Gao Beibei, Qian Xingyi, Guo Yuanyuan, Dong Wei, Yang Ming, Yang Huda, Huang Xiaoying, Liang Xinli
Jiangxi University of Chinese Medicine, Jiangxi, 330004, China.
Jiaxing Hospital of Traditional Chinese Medicine, Zhejiang, 314000, China.
J Ethnopharmacol. 2024 Oct 28;333:118470. doi: 10.1016/j.jep.2024.118470. Epub 2024 Jun 21.
Initial investigative research indicated that the essential oil from Chimonanthus nitens Oliv. Leaves (CLO) significantly reduces lung tissues inflammation and effectively repairs Acute lung injury (ALI) mice model. However, the mechanism underlying is not clear, and the impacts of CLO on oxidative stress require further investigation.
The purpose of the experiment was to validate the influence of CLO in ALI model mice, as well as its potential mechanisms.
Lipopolysaccharide-induced establishment of the A549 cell inflammation model, and ALI mice model was established by intrathecal administration of LPS.
CLO significantly reduced the release of inflammatory cytokines in A549 cells, lowered MDA and ROS levels, and enhanced SOD activity. Animal experiment results showed that CLO dramatically decreased white blood cell count, the expression of inflammatory cytokines, and the destruction of alveolar structures. CLO enhances the activity of antioxidant enzymes. Western Blot and q-PCR analyses have revealed that the mechanism of CLO is correlation with the NF-κB and Nrf2 signaling pathways in cellular and animal models. Pathway inhibitor experiments indicated that there might be functional crosstalk between these two pathways.
CLO may regulate inflammation and oxidative stress in LPS-induced ALI through NF-κB and Nrf2 signaling pathways. This finding could be novel in the pharmacological treatment of ALI.
初步调查研究表明,山蜡梅叶挥发油(CLO)能显著减轻肺组织炎症,并有效修复急性肺损伤(ALI)小鼠模型。然而,其潜在机制尚不清楚,CLO对氧化应激的影响需要进一步研究。
本实验旨在验证CLO对ALI模型小鼠的影响及其潜在机制。
通过脂多糖诱导建立A549细胞炎症模型,并通过鞘内注射LPS建立ALI小鼠模型。
CLO显著降低A549细胞中炎性细胞因子的释放,降低丙二醛(MDA)和活性氧(ROS)水平,并增强超氧化物歧化酶(SOD)活性。动物实验结果表明,CLO显著降低白细胞计数、炎性细胞因子表达以及肺泡结构破坏。CLO增强抗氧化酶的活性。蛋白质免疫印迹法(Western Blot)和实时荧光定量聚合酶链反应(q-PCR)分析表明,在细胞和动物模型中,CLO的作用机制与核因子κB(NF-κB)和核因子E2相关因子2(Nrf2)信号通路有关。通路抑制剂实验表明这两条通路之间可能存在功能串扰。
CLO可能通过NF-κB和Nrf2信号通路调节脂多糖诱导的ALI中的炎症和氧化应激。这一发现可能为ALI的药物治疗提供新方法。