We previously found that fish oil (FO) facilitated memory recovery in the absence of pyramidal neuron rescue after transient, global cerebral ischemia (TGCI). Fish oil preserved the expression of microtubule-associated protein 2 (MAP-2), suggesting a relationship between dendritic plasticity and memory recovery that is mediated by FO after TGCI. The present study examined whether postischemic treatment with FO prevents ischemia-induced loss of dendritic processes in remaining pyramidal neurons. The effects of FO on neuroplasticity-related proteins were also examined after TGCI. Rats were subjected to TGCI (15 min, four-vessel occlusion model) and then received vehicle or FO (300 mg/kg docosahexaenoic acid) once daily for 7 days. The first dose was administered 4 h postischemia. Golgi-Cox staining was used to evaluate dentrict morphology in the pyramidal neurons of hippocampus (CA1 and CA3 subfields) and prefrontal cortex (PFC). Neuronal nuclei protein (NeuN), brain-derived neurotrophic factor (BDNF), growth-associated protein 43 (GAP-43), synaptophysin (SYP), and postsynaptic density protein 95 (PSD-95) levels were measured by Western blot in both structures. Fifteen minutes of TGCI reduced consistently the length of dendrites, number of dendritic branches and dendritic spine density (average of 25%, 43%, 32%, respectively) 7, 14, and 21 days postischemia, indicating that they did not recover spontaneously. This outcome of TGCI was reversed by FO treatment, an effect that was sustained even after treatment cessation. The NeuN and BDNF protein levels were reduced in both the hippocampus and PFC, which were recovered by FO treatment. GAP-43 protein levels decreased after ischemia in the PFC only, and this effect was also mitigated by FO. Neither SYP nor PSD-95 levels were altered by ischemia, but PDS-95 levels almost doubled after FO treatment in the ischemic group. These data support our hypothesis that synaptic plasticity at the level of dendrites may at least partially underlie the memory-protective effect of FO after TGCI and strengthen the possibility that FO has therapeutic potential for treating the sequelae of brain ischemia/reperfusion injury.

中文翻译：

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缺血后鱼油治疗可在大鼠短暂的全脑缺血后恢复树突完整性和突触蛋白水平

我们以前发现鱼油 (FO) 在短暂的全脑缺血 (TGCI) 后没有锥体神经元救援的情况下促进记忆恢复。鱼油保留了微管相关蛋白 2 (MAP-2) 的表达，表明树突可塑性与 TGCI 后由 FO 介导的记忆恢复之间存在关系。本研究检查了用 FO 进行缺血后治疗是否可以防止缺血引起的剩余锥体神经元中树突状突起的丢失。TGCI 后还检查了 FO 对神经可塑性相关蛋白的影响。大鼠接受 TGCI（15 分钟，四血管闭塞模型），然后每天一次接受载体或 FO（300 毫克/千克二十二碳六烯酸），持续 7 天。第一次给药是在缺血后 4 小时给药。Golgi-Cox 染色用于评估海马锥体神经元（CA1 和 CA3 亚区）和前额叶皮层 (PFC) 的牙体形态。通过蛋白质印迹法测量神经元核蛋白 (NeuN)、脑源性神经营养因子 (BDNF)、生长相关蛋白 43 (GAP-43)、突触素 (SYP) 和突触后密度蛋白 95 (PSD-95) 水平结构。15 分钟的 TGCI 持续降低树突长度、树突分支数量和树突棘密度（分别为 25%、43%、32% 的平均值）在缺血后 7、14 和 21 天，表明它们没有自发恢复。TGCI 的这一结果被 FO 治疗逆转，这种效果即使在治疗停止后也能持续。海马体和 PFC 中的 NeuN 和 BDNF 蛋白水平降低，通过 FO 处理恢复。仅在 PFC 缺血后 GAP-43 蛋白水平降低，这种影响也被 FO 减轻。SYP 和 PSD-95 水平均未因缺血而改变，但缺血组中的 FO 治疗后 PDS-95 水平几乎翻了一番。这些数据支持我们的假设，即树突水平的突触可塑性可能至少部分是 TGCI 后 FO 的记忆保护作用的基础，并加强了 FO 具有治疗脑缺血/再灌注损伤后遗症的治疗潜力的可能性。