Objective

The effects of aminoguanidine (AG) were investigated in a rat model of lipopolysaccharide (LPS)-induced anxiety- and depression-like behaviors.

Materials and methods

The animals were allocated to five groups (n = 10 in each) and treated by: (1) saline as a control group, (2) LPS 1 mg/kg injected two hours before behavioral tests, (3–5) AG 50, 100 or 150 mg/kg before LPS. The open-field test (OFT), elevated plus maze test (EPT), and forced swimming (FS) tests were performed. The brains and blood were then collected to examine oxidative stress and inflammation criteria.

Results

LPS increased the immobility while decreased the active time in the FS test. In EPT, LPS decreased the time spent in the open arms, whereas it increased the time spent in the closed arms. In OFT, LPS decreased the time spent in the central zone compared with the controls. A higher dose of selenium improved the performances of the rats in behavioral tests. LPS injection also increased malondialdehyde (MDA) while it decreased thiol, superoxide dismutase (SOD), and catalase. LPS also increased interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-α), but decreased IL-10 in the LPS group. AG protected the brain from inflammation and oxidative damage.

Conclusion

It was demonstrated that AG improves the behaviors of depression and anxiety in a rat model of LPS-induced anxiety- and depression-like behaviors. Moreover, the effects of AG were accompanied by improved inflammation and oxidative damage biomarkers in brain tissues.

中文翻译：

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诱导型一氧化氮合酶在大鼠脂多糖慢性诱导的抑郁和焦虑样行为中起作用：来自炎症和氧化应激的证据。

客观的

在脂多糖 (LPS) 诱导的焦虑和抑郁样行为的大鼠模型中研究了氨基胍 (AG) 的作用。

材料和方法

将动物分为五组（每组 n = 10）并通过以下方式处理：（1）盐水作为对照组，（2）在行为测试前两小时注射 LPS 1 mg/kg，（3-5）AG 50， LPS 前 100 或 150 mg/kg。进行了旷场试验（OFT）、高架十字迷宫试验（EPT）和强迫游泳（FS）试验。然后收集大脑和血液以检查氧化应激和炎症标准。

结果

在 FS 测试中，LPS 增加了不动性，同时减少了活动时间。在 EPT 中，LPS 减少了张开手臂的时间，而增加了闭合手臂的时间。在 OFT 中，与对照组相比，LPS 减少了在中央区域花费的时间。较高剂量的硒改善了大鼠在行为测试中的表现。LPS 注射还增加了丙二醛 (MDA)，同时降低了硫醇、超氧化物歧化酶 (SOD) 和过氧化氢酶。LPS 还增加了白细胞介素 (IL)-6 和肿瘤坏死因子-α (TNF-α)，但在 LPS 组中降低了 IL-10。AG 保护大脑免受炎症和氧化损伤。

结论

结果表明，在 LPS 诱导的焦虑和抑郁样行为的大鼠模型中，AG 改善了抑郁和焦虑的行为。此外，AG 的作用伴随着脑组织中炎症和氧化损伤生物标志物的改善。