Microglia-mediated neuroinflammation is an important pathological feature in many neurological diseases; thus, suppressing microglial activation is considered a possible therapeutic strategy for reducing neuronal damage. Oxyimperatorin (OIMP) is a member of furanocoumarin, isolated from the medicinal herb . However, it is unknown whether OIMP can suppress the neuroinflammation. To investigate the neuroprotective activity of oxyimperatorin (OIMP) in LPS-induced neuroinflammation and models. inflammation-related assays were performed with OIMP in LPS-induced BV-2 microglia. In addition, intraperitoneal injection of LPS-induced microglial activation in the mouse brain was used to validate the anti-neuroinflammatory activity of OIMP. OIMP was found to suppress LPS-induced neuroinflammation and . OIMP significantly attenuated LPS-induced the production of free radicals, inducible nitric oxide synthase, cyclooxygenase-2, and pro-inflammatory cytokines in BV-2 microglia without causing cytotoxicity. In addition, OIMP could reduce the M1 pro-inflammatory transition in LPS-stimulated BV-2 microglia. The mechanistic study revealed that OIMP inhibited LPS-induced NF-κB p65 phosphorylation and nuclear translocation. However, OIMP did not affect LPS-induced IκB phosphorylation and degradation. In addition, OIMP also was able to reduce LPS-induced microglial activation in mice brain. Our findings suggest that OIMP suppresses microglia activation and attenuates the production of pro-inflammatory mediators and cytokines via inhibition of NF-κB p65 signaling.

中文翻译：

---

氧化欧前胡素通过抑制 NF-κB p65 信号传导在体外和体内减弱 LPS 诱导的小胶质细胞活化


小胶质细胞介导的神经炎症是许多神经系统疾病的重要病理特征；因此，抑制小胶质细胞活化被认为是减少神经元损伤的一种可能的治疗策略。氧化欧前胡素 (OIMP) 是从草药中分离出来的呋喃香豆素的成员。然而，OIMP 是否可以抑制神经炎症尚不清楚。研究氧欧前胡素 (OIMP) 在 LPS 诱导的神经炎症和模型中的神经保护活性。使用 OIMP 在 LPS 诱导的 BV-2 小胶质细胞中进行炎症相关测定。此外，通过腹腔注射 LPS 诱导小鼠大脑小胶质细胞活化来验证 OIMP 的抗神经炎症活性。 OIMP 被发现可以抑制 LPS 诱导的神经炎症。 OIMP 显着减弱 BV-2 小胶质细胞中 LPS 诱导的自由基、诱导型一氧化氮合酶、环氧合酶 2 和促炎细胞因子的产生，而不引起细胞毒性。此外，OIMP 可以减少 LPS 刺激的 BV-2 小胶质细胞中的 M1 促炎转变。机制研究表明，OIMP 抑制 LPS 诱导的 NF-κB p65 磷酸化和核转位。然而，OIMP 并不影响 LPS 诱导的 IκB 磷酸化和降解。此外，OIMP 还能够减少 LPS 诱导的小鼠大脑中小胶质细胞的激活。我们的研究结果表明，OIMP 通过抑制 NF-κB p65 信号传导来抑制小胶质细胞活化并减弱促炎介质和细胞因子的产生。