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. 2019 Mar 14;19:58. doi: 10.1186/s12935-019-0777-2

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© The Author(s) 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 5 — Mitophagy was modulated by melatonin via the CaMKII-Parkin pathway. a–d Western blotting was used to analyze the expression of CaMKII and Parkin in response to melatonin and/or TNF-α treatment. siRNA against Parkin was transfected into TNF-α-treated cells to inhibit Parkin-related mitophagy. e–g Proteins were isolated from cells and the expression of p-CaMKII and Parkin was determined via western blotting. CaMKII specific agonist bradykinin (Brad) was added into melatonin-treated cells to re-activate the CaMKII pathway. H-J. Immunofluorescence assay for p-CaMKII and Parkin under melatonin and/or TNF-α treatment. CaMKII specific agonist bradykinin (Brad) was added into melatonin-treated cells to re-activate the CaMKII pathway. *P < 0.05 vs. ctrl group, ^#P < 0.05 vs. TNF-α group, ^@P < 0.05 vs. TNF-α + melatonin group