Impact of High Fat Consumption on Neurological Functions after Traumatic Brain Injury in Rats
Impact of High Fat Consumption on Neurological Functions after Traumatic Brain Injury in Rats
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DOI：
10.1089/neu.2022.0080
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发表时间：
2022-07-14
影响因子：
4.2
通讯作者：
Chen，Hui
中科院分区：
文献类型：
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作者：
Thomson，Shannon;Chan，Yik Lung;Chen，Hui
创伤性脑损伤（TBI）和肥胖是现代社会常见的两种疾病；两者都会损害神经元完整性和神经功能。然而，目前尚不清楚这两种情况的共存是否会使结果恶化。因此，在大鼠模型中，我们旨在研究TBI和高脂肪饮食（HFD）共存是否具有累加效应，导致更严重的神经损伤，以及它们是否与氧化应激、炎症和突触可塑性等脑蛋白标志物的变化有关。sd - dawley大鼠（雌性，~ 250 g）分为HFD（43%脂肪）组和CD（17%脂肪）组，持续6周。在每个饮食组中，一半的人接受了减肥装置的创伤性脑损伤，另一半接受了假手术。分别于创伤后24小时、1周、3周和6周测量短期记忆和感觉功能。分别于脑损伤后24小时和6周采集脑组织，通过免疫染色和Western blotting检测氧化应激、细胞凋亡、炎症和突触可塑性标志物。在没有TBI的大鼠中，HFD增加了突触前蛋白synaptophysin。在TBI大鼠中，HFD导致感觉和记忆功能恶化，活化巨噬细胞增加，内源性抗氧化剂锰超氧化物歧化酶（MnSOD）降低。我们的研究结果表明，HFD和TBI的叠加效应加重了短期记忆和感觉缺陷，这可能是由氧化应激和炎症增强所驱动的。
Traumatic brain injury (TBI) and obesity are two common conditions in modern society; both can impair neuronal integrity and neurological function. However, it is unclear whether the coexistence of both conditions will worsen outcomes. Therefore, in a rat model, we aimed to investigate whether the coexistence of TBI and a high-fat diet (HFD) has an additive effect, leading to more severe neurological impairments, and whether they are related to changes in brain protein markers of oxidative stress, inflammation, and synaptic plasticity. Sprague–Dawley rats (female, ∼250 g) were divided into HFD (43% fat) and diet (CD) (17% fat) groups for 6 weeks. Within each dietary group, half underwent a TBI by a weight-drop device, and the other half underwent sham surgery. Short-term memory and sensory function were measured at 24 h, 1 week, 3 weeks, and 6 weeks post-TBI. Brain tissues were harvested at 24 h and 6 weeks post-TBI, and markers of oxidative stress, apoptosis, inflammation, and synaptic plasticity were measured via immunostaining and Western blotting. In rats without TBI, HFD increased the pre-synaptic protein synaptophysin. In rats with TBI, HFD resulted in worsened sensory and memory function, an increase in activated macrophages, and a decrease in the endogenous antioxidant manganese superoxide dismutase (MnSOD). Our findings suggest that the additive effect of HFD and TBI worsens short term memory and sensation deficits, and may be driven by enhanced oxidative stress and inflammation.