目的 基于脂多糖誘導小鼠單核巨噬細胞（RAW 264.7）構建的體外細胞炎癥模型，探討牡蒿Artemisia japonica Thunb.水提物的抗炎作用及其機制。方法 通過CCK-8法檢測牡蒿水提物對RAW 264.7細胞活力的影響以篩選合適的牡蒿水提物給藥質量濃度。采用脂多糖200 ng/mL誘導RAW 264.7細胞建立體外炎癥細胞模型。將細胞分為對照組、模型組和牡蒿水提物（240、480、960μg/mL）組，用Griess試劑法檢測RAW 264.7細胞一氧化氮（NO）釋放水平，ELISA法檢測細胞白細胞介素（IL）-6、IL-1β含量。采用Western blotting法檢測誘導型一氧化氮合成酶（iNOS）、環(huán)氧合酶-2(COX-2)以及Toll樣受體4(TLR4)/核因子-κB(NF-κB)信號通路中TLR4、核因子κB抑制蛋白α(IκBα)、p-IκBα、p65蛋白（p65）、p-p65蛋白相對表達量。結果 牡蒿水提物質量濃度為0～960μg/mL時對RAW 264.7細胞活力沒有顯著影響。與模型組相比，牡蒿水提物480、960μg/mL組能顯著抑制IL-6的釋放以及COX-2的蛋白相對表達量（P<0.01）；各質量濃度牡蒿水提物均能顯著抑制NO、IL-1β的釋放，iNOS、p-IκBα、p65、p-p65蛋白的表達以及IκBα蛋白的降解（P<0.01）。結論 牡蒿水提物能抑制脂多糖誘導的RAW 264.7細胞炎性因子的分泌，其作用機制與抑制炎性蛋白iNOS和COX-2的表達及TLR4/NF-κB信號通路的激活有關。

Objective To explore the effects and mechanisms of A. japonica water extract on lipopolysaccharide-induced RAW 264.7macrophages model. Methods CCK-8 colorimetric method was used to select the appropriate concentration of A. japonica on the activity of RAW 264.7 macrophages. RAW 264.7 cells were induced by lipopolysaccharide 200 ng/mL to establish in vitro inflammatory cell model. Cells were divided into control group, model group, and A. japonica（240, 480, and 960 μg/mL） groups.Griess assay was used to assess NO concentration, IL-1β, and IL-6 content was measured by ELISA. The expression of iNOS, COX-2, and TLR4/NF-κB pathway-related proteins（TLR4, IκBα, p-IκBα, p65, p-P65） were detected by Western blotting. Results A.japonica had no significant effect on the viability of RAW 264.7 cells at the concentrations of 0 — 960 μg/mL. Compared with model group, A. japonica water extract 480 and 960 μg/mL groups significantly inhibitory effects on the release of IL-6 and protein expression of COX-2（P＜0.01）. Each dose group of A. japonica water extract displayed favorable inhibitory decreased effects on release of NO and IL-1β, expression of iNOS, p-IκBα, p65, and p-p65 proteins and degradation of IκBα. Conclusion A. japonica water extract could inhibit lipopolysaccharide-induced secretion of inflammatory factors in RAW 264.7 cells, the mechanism of which is related to inhibiting the expression of inflammatory proteins iNOS and COX-2 and inhibiting the activation of TLR4/NF-κB signaling pathway.

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國家自然科學基金資助項目(32260925); 貴州省科技計劃項目(黔科合基礎-ZK[2022]一般507); 貴州中醫(yī)藥大學大學生創(chuàng)新創(chuàng)業(yè)訓練計劃項目[貴中醫(yī)大創(chuàng)合字(2021)84號