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. 2018 Sep 4;16(5):3913–3920. doi: 10.3892/etm.2018.6692

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Copyright: © Yang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — miR-140-5p regulates inflammation in the in vitro acute lung injury model through the MyD88/NF-KB signaling pathway by targeting TLR4. (A) TLR4, (B) MyD88 and (C) NF-κB protein expression was statistically analyzed. (D) Western blotting assays for the (E) TLR4, (F) MyD88 and (G) NF-κB signaling pathway were performed following miR-140-5p downregulation, as well as following (H) the overexpression of miR-140-5p. **P<0.01 vs. negative control group. miR, microRNA; Anti-140-5p, downregulation of miR-140-5p group; miR-140-5p, over-expression of miR-140-5p; TLR4, Toll-like receptor 4; MyD88, myeloid differentiation primary response 88; NF-κB, nuclear factor-κB.