Department of Pharmacology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Department of Internal Medicine, School of Medicine, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Neuroimmunomodulation. 2020;27(2):87-96. doi: 10.1159/000511181. Epub 2020 Nov 11.
Major depressive disorder is considered a global public health problem. Inflammatory processes are likely involved in its pathophysiology, but the underlying mechanisms have remained uncertain.Here, we used the model of systemic lipopolysaccharide (LPS) injection to test the hypothesis that depressive-like behaviors occur along with changes in the levels of cytokines and brain-derived neurotrophic factor (BDNF) in the hippocampus (HC), prefrontal cortex (PFC), and hypothalamus (HT), and can be prevented by dexamethasone administration.
Adult C57Bl/6 male mice were first isolated for 10 days, and thereafter received an injection of dexamethasone (6 mg/kg, intraperitoneal [i.p.]), saline followed by LPS (0.83 mg/kg, i.p.), or saline. After 6 h, animals were subjected to the forced-swim test (FST) and open-field tests. Immediately after the behavioral tests, they were euthanized and their brains were collected for the biochemical analyses.
LPS increased the immobility time and reduced the distance travelled in the FST and open-field test, respectively. Dexamethasone increased the immobility time in saline-treated mice but reduced this behavior in the LPS group. LPS increased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and interferon (IFN)-γ in most of the regions evaluated. Dexamethasone prevented LPS-induced IL-6 in the HC, PFC, and HT. Interestingly, dexamethasone increased IL-4 and IL-10 levels in both the LPS- and saline-treated groups. Although dexamethasone reduced BDNF in saline-treated mice, it prevented LPS-induced reduction in this neurotrophic factor.
In summary, dexamethasone decreased proinflammatory and increased anti-inflammatory levels of cytokines and prevented a reduction in BDNF levels induced by the inflammatory stimulus. Thus, the attenuation of depressive-like behavior induced by dexamethasone may be related to the effects on these parameters.
重度抑郁症被认为是全球公共卫生问题。炎症过程可能参与其病理生理学,但潜在机制仍不确定。在这里,我们使用全身脂多糖(LPS)注射模型来检验以下假说,即抑郁样行为的发生伴随着海马(HC)、前额叶皮层(PFC)和下丘脑(HT)中细胞因子和脑源性神经营养因子(BDNF)水平的变化,并且可以通过给予地塞米松来预防。
成年 C57Bl/6 雄性小鼠首先被隔离 10 天,然后接受地塞米松(6mg/kg,腹腔内[ip.])、盐水后 LPS(0.83mg/kg,ip.])或盐水。6 小时后,动物进行强迫游泳试验(FST)和旷场试验。行为测试后,立即处死动物并采集其大脑进行生化分析。
LPS 增加了 FST 和旷场试验中的不动时间,并分别减少了动物的移动距离。地塞米松增加了盐水处理组小鼠的不动时间,但减少了 LPS 组的这种行为。LPS 增加了大多数评估区域的肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6 和干扰素(IFN)-γ的水平。地塞米松可预防 LPS 诱导的 HC、PFC 和 HT 中的 IL-6。有趣的是,地塞米松增加了 LPS 和盐水处理组的 IL-4 和 IL-10 水平。尽管地塞米松减少了盐水处理组小鼠的 BDNF,但它预防了 LPS 诱导的这种神经营养因子的减少。
总之,地塞米松降低了促炎细胞因子的水平,增加了抗炎细胞因子的水平,并防止了炎症刺激引起的 BDNF 水平降低。因此,地塞米松减轻抑郁样行为可能与这些参数的影响有关。