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Trazodone treatment protects neuronal-like cells from inflammatory insult by inhibiting NF-kappa B, p38 and JNK

机译:曲唑酮处理通过抑制NF-Kappa B,P38和JNK保护神经元样细胞免受炎症性损伤

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Growing evidence suggests that alterations of the inflammatory/immune system contribute to the pathogenesis of major depression and that inflammatory processes may influence the antidepressant treatment response. Depressed patients exhibit increased levels of inflammatory markers in both the periphery and brain, and high co-morbidity exists between depression and diseases associated with inflammatory alterations. Trazodone (TDZ) is a triazolopyridine derivative that belongs to the class of serotonin receptor antagonists and reuptake inhibitors. Although the trophic and protective properties of classic antidepressants have extensively been exploited, the effects of TDZ remain to be fully elucidated. In this study, the pharmacological activities of TDZ on human neuronal-like cells were investigated under both physiological and inflammatory conditions. An in vitro inflammatory model was established using lipopolysaccharide (LPS) and tumour necrosis factor-alpha (TNF-alpha), which efficiently mimic the stress-related changes in neurotrophic and pro-inflammatory genes.
机译:日益增长的证据表明,炎症/免疫系统的改变有助于重大抑郁的发病机制,炎症过程可能影响抗抑郁药治疗反应。抑郁症患者表现出周围和大脑的炎症标记水平增加,抑郁和与炎症改变相关的疾病之间存在高的共发病率。曲唑酮(TDZ)是三唑吡啶衍生物,属于血清素受体拮抗剂和再摄取抑制剂的类。虽然经典抗抑郁药的营养和保护性具有广泛的利用,但TDZ的效果仍然被完全阐明。在这项研究中,在生理和炎症条件下研究了TDZ对人神经元样细胞的药理活性。使用脂多糖(LPS)和肿瘤坏死因子-α(TNF-α)建立体外炎症模型,其有效地模仿神经营养和促炎基因的应力相关变化。

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