Department of Emergency, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China.
Department of Critical Care Medicine, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, China;
Allergol Immunopathol (Madr). 2022 May 1;50(3):113-118. doi: 10.15586/aei.v50i3.587. eCollection 2022.
Pneumonia is a continuous and widespread disease with higher incidence, the effects of it on human life can be fearful. Tricin has been demonstrated to take part in the progression and development of diseases. However, the function of Tricin and its related regulatory pathways remain unclear. This study was planned to investigate the effects of Tricin on severe pneumonia.
The cell viability was detected through CCK-8 assay. The TNF-α, IL-1β and IL-6 levels were assessed through ELISA and RT-qPCR. The levels of MDA, SOD and GSH were tested through corresponding commercial kits. The protein expressions were examined through western blot.
In our study, the lipopolysaccharide (LPS) was firstly used to stimulate cell model for severe pneumonia. We discovered that Tricin had no toxic effects on BEAS-2B cells and the decreased cell viability induced by LPS was relieved by a dose-dependent Tricin treatment. Additionally, through ELISA and RT-qPCR, it was uncovered that Tricin reduced the LPS-induced inflammation through regulating TNF-α, IL-1β and IL-6. Furthermore, Tricin relieved LPS-induced oxidative stress through reducing MDA level and enhancing SOD and GSH levels. Finally, it was demonstrated that Tricin retarded LPS-activated AKT and MAPK pathways.
Our findings revealed that Tricin attenuated the progression of LPS induced severe pneumonia through modulating AKT and MAPK signaling pathways. This discovery might afford one novel sight for the treatment of severe pneumonia.
肺炎是一种发病率较高、持续广泛的疾病，其对人类生命的影响可能是可怕的。三荆素已被证明参与了疾病的进展和发展。然而，三荆素的功能及其相关调节途径仍不清楚。本研究旨在探讨三荆素对重症肺炎的影响。
通过 CCK-8 检测细胞活力。通过 ELISA 和 RT-qPCR 评估 TNF-α、IL-1β 和 IL-6 水平。通过相应的商业试剂盒测试 MDA、SOD 和 GSH 的水平。通过 Western blot 检测蛋白表达。
在我们的研究中，首先使用脂多糖（LPS）刺激重症肺炎细胞模型。我们发现三荆素对 BEAS-2B 细胞没有毒性作用，并且 LPS 诱导的细胞活力下降被剂量依赖性的三荆素处理所缓解。此外，通过 ELISA 和 RT-qPCR，发现三荆素通过调节 TNF-α、IL-1β 和 IL-6 减轻 LPS 诱导的炎症。此外，三荆素通过降低 MDA 水平和增强 SOD 和 GSH 水平来缓解 LPS 诱导的氧化应激。最后，证明三荆素抑制了 LPS 激活的 AKT 和 MAPK 途径。
我们的研究结果表明，三荆素通过调节 AKT 和 MAPK 信号通路，减轻 LPS 诱导的重症肺炎的进展。这一发现可能为重症肺炎的治疗提供了一个新的视角。
