Luteolin reversed anxiety and depressive-like behavior via modulation of the NF-κB/NLRP3 inflammasome axis in the hippocampus of rats subjected to sleep deprivation

• Published in: Iranian journal of basic medical sciences Vol. 27; no. 8; pp. 1050 - 1058
• Main Authors: Xiong, Fang, Lv, Xuewen
• Format: Journal Article
• Language: English
• Published: Iran Mashhad University of Medical Sciences 01.01.2024
• Subjects: Animals; Anxiety; depression; hippocampus; luteolin; neuroinflammation; Original; Sleep deprivation; Depression; Neuroinflammation; Anxiety; Luteolin; Hippocampus; Sleep deprivation
• ISSN: 2008-3866; 2008-3874
• DOI: 10.22038/IJBMS.2024.75068.16277

In this study, we assessed the impact of luteolin (LUT) on mood disorders (specifically anxiety and depression) induced by sleep deprivation (SD) by regulating pathways associated with neuroinflammation. Rapid eye movement (REM) SD was employed to induce anxiety and depression in the animal subjects. The animals were treated with PAX (15 mg/kg, positive control) and LUT (10 and 20 mg/kg) for a duration of 21 days. The anxiety and depressive disorders were evaluated using behavioral tests. Following the sacrifice of the animals, hippocampal tissues were stored for molecular investigations. SD resulted in anxiety, as evidenced by the elevated plus maze test and open field test. Furthermore, the findings from the sucrose performance test, forced swimming test, and tail suspension test confirmed the presence of depressive-like behaviors in the animals. The nuclear factor kappa B (NF-κB) and NLR family pyrin domain containing 3 (NLRP3) inflammasome components, including apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC), NLRP3, and active Caspase-1, were up-regulated in the hippocampus (HC) of the animals subjected to REM SD. However, treatment with LUT demonstrated a significant reversal of the behavioral changes by modulating the NF-κB and NLRP3 inflammasome components in the HC. It can be concluded that LUT demonstrated antidepressant effects via regulation of the NF-κB/NLRP3 inflammasome axis components in the HC.