Department of Food Nutrition and Safety, Dalian Medical University, Dalian, China.
Department of Cardiology, The First Affiliated Hospital of Dalian Medical University, Dalian, China.
Environ Toxicol. 2022 Jul;37(7):1642-1652. doi: 10.1002/tox.23513. Epub 2022 Mar 14.
Exposure to air pollution has been closely associated with some cardiovascular disease. One of the mechanisms of PM -mediated heart injury may be to promote inflammation. We aim to investigate whether the main extract of Houttuynia cordata, 2-undecanone, can prevent the inflammation caused by PM , and to reveal the underlying mechanisms. The results showed that PM increased the expression of certain inflammatory cytokines, and caused oxidative damage in BALB/c mice and H9C2 cells. Supplementation with 2-undecanone attenuated this PM -induced inflammatory injury and oxidative damage. Further, we elucidated that the protective effect of 2-undecanone may be associated with NF-κB and Nrf2/HO-1 pathways. The NF-κB pathway was distinctly activated after treated by PM , which can be blocked by 2-undecanone, accompanied by increasing Nrf2 and HO-1 levels. To figure out the relationship between NF-κB and Nrf2/HO-1 pathways, we knocked down Nrf2 gene. NF-κB pathway proteins and downstream inflammatory cytokines were significantly increased after treatment with PM , while 2-undecanone could decrease expression of these proteins. In conclusion, it is possible that 2-undecanone can induce the expression of the antioxidant enzyme HO-1 by activating Nrf2, thereby reducing NF-κB pathway and inflammatory damage of mouse myocardium caused by PM exposure.
暴露于空气污染与一些心血管疾病密切相关。PM 介导的心脏损伤的机制之一可能是促进炎症。我们旨在研究鱼腥草的主要提取物 2-十一酮是否可以预防 PM 引起的炎症,并揭示其潜在机制。结果表明,PM 增加了某些炎症细胞因子的表达,并在 BALB/c 小鼠和 H9C2 细胞中引起氧化损伤。用 2-十一酮补充可减轻 PM 引起的这种炎症损伤和氧化损伤。此外,我们阐明了 2-十一酮的保护作用可能与 NF-κB 和 Nrf2/HO-1 途径有关。PM 处理后 NF-κB 途径明显激活,可被 2-十一酮阻断,同时 Nrf2 和 HO-1 水平增加。为了弄清 NF-κB 和 Nrf2/HO-1 途径之间的关系,我们敲低了 Nrf2 基因。PM 处理后 NF-κB 途径蛋白和下游炎症细胞因子显著增加,而 2-十一酮可降低这些蛋白的表达。总之,2-十一酮可能通过激活 Nrf2 诱导抗氧化酶 HO-1 的表达,从而减少 PM 暴露引起的小鼠心肌 NF-κB 途径和炎症损伤。