LncRNA MEG3 ameliorates NiO nanoparticles-induced pulmonary inflammatory damage via suppressing the p38 mitogen activated protein kinases pathway

The lung inflammatory damage could result from the nickel oxide nanoparticles (NiO NPs), in which the underlying mechanism is still unclear. This article explored the roles of long noncoding RNA maternally expressed gene 3 (lncRNA MEG3) and p38 mitogen activated protein kinases (p38 MAPK) pathway in pulmonary inflammatory injury induced by NiO NPs. Wistar rats were treated with NiO NPs suspensions (0.015, 0.06, and 0.24 mg/kg) by intratracheal instillation twice-weekly for 9 weeks. Meanwhile, A549 cells were treated with NiO NPs suspensions (25, 50, and 100 mu g/ml) for 24 h. It can be concluded that the NiO NPs did trigger pulmonary inflammatory damage, which was confirmed by the histopathological examination, abnormal changes of inflammatory cells and inflammatory cytokines (IL-1 beta, IL-6, TGF-beta 1, TNF-alpha, IFN-gamma, IL-10, CXCL-1 and CXCL-2) in bronchoalveolar lavage fluid (BALF), pulmonary tissue and cell culture supernatant. Furthermore, NiO NPs activated the p38 MAPK pathway and downregulated MEG3 in vivo and in vitro. However, p38 MAPK pathway inhibitor (10 mu M SB203580) reversed the alterations in the expression levels of inflammatory cytokines induced by NiO NPs. Meanwhile, over-expressed MEG3 significantly suppressed NiO NPs-induced p38 MAPK pathway activation and inflammatory cytokines changes. Overall, the above results proved that over-expression of lncRNA MEG3 reduced NiO NPs-induced inflammatory damage by preventing the activation of p38 MAPK pathway.

Automated summary

This study found that nickel oxide nanoparticles (NiO NPs) can cause lung inflammatory damage, and over-expression of lncRNA MEG3 can reduce this damage by preventing the activation of the p38 MAPK pathway.