Dietary menhaden fish oil supplementation suppresses lipopolysaccharide-induced neuroinflammation and cognitive impairment in diabetic rats.

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
ACS Applied Electronic Materials Pub Date : 2024-12-01 Epub Date: 2024-05-16 DOI:10.1080/13880209.2024.2351933
Nurina Titisari, Ahmad Fauzi, Intan Shameha Abdul Razak, Mohd Hezmee Mohd Noor, Nurdiana Samsulrizal, Hafandi Ahmad
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Abstract

Context: Menhaden fish oil (FO) is widely recognized for inhibiting neuroinflammatory responses and preserving brain function. Nevertheless, the mechanisms of FO influencing brain cognitive function in diabetic states remain unclear.

Objective: This study examines the potential role of FO in suppressing LPS-induced neuroinflammation and cognitive impairment in diabetic animals (DA).

Materials and methods: Thirty male Wistar rats were divided into 5 groups: i) DA received LPS induction (DA-LPS); ii) DA received LPS induction and 1 g/kg FO (DA-LPS-1FO); iii) DA received LPS induction and 3 g/kg FO (DA-LPS-3FO); iv) animals received normal saline and 3 g/kg FO (NS-3FO) and v) control animals received normal saline (CTRL). Y-maze test was used to measure cognitive performance, while brain samples were collected for inflammatory markers and morphological analysis.

Results: DA received LPS induction, and 1 or 3 g/kg FO significantly inhibited hyperglycaemia and brain inflammation, as evidenced by lowered levels of pro-inflammatory mediators. Additionally, both DA-LPS-1FO and DA-LPS-3FO groups exhibited a notable reduction in neuronal damage and glial cell migration compared to the other groups. These results were correlated with the increasing number of entries and time spent in the novel arm of the Y-maze test.

Discussion and conclusion: This study indicates that supplementation of menhaden FO inhibits the LPS signaling pathway and protects against neuroinflammation, consequently maintaining cognitive performance in diabetic animals. Thus, the current study suggested that fish oil may be effective as a supporting therapy option for diabetes to avoid diabetes-cognitive impairment.

补充黑线鳕鱼油能抑制脂多糖诱导的糖尿病大鼠神经炎症和认知障碍。
背景:人们普遍认为孟加拉鱼油(FO)可抑制神经炎症反应并保护大脑功能。然而,FO 影响糖尿病患者大脑认知功能的机制仍不清楚:本研究探讨了鱼油在抑制 LPS 诱导的糖尿病动物(DA)神经炎症和认知障碍中的潜在作用:将 30 只雄性 Wistar 大鼠分为 5 组:①接受 LPS 诱导的 DA(DA-LPS);②接受 LPS 诱导和 1 g/kg FO 的 DA(DA-LPS-1FO);③接受 LPS 诱导和 3 g/kg FO 的 DA(DA-LPS-3FO);④接受正常生理盐水和 3 g/kg FO 的动物(NS-3FO);⑤接受正常生理盐水的对照动物(CTRL)。用Y-迷宫试验测量动物的认知能力,同时采集脑样本进行炎症标记物和形态学分析:结果:接受 LPS 诱导的 DA 和 1 或 3 g/kg FO 能显著抑制高血糖和脑部炎症,这体现在促炎症介质水平的降低。此外,与其他组相比,DA-LPS-1FO 组和 DA-LPS-3FO 组的神经元损伤和胶质细胞迁移均明显减少。这些结果与进入 Y 型迷宫试验新颖臂的次数和时间的增加相关:本研究表明,补充黑线鳕鱼油能抑制 LPS 信号通路,防止神经炎症,从而维持糖尿病动物的认知能力。因此,本研究认为鱼油可作为糖尿病的辅助疗法,有效避免糖尿病导致的认知障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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