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. 2020 Jul 16;11:2040622320942042. doi: 10.1177/2040622320942042

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© The Author(s), 2020

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 4. — GNS561 inhibits hepatic stellate cell stimulation and ECM deposition in LX-2. Cell lysates were prepared after both GNS561 treatment (24 h) and transforming growth factor-beta 1 (TGF-β1) stimulation (22 h, 5 ng/μL) and analyzed by real-time polymerase chain reaction (PCR) and western blotting. mRNA (a and c) and protein (b and d) fold changes of alpha smooth muscle actin (α-SMA) (a and b) and collagen type I alpha 1 chain (COL1A1) (c and d) were measured in comparison with the untreated condition (neither GNS561 nor TGF-β1 stimulation). The mRNA levels of TGF-β1 (e) and metalloproteinases (MMPs) 2 and 9 (f) and tissue inhibitors of MMP (TIMP) 1 and 3 (f) were analyzed using real-time PCR and compared against the untreated condition (neither GNS561 nor TGF-β1 stimulation). The data are presented as median values of three separate experiments surrounded by upper and lower confidence limits (95%). For all blots, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) immunoblotting was used as a loading control.