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. 2022 Aug 12;20:117. doi: 10.1186/s12958-022-00991-6

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 5 — Sirt1 knockdown prevented the protective effect of melatonin on mitochondrial dysfunction caused by high glucose. A The expression levels of mitochondrial function-related proteins in TM3 cells were detected by Western blot and their gray values were analyzed. B and D Mitochondria in TM3 cells were stained by MitoTracker fluorescent probe and the percentage of cells with mitochondrial fragmentation (n = 150) was statistically analyzed. C and E Mitochondrial reactive oxygen species in TM3 cells were detected by MitoSOX, and the average fluorescence intensity was statistically analyzed. NG, normal glucose control group; HG, high glucose treatment group; HG + MT, high glucose and melatonin treatment group; siSirt1, HG + MT + siSirt1 group. A, Data are expressed as fold change relative to NG. *, P < 0.05; #, P < 0.01. Bar: B&C, 50 μm