甘草查尔酮 B 通过 Keap1/Nrf2 通路赋予细胞和小鼠对抗 LPS 诱导的急性肺损伤的保护作用。
Licochalcone B confers protective effects against LPS-Induced acute lung injury in cells and mice through the Keap1/Nrf2 pathway.
机构信息
Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, People's Republic of China.
Chengdu sport university, Chengdu, People's Republic of China.
出版信息
Redox Rep. 2023 Dec;28(1):2243423. doi: 10.1080/13510002.2023.2243423.
BACKGROUND
Acute lung injury (ALI) is a severe and often fatal pulmonary disease. Current treatments for ALI and acute respiratory distress syndrome (ARDS) are limited. Natural product metabolites have shown promise as therapeutic alternatives. However, the effects of Licochalcone B (LCB) on ALI are largely unknown.
METHODS
We investigated the effects of LCB on lipopolysaccharide-challenged mice and human pulmonary microvascular endothelial cells. Cell viability, apoptosis, and ROS production were assessed. Lung tissue histopathology and oxidative stress and inflammation markers were evaluated. Protein expression levels were measured.
RESULTS
LCB had no cytotoxic effects on cells and increased cell viability. It reduced apoptosis and ROS levels in cells. In mice with ALI, LCB decreased lung tissue weight and improved oxidative stress and inflammation markers. It also enhanced expression levels of Nrf2, HO-1, and NQO1 while reducing Keap1.
CONCLUSION
LCB protects against LPS-induced acute lung injury in cells and mice. The Keap1/Nrf2 pathway may be involved in its protective effects. LCB shows potential as a strategy to alleviate ALI caused by LPS.
背景
急性肺损伤（ALI）是一种严重且常致命的肺部疾病。目前对 ALI 和急性呼吸窘迫综合征（ARDS）的治疗方法有限。天然产物代谢物已被证明是有希望的治疗替代品。然而，甘草查尔酮 B（LCB）对 ALI 的影响在很大程度上尚不清楚。
方法
我们研究了 LCB 对脂多糖刺激的小鼠和人肺微血管内皮细胞的影响。评估了细胞活力、细胞凋亡和 ROS 产生。评估了肺组织组织病理学以及氧化应激和炎症标志物。测量了蛋白质表达水平。
结果
LCB 对细胞无细胞毒性作用，可增加细胞活力。它降低了细胞中的细胞凋亡和 ROS 水平。在患有 ALI 的小鼠中，LCB 降低了肺组织重量，改善了氧化应激和炎症标志物。它还增强了 Nrf2、HO-1 和 NQO1 的表达水平，同时降低了 Keap1。
结论
LCB 可预防 LPS 诱导的细胞和小鼠急性肺损伤。Keap1/Nrf2 通路可能与其保护作用有关。LCB 显示出作为减轻 LPS 引起的 ALI 的策略的潜力。
Zotero 插件