مقاله انگلیسی کاهش رفتارهای شبه افسردگی در موشهای CUMS با لیکویریتین
Introduction
Materials and Methods
Results
Discussion
References
Introduction
Accumulating evidence suggests that mitigation of neuroinflammation could be a potential therapeutic approach for depression [1]. Clinical studies have shown that inflammatory cytokines in the central nervous system are significantly elevated, such as IL-1β and IL-6, in patients with depression. Recent studies consider that inhibition of NLRP3 inflammasome activation may be a promising strategy for the therapy of depression [2]. Liquiritin, a flavonoid isolated from the root of liquorice, has exhibited various biological activities, such as anti-inflammatory, antiaging, and antitumor activity [3–5]. .e neuroprotective activity of liquiritin has attracted considerable attention. Studies have shown that liquiritin could resist the death of cortical neurons induced by glutamate and promote the axon growth of PC12 cells triggered by nerve growth factor [6, 7]. Notably, an early study reported that liquiritin showed antidepressant effect via enhancement of 5-hydroxytryptamine and norepinephrine levels in the hippocampus, hypothalamus, and cortex [8]. In Hindawi Evidence-Based Complementary and Alternative Medicine Volume 2022, Article ID 7558825, 10 pages https://doi.org/10.1155/2022/7558825 another study, liquiritin also showed antidepressant effects, which might be related to the defense of liquiritin against oxidative stress [9]. Although some evidence confirms the antidepressant effect of liquiritin, it is unclear whether the alleviation of central inflammation is involved in this effect. .erefore, we established an CUMS model to confirm the antidepression effects of liquiritin and explore the effects on cytokine release and NLRP3 inflammasome associate protein expression in the hippocampus.
Materials and Methods
2.1. Drugs and Reagents. Liquiritin (CAS: 551-15-5, molecular formula is shown in Figure 1(a)) and fluoxetine hydrochloride (CAS: 56296-78-7), purity ≥98%, were purchased from Selleck China (Shanghai, China). PC12 cell was purchased from Procell Life Science&Technology Co., Ltd. DMSO (D4540) was got from Sigma-Aldrich (Shanghai) Trading Co., Ltd. Superoxide dismutase (SOD) detection kit (A001-1-2), glutathione peroxidase (GSH-Px) detection kit (A005-1-2), and malondialdehyde (MDA) detection kit (A003-1-2) were all purchased from Nanjing Jiancheng Institute of Biological Engineering (Nanjing, China). BCA protein concentration detection kit (P0012S) and RIPA Lysis Buffer (P0013B) were purchased from Beyotime Biotechnology Co., Ltd.