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. 2020 Jun 2;26(6):528–536. doi: 10.1177/1753425920928449

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© The Author(s) 2020

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 4. — MiR-128-3p activates the NF-κB pathway by inhibiting Rnd3 expression in a mouse liver I/R-treated model. (a) Relative miR-128-3p mRNA level after being treated with miR-128-3p agomir and miR-128-3p NC. (b) Relative Rnd3 mRNA level after being treated with ADV-Rnd3 and ADV control. (c) Relative Rnd3 mRNA level in a mouse liver I/R model treated with miR-128-3p agomir and ADV-Rnd3. (d) and (e) Serum ALT and AST levels after being treated with miR-128-3p agomir and ADV-Rnd3. (f) and (g) Serum TNF-α and IL-6 levels after being treated with miR-128-3p agomir and ADV-Rnd3. (h)–(j) Relative Rnd3 and NF-κB (p65) protein expression in a mouse liver I/R model after being treated with miR-128-3p agomir and ADV-Rnd3. (k) and (l) Histological changes of the liver in the sham, I/R, I/R+miR-128-3p agomir and I/R+miR-128-3p agomir+ADV-Rnd3 groups. Original magnification ×200. n = 5. *P < 0.05; **P < 0.01; ***P < 0.001; ns. P > 0.05.