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. 2020 Jun 11;33(4):1006–1016. doi: 10.1007/s13577-020-00387-x

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© The Author(s) 2020

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/.

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Fig. 3 — HDAC inhibition promoted apoptosis of pancreatic stellate cells and elevated transcription of miR-15 and miR-16. a The cell viability of PSCs treated with an assigned concentration of SAHA (left) or TSA (right). b The percentage of apoptosis PSCs treated with SAHA or TSA. c The mRNA levels of α-SMA in PSCs treated with SAHA (left) or TSA (right). d The protein levels and the related quantification of α-SMA in PSCs treated with SAHA or TSA. e The levels of miR15 (left) and miR-16 (right) in PSCs treated with an assigned concentration of TSA. f The protein levels of ac-H3 and ac-H4 in PSCs treated with SAHA or TSA. All data are presented as the mean ± S.D. (n = 3). ***P < 0.001, compared with control. Each assay was performed in triplicate