期刊
SCIENTIFIC REPORTS
卷 11, 期 1, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/s41598-021-86514-6
关键词
-
资金
- Arab Republic of Egypt (Egyptian Culture Affairs & Missions Sector) Scholarship
- University of Tubingen
The research highlights that urolithin A (UA) shows promising therapeutic potential for treating inflammatory diseases by inhibiting pro-inflammatory molecules and NF-kappa B activation, as well as maintaining intracellular calcium and ROS homeostasis.
Inflammation is a natural defense process of the innate immune system, associated with the release of proinflammatory cytokines such as interleukin-1 beta, interleukin-6, interleukin-12 and TNF alpha; and enzymes including iNOS through the activation and nuclear translocation of NF-kappa B p65 due to the phosphorylation of I kappa B alpha. Regulation of intracellular Ca2+ is considered a promising strategy for the prevention of reactive oxygen species (ROS) production and accumulation of DNA double strand breaks (DSBs) that occurs in inflammatory-associated-diseases. Among the metabolites of ellagitannins that are produced in the gut microbiome, urolithin A (UA) has received an increasing attention as a novel candidate with anti-inflammatory and anti-oxidant effects. Here, we investigated the effect of UA on the suppression of pro-inflammatory molecules and NF-kappa B activation by targeting TLR4 signalling pathway. We also identified the influence of UA on Ca2+ entry, ROS production and DSBs availability in murine bone-marrow-derived macrophages challenged with lipopolysaccharides (LPS). We found that UA inhibits I kappa B alpha phosphorylation and supresses MAPK and PI3K activation. In addition, UA was able to reduce calcium entry, ROS production and DSBs availability. In conclusion, we suggest that urolithin A is a promising therapeutic agent for treating inflammatory diseases through suppression of NF-kappa B and preserving DNA through maintaining intracellular calcium and ROS homeostasis.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据