Bussmann Hendrik, Bremer Swen, Hernier Anne Marie, Drewe Jürgen, Häberlein Hanns, Franken Sebastian, Freytag Virginie, Boonen Georg, Butterweck Veronika
Medical Department, Max Zeller Soehne AG, Seeblickstrasse 4, 8590 Romanshorn, Switzerland.
Institute of Biochemistry and Molecular Biology, Medical Faculty, University of Bonn, Nussallee 11, 53115 Bonn, Germany.
Int J Mol Sci. 2024 Nov 26;25(23):12667. doi: 10.3390/ijms252312667.
Chronic stress is a key factor in the development of depression. It leads to hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis, which in turn increases the formation of glucocorticoids (GCs). Chronically elevated GC levels disrupt neuroplasticity and affect brain lipid metabolism, which may, ultimately, contribute to the development of depression. This study aimed to investigate the effects of the antidepressants St. John's Wort extract and escitalopram on lipid metabolism in vivo. Therefore, repeated corticosterone injections were used to induce depression-like behavior in rats. Male Sprague-Dawley rats were stressed with corticosterone injections (40 mg/kg, s.c.) over 22 consecutive days and were concomitantly treated with varying doses of the St. John's wort extract Ze 117 (30, 90 or 180 mg/kg, p.o.) or escitalopram (10 mg/kg, p.o.) and behavioral changes were evaluated using a modified forced swim test. The results indicate that repeated corticosterone injections significantly decreased the latency to first immobility. Furthermore, co-treatment of corticosterone with Ze 117 increased latency to first immobility significantly compared to rats treated with corticosterone alone. To further investigate the biochemical effects of corticosterone-induced stress, as well as the possible counter-regulation by antidepressants, the lipidomes of the plasma and hippocampus samples were analyzed by shotgun mass spectrometry. Corticosterone-induced stress significantly altered key lipid metabolites in the plasma but not in the hippocampal samples. In the hippocampus, however, specific glycerophospholipids such as lysophosphatidylethanolamines (LPEs) increased with escitalopram treatment and with Ze 117, both showing significant correlations with behavioral parameters. In summary, our study shows significant behavioral- and lipidome-altering processes with Ze 117 and escitalopram in rat plasma and hippocampal samples, thereby providing new targets and biomarker ideas for clinical diagnosis and antidepressant intervention.
慢性应激是抑郁症发病的关键因素。它会导致下丘脑 - 垂体 - 肾上腺(HPA)轴过度激活,进而增加糖皮质激素(GCs)的生成。长期升高的GC水平会破坏神经可塑性并影响脑脂质代谢,这最终可能导致抑郁症的发生。本研究旨在探讨抗抑郁药圣约翰草提取物和艾司西酞普兰对体内脂质代谢的影响。因此,采用重复注射皮质酮的方法在大鼠中诱导出类似抑郁的行为。雄性Sprague-Dawley大鼠连续22天接受皮质酮注射(40mg/kg,皮下注射)进行应激处理,并同时给予不同剂量的圣约翰草提取物Ze 117(30、90或180mg/kg,口服)或艾司西酞普兰(10mg/kg,口服),使用改良的强迫游泳试验评估行为变化。结果表明,重复注射皮质酮显著缩短了首次不动的潜伏期。此外,与单独接受皮质酮治疗的大鼠相比,皮质酮与Ze 117联合治疗显著延长了首次不动的潜伏期。为了进一步研究皮质酮诱导应激的生化效应以及抗抑郁药可能的反向调节作用,通过鸟枪法质谱分析了血浆和海马样本的脂质组。皮质酮诱导的应激显著改变了血浆中的关键脂质代谢物,但未改变海马样本中的关键脂质代谢物。然而,在海马中,特定的甘油磷脂,如溶血磷脂酰乙醇胺(LPEs),在接受艾司西酞普兰治疗和Ze 117治疗时均增加,且二者均与行为参数显示出显著相关性。总之,我们的研究表明,Ze 117和艾司西酞普兰在大鼠血浆和海马样本中具有显著的行为和脂质组改变过程,从而为临床诊断和抗抑郁干预提供了新的靶点和生物标志物思路。