Dihydrotanshinone (DIH) is an extract of Salvia miltiorrhiza Bunge. It has been reported that DIH could regulate NF-κB signaling pathway. The aim of this study was to investigate whether DIH could protect mice from lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. In this study, sixty mice were randomly divided into five groups, one group as blank control group, the second group as LPS control group, and the last three groups were pre-injected with different doses of DIH and then inhaled LPS for experimental comparison. After 12 h of LPS treatment, the wet-dry ratio, histopathlogical changes, and myeloperoxidase (MPO) activity of lungs were measured. In addition, ELISA kits were used to measure the levels of TNF-α and IL-1β inflammatory cytokines in bronchoalveolar lavage fluids (BALF), and western blot analysis was used to measure the activity of NF-κB signaling pathway. The results demonstrated that DIH could effectively reduce pulmonary edema, MPO activity, and improve the lung histopathlogical changes. Furthermore, DIH suppressed the levels of inflammatory cytokines in BALF, such as TNF-α and IL-1β. In addition, DIH could also downregulate the activity of NF-κB signaling pathway. We also found that DIH dose-dependently increased the expression of LXRα. In addition, DIH could inhibit LPS-induced IL-8 production and NF-κB activation in A549 cells. And the inhibitory effects were reversed by LXRα inhibitor geranylgeranyl pyrophosphate (GGPP). Therefore, we speculate that DIH regulates LPS-induced ALI in mice by increasing LXRα expression, which subsequently inhibiting NF-κB signaling pathway.

二氢丹参酮 (DIH) 是丹参的提取物. 据报道，DIH可以调节NF-κB信号通路。本研究的目的是调查 DIH 是否可以保护小鼠免受脂多糖 (LPS) 诱导的小鼠急性肺损伤 (ALI)。本研究将60只小鼠随机分为5组，一组为空白对照组，第二组为LPS对照组，最后三组分别预先注射不同剂量的DIH后吸入LPS进行实验比较。LPS 处理 12 h 后，测量肺的干湿比、组织病理学变化和髓过氧化物酶 (MPO) 活性。此外，采用ELISA试剂盒测定支气管肺泡灌洗液（BALF）中TNF-α和IL-1β炎性细胞因子的水平，采用western blot分析测定NF-κB信号通路的活性。结果表明，DIH可有效降低肺水肿、MPO活性，改善肺组织病理学改变。此外，DIH 抑制了 BALF 中炎性细胞因子的水平，例如 TNF-α 和 IL-1β。此外，DIH还可以下调NF-κB信号通路的活性。我们还发现 DIH 剂量依赖性地增加了 LXRα 的表达。此外，DIH 可以抑制 A549 细胞中 LPS 诱导的 IL-8 产生和 NF-κB 活化。LXRα抑制剂香叶基香叶基焦磷酸盐（GGPP）逆转了抑制作用。因此，我们推测DIH通过增加LXRα表达来调节LPS诱导的小鼠ALI，从而抑制NF-κB信号通路。DIH 抑制 BALF 中炎性细胞因子的水平，例如 TNF-α 和 IL-1β。此外，DIH还可以下调NF-κB信号通路的活性。我们还发现 DIH 剂量依赖性地增加了 LXRα 的表达。此外，DIH 可以抑制 A549 细胞中 LPS 诱导的 IL-8 产生和 NF-κB 活化。LXRα抑制剂香叶基香叶基焦磷酸盐（GGPP）逆转了抑制作用。因此，我们推测DIH通过增加LXRα表达来调节LPS诱导的小鼠ALI，从而抑制NF-κB信号通路。DIH 抑制 BALF 中炎性细胞因子的水平，例如 TNF-α 和 IL-1β。此外，DIH还可以下调NF-κB信号通路的活性。我们还发现 DIH 剂量依赖性地增加了 LXRα 的表达。此外，DIH 可以抑制 A549 细胞中 LPS 诱导的 IL-8 产生和 NF-κB 活化。LXRα抑制剂香叶基香叶基焦磷酸盐（GGPP）逆转了抑制作用。因此，我们推测DIH通过增加LXRα表达来调节LPS诱导的小鼠ALI，从而抑制NF-κB信号通路。DIH 可以抑制 A549 细胞中 LPS 诱导的 IL-8 产生和 NF-κB 活化。LXRα抑制剂香叶基香叶基焦磷酸盐（GGPP）逆转了抑制作用。因此，我们推测DIH通过增加LXRα表达来调节LPS诱导的小鼠ALI，从而抑制NF-κB信号通路。DIH 可以抑制 A549 细胞中 LPS 诱导的 IL-8 产生和 NF-κB 活化。LXRα抑制剂香叶基香叶基焦磷酸盐（GGPP）逆转了抑制作用。因此，我们推测DIH通过增加LXRα表达来调节LPS诱导的小鼠ALI，从而抑制NF-κB信号通路。