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. 2022 Jan 18;13(2):2927–2942. doi: 10.1080/21655979.2021.2017698

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© 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — miR-665-3p modulates oxidative stress, inflammation and cellular injury in PO-treated primary hepatocytes. (a) LDH releases in PO-stimulated hepatocytes treated with or without the miR-665-3p antagomir. (b) Intracellular TG and TC levels in the miR-665-3p antagomir-treated hepatocytes upon PO stimulation. (c) Cellular ROS levels determined by DCFH-DA probe. (d) MDA levels in the miR-665-3p antagomir-treated hepatocytes. (e) The levels of IL-1β, IL-6, MCP-1, TNF-α and IL-10 in the miR-665-3p antagomir-treated hepatocytes. (f) LDH releases in PO-stimulated hepatocytes treated with or without the miR-665-3p agomir. (g) Intracellular TG and TC levels in the miR-665-3p agomir-treated hepatocytes upon PO stimulation. (h) Cellular ROS levels determined by DCFH-DA probe. (i) MDA levels in the miR-665-3p agomir-treated hepatocytes. (j) The levels of IL-1β, IL-6, MCP-1, TNF-α and IL-10 in the miR-665-3p agomir-treated hepatocytes. All results were expressed as the means ± standard deviations, n = 6 for each group, and *P < 0.05 was considered statistically significant.