Objective: Apigenin is a natural flavonoid compound extracted from Matricaria chamomilla. We evaluated the anti-inflammatory effects of apigenin in this study using the Lipopolysaccharide (LPS)-stimulated BV2 microglia.Methods: BV2 cells were treated with apigenin for 1 h and then treated with LPS. The inflammatory cytokine productions were tested by qRT-PCR and ELISA. The expression of GSK3β, Nrf2, and NF-κB signaling pathways were measured by western blot analysis.Results: Apigenin significantly attenuated LPS-induced TNF-α, IL-1β, and IL-6 production. Apigenin suppressed LPS-induced NF-κB activation. Furthermore, GSK3β, Nrf2, and HO-1 were concentration-dependently increased by apigenin. The suppression of apigenin on LPS-induced inflammatory response and NF-κB activation were prevented when Nrf2 was knocked out or by GSK3β inhibitor.Conclusions: Collectively, apigenin suppressed LPS-induced microglia activation via activating GSK3β/Nrf2 signaling pathway.

中文翻译：

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芹菜素通过激活GSK3β/ Nrf2信号通路在LPS刺激的BV2小胶质细胞中表现出抗炎作用。

目的：芹菜素是从洋母菊提取的天然黄酮类化合物。我们使用脂多糖（LPS）刺激的B​​V2小胶质细胞评估芹菜素的抗炎作用。方法：将芹菜素处理BV2细胞1 h，然后再用LPS处理。通过qRT-PCR和ELISA测试炎性细胞因子的产生。Western blot检测GSK3β，Nrf2和NF-κB信号通路的表达。结果：芹菜素显着减弱LPS诱导的TNF-α，IL-1β和IL-6的产生。芹菜素抑制LPS诱导的NF-κB活化。此外，芹菜素对GSK3β，Nrf2和HO-1的浓度依赖性增加。当敲除Nrf2或用GSK3β抑制剂抑制芹菜素对LPS诱导的炎症反应和NF-κB活化的抑制作用。