Overexpression of miR‑200a‑3p promoted inflammation in sepsis‑induced brain injury through ROS‑induced NLRP3
- Jianhua Yu
- Jinlong Chen
- Hualing Yang
- Sifang Chen
- Zhanxiang Wang
Affiliations: Department of ICU, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361000, P.R. China, Department of Neurosurgery, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361000, P.R. China
- Published online on: August 30, 2019 https://doi.org/10.3892/ijmm.2019.4326
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Sepsis, a systemic inflammatory response syndrome induced by infection, is a common complication of trauma, burns, postoperative infection and critical disease, and is characterized by an acute onset and high fatality rate. The aim of the present study was to explore the possible molecular mechanisms of microRNA‑200a‑3p (miRNA‑200a‑3p) on inflammation during sepsis. Reverse transcription‑quantitative PCR and gene microarray were used to measure the expression of miRNA‑200a‑3p. Tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 were searched by ELISA. The related proteins expression was measured using western blotting. The expression of miRNA‑200a‑3p was markedly higher in the sepsis model when compared with the normal control group. In addition, the expression of miRNA‑200a‑3p was upregulated by the miRNA‑200a‑3p plasmid in human brain microvascular endothelial cells treated with lipopolysaccharide, which further induced inflammation via the induction of NLR family pyrin domain containing 3 (NLRP3) and suppression of Kelch like ECH associated protein (Keap)‑1/nuclear factor erythroid 2 like 2 (Nrf2)/heme oxygenase (HO)‑1. The inhibition of Keap1/Nrf2/HO‑1 attenuated the effects of anti‑miRNA‑200a‑3p on inflammation. However, the inhibition of NLRP3 attenuated the effects of miRNA‑200a‑3p on inflammation. In conclusion, to the best of our knowledge, the results of the present study demonstrated for the first time that overexpression of miRNA‑200a‑3p promoted inflammation in sepsis‑induced brain injury through reactive oxygen species‑induced NLRP3.