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. 2022 Nov 21;6(1):e202201665. doi: 10.26508/lsa.202201665

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© 2022 Yang et al.

This article is available under a Creative Commons License (Attribution 4.0 International, as described at https://creativecommons.org/licenses/by/4.0/).

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Figure 3. — (A, B, C) Under DKK1 knockout conditions, cell steatosis was induced by FFA (A, B, C), n = 3 in each group. (A, B, C) Oil red O staining (A) scale bar = 50 µm; TG measurements in DKK1^−/− AML12 (B) and DKK1^−/− HepG2 (C) cells. n = 3 in each group. (D, E) The changed TG was further confirmed with administration of a DKK1 inhibitor, WAY262611 in AML12 (D) and HepG2 (E) cells. n = 3 in each group. (F, G, H) On other hand, under DKK1 overexpression condition, the induced steatosis status was parallel analyzed, oil red O staining (F), and TG measurements in DKK1^−/− AML12 (G) and DKK1^−/− HepG2 (H) cells. n = 3 in each group. (I, J) Furthermore, the changed trend of TG was further confirmed with administration of recombinant DKK1 protein in AML12 (I) and HepG2 (J) cells. n = 3 in each group. *P < 0.05, **P < 0.01, ***P < 0.001 as compared with the indicated controls by two-tailed t tests. All data are shown as the means ± SD.

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