Alzheimer's disease is a chronic neurological ailment that seriously threatens human health and imposes a huge burden on families and the society at large. Emerging evidence suggests that neuroinflammation is an important pathological manifestation of neurodegenerative diseases, and currently considered a new research target. We previously found that artemisinin B from Artemisia annua Linn. has strong anti-inflammatory and immunological activities. In the present study, we assessed the anti-neuroinflammatory effects of artemisinin B in vitro and in vivo, exploring the underlying mechanisms. The results demonstrated that artemisinin B inhibited NO secretion from LPS-induced BV2 cells and significantly reduced the expression levels of the inflammatory cytokines IL-1β, IL-6 and TNF-α. This was accompanied by reduced gene expression levels of MyD88 and NF-κB as well as TLR4 and MyD88 protein levels. These inhibitory effects were further confirmed in AD model mice. This study also showed that artemisinin B improved spatial memory in dementia mice in the water maze and step-through tests, and altered the pathological features and the levels of inflammatory cytokines in the hippocampus and the cortex. These results suggested that artemisinin B might inhibit neuroinflammation and exert neuroprotective effects on cognitive functions by modulating the TLR4-MyD88-NF-κB signaling pathway. This study provides direct evidence for the potential application of artemisinin B in the treatment of neuroinflammatory diseases.

译文

阿尔茨海默病是一种慢性神经系统疾病,严重威胁人类健康,给家庭和整个社会带来巨大负担。新兴证据表明,神经炎症是神经退行性疾病的重要病理表现,目前被认为是一个新的研究目标。我们以前发现青蒿中的青蒿素B。具有很强的抗炎和免疫活性。在本研究中,我们评估了青蒿素B在体外和体内的抗神经炎症作用,并探索了潜在的机制。结果表明,青蒿素B可抑制LPS诱导的BV2细胞的NO分泌,并显着降低炎性细胞因子IL-1β,IL-6和TNF-α 的表达水平。伴随着MyD88和NF-κ b的基因表达水平以及TLR4和MyD88蛋白水平降低。这些抑制作用在AD模型小鼠中得到进一步证实。这项研究还表明,青蒿素B在水迷宫和步进测试中改善了痴呆小鼠的空间记忆,并改变了海马和皮质的病理特征和炎性细胞因子的水平。这些结果表明,青蒿素B可能通过调节TLR4-MyD88-NF-κB信号通路来抑制神经炎症并对认知功能发挥神经保护作用。这项研究为青蒿素B在治疗神经炎性疾病中的潜在应用提供了直接证据。

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