Lung injury associated with systemic inflammatory response is a common problem affecting human health. Previous studies have shown that lycorine exerts a anti-inflammatory effect. However, whether lycorine alleviates lung injury remains unclear. To explore this issue, BALB/c mice and MLE-12 cells were treated with lipopolysaccharide (LPS) to establish lung injury mouse model and cell model, respectively. Glycyrrhizic acid, known as an inhibitor of ALI, was also used to study the effects of lycorine in vitro. Our results showed that after LPS treatment, the lung injury score, lung wet-to-dry weight ratio, and malondialdehyde (MDA) production in the lung tissues and the expression levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6 in bronchoalveolar lavage fluid were significantly increased, whereas their levels were decreased by lycorine. Additionally, LPS injection activated the high-mobility group box 1 (HMGB1)/Toll-like receptors (TLRs)/NF-κB pathway. However, lycorine treatment attenuated the activity of the HMGB1/TLRs/NF-κB pathway in the lung tissues. In vitro studies showed that lycorine administration significantly decreased the levels of inflammatory cytokines and MDA and attenuated the activity of the HMGB1/TLRs/NF-κB pathway in LPS-treated cells. Moreover, the inhibitory effects of lycorine on the inflammatory response and oxidative stress in LPS-treated lung cells were similar with that of glycyrrhizic acid, and this inhibition was intensified by both lycorine and glycyrrhizic acid treatment. We suggest that lycorine could alleviate LPS-induced lung injury of inflammation and oxidative stress by blocking the HMGB1/TLRs/NF-κB pathway, which gives a new perspective for ALI therapy to treat lycorine as a potential treatment clinically.

与全身性炎症反应相关的肺损伤是影响人类健康的普遍问题。先前的研究表明，茄碱具有抗炎作用。然而，尚无研究表明，番石榴碱是否能减轻肺损伤。为了探讨这个问题，分别用脂多糖（LPS）处理BALB / c小鼠和MLE-12细胞，以建立肺损伤小鼠模型和细胞模型。甘草酸，被称为ALI的抑制剂，也被用来研究肾上腺素在体外的作用。我们的研究结果表明，LPS处理后，肺组织中的肺损伤评分，肺干重比和肺中丙二醛（MDA）的产生以及肿瘤坏死因子-α，白介素-1β和白介素- 6支支气管肺泡灌洗液中明显增多，而他们的水平由lycorine降低。此外，LPS注射激活了高迁移率族框1（HMGB1）/ Toll样受体（TLRs）/NF-κB通路。然而，蛋氨酸处理减弱了肺组织中HMGB1 / TLRs /NF-κB通路的活性。体外研究表明，在LPS处理的细胞中，施用蛋黄素可显着降低炎症细胞因子和MDA的水平，并减弱HMGB1 / TLRs /NF-κB途径的活性。而且，在经LPS处理的肺细胞中，番红花碱对炎症反应和氧化应激的抑制作用与甘草酸相似，而这种抑制作用通过番荔枝碱和甘草酸的处理均得到增强。