Department of Pharmacology, School of Pharmacy, International University of Health and Welfare, 2600-1 Kitakanemaru, Ohtawara, Tochigi, 324-8501, Japan.
Division of Pharmacology, Faculty of Pharmaceutical Sciences, Tohoku Medical and Pharmaceutical University, 4-4-1 Komatsushima, Aoba-Ku, Sendai, Miyagi, 981-8558, Japan.
Sci Rep. 2024 May 21;14(1):11519. doi: 10.1038/s41598-024-62309-3.
Ulcerative colitis (UC) is a refractory inflammatory bowel disease, which is known to cause psychiatric disorders such as anxiety and depression at a high rate in addition to peripheral inflammatory symptoms. However, the pathogenesis of these psychiatric disorders remains mostly unknown. While prior research revealed that the Enterococcus faecalis 2001 (EF-2001) suppressed UC-like symptoms and accompanying depressive-like behaviors, observed in a UC model using dextran sulfate sodium (DSS), whether it has an anxiolytic effect remains unclear. Therefore, we examined whether EF-2001 attenuates DSS-induced anxiety-like behaviors. Treatment with 2% DSS for seven days induced UC-like symptoms and anxiety-like behavior through the hole-board test, increased serum lipopolysaccharide (LPS) and corticosterone concentration, and p-glucocorticoid receptor (GR) in the prefrontal cortex (PFC), and decreased N-methyl-D-aspartate receptor subunit (NR) 2A and NR2B expression levels in the PFC. Interestingly, these changes were reversed by EF-2001 administration. Further, EF-2001 administration enhanced CAMKII/CREB/BDNF-Drebrin pathways in the PFC of DSS-treated mice, and labeling of p-GR, p-CAMKII, and p-CREB showed colocalization with neurons. EF-2001 attenuated anxiety-like behavior by reducing serum LPS and corticosterone levels linked to the improvement of UC symptoms and by facilitating the CAMKII/CREB/BDNF-Drebrin pathways in the PFC. Our findings suggest a close relationship between UC and anxiety.
溃疡性结肠炎(UC)是一种难治性炎症性肠病,除外周炎症症状外,已知其还会以高发病率引起焦虑和抑郁等精神障碍。然而,这些精神障碍的发病机制在很大程度上仍然未知。虽然先前的研究表明粪肠球菌 2001(EF-2001)可抑制葡聚糖硫酸钠(DSS)诱导的 UC 样症状和伴随的抑郁样行为,但它是否具有抗焦虑作用尚不清楚。因此,我们研究了 EF-2001 是否能减轻 DSS 诱导的焦虑样行为。用 2%的 DSS 处理 7 天,通过洞板试验诱导 UC 样症状和焦虑样行为,增加血清脂多糖(LPS)和皮质酮浓度,以及前额叶皮质(PFC)中的 p-糖皮质激素受体(GR),并降低 PFC 中的 N-甲基-D-天冬氨酸受体亚单位(NR)2A 和 NR2B 的表达水平。有趣的是,EF-2001 的给药逆转了这些变化。此外,EF-2001 的给药增强了 DSS 处理的小鼠 PFC 中的钙调蛋白激酶 II/CREB/BDNF-Drebrin 途径,p-GR、p-CAMKII 和 p-CREB 的标记与神经元共定位。EF-2001 通过降低与 UC 症状改善相关的血清 LPS 和皮质酮水平以及促进 PFC 中的 CAMKII/CREB/BDNF-Drebrin 途径来减轻焦虑样行为。我们的研究结果表明 UC 与焦虑之间存在密切关系。