Institute for Behavioral Medicine Research, The Ohio State University, Columbus, OH, USA; Biomedical Sciences Graduate Program, The Ohio State University, Columbus, OH, USA; Department of Neuroscience, The Ohio State University, Columbus, OH, USA.
Institute for Behavioral Medicine Research, The Ohio State University, Columbus, OH, USA.
Brain Behav Immun. 2024 Feb;116:385-401. doi: 10.1016/j.bbi.2023.12.028. Epub 2023 Dec 23.
Post-operative cognitive dysfunction (POCD) is an abrupt decline in neurocognitive function arising shortly after surgery and persisting for weeks to months, increasing the risk of dementia diagnosis. Advanced age, obesity, and comorbidities linked to high-fat diet (HFD) consumption such as diabetes and hypertension have been identified as risk factors for POCD, although underlying mechanisms remain unclear. We have previously shown that surgery alone, or 3-days of HFD can each evoke sufficient neuroinflammation to cause memory deficits in aged, but not young rats. The aim of the present study was to determine if HFD consumption before surgery would potentiate and prolong the subsequent neuroinflammatory response and memory deficits, and if so, to determine the extent to which these effects depend on activation of the innate immune receptor TLR4, which both insults are known to stimulate. Young-adult (3mo) & aged (24mo) male F344xBN F1 rats were fed standard chow or HFD for 3-days immediately before sham surgery or laparotomy. In aged rats, the combination of HFD and surgery caused persistent deficits in contextual memory and cued-fear memory, though it was determined that HFD alone was sufficient to cause the long-lasting cued-fear memory deficits. In young adult rats, HFD + surgery caused only cued-fear memory deficits. Elevated proinflammatory gene expression in the hippocampus of both young and aged rats that received HFD + surgery persisted for at least 3-weeks after surgery. In a separate experiment, rats were administered the TLR4-specific antagonist, LPS-RS, immediately before HFD onset, which ameliorated the HFD + surgery-associated neuroinflammation and memory deficits. Similarly, dietary DHA supplementation for 4 weeks prior to HFD onset blunted the neuroinflammatory response to surgery and prevented development of persistent memory deficits. These results suggest that HFD 1) increases risk of persistent POCD-associated memory impairments following surgery in male rats in 2) a TLR4-dependent manner, which 3) can be targeted by DHA supplementation to mitigate development of persistent POCD.
术后认知功能障碍(POCD)是指手术后不久出现的神经认知功能突然下降,并持续数周至数月,增加了痴呆诊断的风险。高龄、肥胖以及与高脂肪饮食(HFD)消费相关的合并症,如糖尿病和高血压,已被确定为 POCD 的危险因素,尽管其潜在机制尚不清楚。我们之前已经表明,单独手术或 3 天的 HFD 都可以引起足够的神经炎症,导致老年但不是年轻大鼠的记忆缺陷。本研究的目的是确定 HFD 在手术前的消费是否会增强和延长随后的神经炎症反应和记忆缺陷,如果是这样,确定这些影响在多大程度上取决于先天免疫受体 TLR4 的激活,这两种刺激物都已知会刺激 TLR4。年轻成年(3 个月)和老年(24 个月)雄性 F344xBN F1 大鼠在假手术或剖腹手术后立即接受标准饲料或 HFD 喂养 3 天。在老年大鼠中,HFD 和手术的组合导致情景记忆和提示性恐惧记忆的持续缺陷,尽管确定 HFD 本身足以引起持久的提示性恐惧记忆缺陷。在年轻成年大鼠中,HFD + 手术仅引起提示性恐惧记忆缺陷。接受 HFD + 手术的年轻和老年大鼠海马中的促炎基因表达升高至少在手术后 3 周后仍持续存在。在另一个实验中,大鼠在 HFD 开始前立即给予 TLR4 特异性拮抗剂 LPS-RS,这改善了 HFD + 手术相关的神经炎症和记忆缺陷。同样,在 HFD 开始前 4 周补充 DHA 饮食可减轻手术引起的神经炎症反应,并防止持续记忆缺陷的发生。这些结果表明,HFD 1)增加了雄性大鼠手术后持续 POCD 相关记忆障碍的风险,2)以 TLR4 依赖性方式,3)可以通过 DHA 补充来靶向减轻持续 POCD 的发展。