fed diets either deficient (DEF) or sufficient (SUF) in omega 3 fatty acids. At postnatal day 21, the F3 offspring remained on the dam's diet or were switched to the opposite diet, creating 4 groups. In addition, 2 groups that remained on the dam's diet were treated with a COX inhibitor. At 19 wk of age, spatial-recognition memory was tested on a Y-maze. Results showed that 16 wk of SUF diet reversed the cognitive impairment of F3 DEF mice. However, 16 wk of omega 3 fatty-acid deficient diet impaired the cognitive performance of the F3 SUF mice, which did not differ from that of the F3 DEF mice. These findings suggest that the cognitive deficits after multigenerational maintenance on omega 3 fatty-acid-deficient diet are not any greater than are those after deficiency during a single generation. In addition, treatment with a COX inhibitor prevented spatial-recognition deficits in F3 DEF mice. Therefore, cognitive impairment due to dietary omega 3 fatty-acid deficiency appears to be mediated by the arachidonic acid-COX pathway and can be prevented by 16 wk of dietary repletion with omega 3 fatty acids or COX inhibition.
机译：在发育过程中饮食中ω-3脂肪酸的缺乏会导致认知功能受损。但是，尚不清楚多代ω3脂肪酸缺乏对认知障碍的影响。另外，我们试图检验以下假设：ω-3脂肪酸缺乏小鼠的认知障碍是通过花生四烯酸环加氧酶（COX）途径介导的。为了解决这些问题，将C57BL / 6J小鼠饲养了3代，并喂食了ω3脂肪酸不足（DEF）或足够（SUF）的饮食。在出生后的第21天，F3的后代仍按大坝的饮食或改用相反的饮食，分成4组。此外，用COX抑制剂治疗了仍保留在大坝饮食中的2组。在19周龄时，在Y型迷宫上测试了空间识别记忆。结果显示16周SUF饮食可以逆转F3 DEF小鼠的认知障碍。然而，16周的欧米伽3脂肪酸缺乏饮食会损害F3 SUF小鼠的认知能力，与F3 DEF小鼠的认知能力没有区别。这些发现表明，在多代维持omega 3脂肪酸缺乏饮食后的认知缺陷并没有比单代缺失后的认知缺陷更大。此外，用COX抑制剂治疗可预防F3 DEF小鼠的空间认知缺陷。因此，由于饮食中ω-3脂肪酸缺乏引起的认知障碍似乎是由花生四烯酸-COX途径介导的，并且可以通过饮食中16周的ω-3脂肪酸补充或抑制COX来预防。

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