特里金
蛋白激酶B
MAPK/ERK通路
医学
活力测定
脂多糖
氧化应激
肺炎
信号转导
药理学
细胞凋亡
免疫学
内科学
生物
细胞生物学
生物化学
抗氧化剂
类黄酮
出处
期刊:Allergologia et immunopathologia
[Codon Publications]
日期:2022-05-01
卷期号:50 (3): 113-118
被引量:3
标识
DOI:10.15586/aei.v50i3.587
摘要
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.
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