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. 2020 Aug 7;22(4):3191–3200. doi: 10.3892/mmr.2020.11423

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Copyright: © Xiao et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 4. — Effects of 11β-HSD1 knockdown and overexpression on LX2-HSC proliferation. (A) 11β-HSD1 knockdown using siRNA-11β-HSD1. (B) 11β-HSD1 overexpression using pSuper-11β-HSD1. ^##P<0.01 vs. N. (C) Effects of 11β-HSD1 knockdown and overexpression on LX2-HSC proliferation under normal culture conditions. (D) Effects of 11β-HSD1 knockdown and overexpression on LX2-HSC proliferation following TGF-β1 induction. ^#P<0.05 and ^##P<0.01 vs. N. 11β-HSD1, 11β-hydroxysteroid dehydrogenase 1; HSCs, hepatic stellate cells; siRNA, small interfering RNA; N, normal control group; NC, non-specific control; Vec, group in which LX2-HSCs were transfected with the pSuper-11β-HSD1-vector plasmid; OD, optical density; TGF-β1, transforming growth factor-β1.