MicroRNA‑223 attenuates LPS‑induced inflammation in an acute lung injury model via the NLRP3 inflammasome and TLR4/NF‑κB signaling pathway via RHOB
- Yurong Yan
- Kexin Lu
- Ting Ye
- Zongwang Zhang
Affiliations: Shandong University, Jinan, Shandong 250012, P.R. China, Department of Obstetrics, Binzhou Medical University Hospital, Binzhou, Shandong 256600, P.R. China, Department of Anesthesiology, Binzhou Medical University Hospital, Binzhou, Shandong 256600, P.R. China, Department of Anesthesiology, Liaocheng People's Hospital, Liaocheng, Shandong 252000, P.R. China
- Published online on: January 23, 2019 https://doi.org/10.3892/ijmm.2019.4075
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Acute lung injury (ALI) and the more severe acute respiratory distress syndrome are common and complex inflammatory lung diseases. MicroRNAs (miRs) have emerged as novel gene regulatory molecules, serving a crucial role in a variety of complex diseases, including ALI. In the present study, the anti‑inflammatory action of miR‑223 on inflammation in ALI was demonstrated and the possible mechanism was further examined. In lipopolysaccharide‑induced ALI, the expression of miR‑223 was reduced compared with that in the control normal group. An in vitro model was used to analyze the effect of miR‑223 downregulation on an ALI model, which increased inflammation, and induced the activation of the NACHT, LRR and PYD domains‑containing protein 3 (NLRP3) inflammasome and Toll‑like receptor 4 (TLR4)/nuclear factor (NF)‑κB signaling pathway via rho‑related GTP‑binding protein RhoB (RHOB). In addition, the overexpression of miR‑223 reduced inflammation and suppressed the NLRP3 inflammasome and TLR4/NF‑κB signaling pathway via RHOB in the in vitro model. Furthermore, TLR4 inhibitor or NLRP3 inhibitor reduced the pro‑inflammatory effect of miR‑223 downregulation in ALI. In conclusion, the results of the present study indicated that miR‑223 functioned as a biological indicator by regulating inflammation in ALI, and may represent a novel potential therapeutic target and prognostic marker of ALI.