Abstract
Neuroinflammation is associated with an increased risk of depression. Lipopolysaccharide (LPS) treatment is known to induce pro-inflammatory cytokine secretion and a depressive-like phenotype in mice. Although Erythronium japonicum exhibits various health benefits, the role of E. japonicum extract (EJE) in inflammation-associated depression is unknown. This study aimed to explore the anti-inflammatory effect of EJE on LPS-induced depressive symptoms in mice using the open field test (OFT), passive avoidance test (PAT), tail suspension test (TST), and forced swim test (FST). LPS-treated mice had significantly increased immobility time in the TST and FST, decreased step-through latency time in the PAT, and decreased locomotor activity in the OFT. However, administration of 100 and 300 mg/kg of EJE significantly improved these depressive-like behaviors. EJE also prevented the increase in mRNA levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and monocyte chemoattractant protein-1 (MCP-1), and the decrease in IL-10 levels by inhibiting nuclear factor-κB (NF-κB) subunit p65 phosphorylation. Additionally, LPS-treated mice showed markedly decreased brain-derived neurotrophic factor (BDNF) levels and phosphorylation of phosphoinositide 3-kinase (PI3K) and Akt, while EJE treatment significantly increased these levels in the hippocampus. These results suggest that EJE ameliorated LPS-induced depressive-like behavior by reducing LPS-induced neuroinflammation and activating the BDNF-PI3K/Akt pathway.
Highlights
Depression is one of the most significant mental disorders worldwide
Pro-inflammatory cytokines including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels have been found to be higher in major depressive patients [6], whereas the antioxidant capacity was lower [7]
We examined the effect of E. japonicum extract (EJE) on LPS-induced abnormal behaviors in the open field test (OFT)
Summary
It is estimated that more than 350 million people have depression worldwide [1], and that depression will be the most important cause of disability by 2020 [2]. The pathogenesis of depression remains unclear, numerous studies have reported the importance of neuroinflammation in the development of depression [3,4]. Continuous inflammation with elevated levels of pro-inflammatory cytokines can cause depressive symptoms [5]. Pro-inflammatory cytokines including interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels have been found to be higher in major depressive patients [6], whereas the antioxidant capacity was lower [7]. It was reported that the cyclooxygenase-2 (COX-2) inhibitor celecoxib may be an effective adjuvant agent in the management of patients with major depression [8].
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