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. 2021 Feb 26;12(2):217. doi: 10.1038/s41419-021-03508-y

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© The Author(s) 2021

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — SIRT1 activation by pretreatment with SRT1720, PD, RSV and SIRT1 inhibition pre-treated with EX527 for 2 h, respectively. A Pathological observation of kidney tissue. H&E staining of kidney cortex (upper panel, 200×; inset: 400×; scale bar = 10 μm) and PAS staining of kidney cortex (lower panel, 200×; inset: 400×; scale bar = 10 μm). The irregular brush border (arrow) and ectasia of the affected tubules (arrowheads) was observed. B Tubular damage scores were evaluated based on H&E and PAS staining (n = 10). C Scr levels (n = 6). D Serum BUN levels (n = 6). Values shown are the mean ± SD. ^*p < 0.05, ^**p < 0.01 and ^***p < 0.001 vs the sham group; ^##p < 0.01 and ^###p < 0.001 vs the vehicle + CLP group. SAKI sepsis-induced acute kidney injury, CLP caecal ligation and puncture, SIRT1 silent mating-type information regulation 2 homologue-1, PD polydatin, RSV resveratrol, PAS periodic acid-Schiff staining, H&E haematoxylin-eosin staining, Scr Serum creatinine, BUN urea nitrogen.