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. 2022 Aug 5;26:372–386. doi: 10.1016/j.omto.2022.08.001

Figure 5.

Figure 5

E2 inhibited the leptin promoter activity and p38 phosphorylation stimulated by LPA

(A) pGL4.17-LP1 transfected cells were treated as above, BBR as 2.5 μM, and E2 at a dose of 100 pM. The luminescence was set as 1 in the vehicle group treated with DMSO. Values are expressed as mean ± SEM, ∗∗p < 0.01 versus the LPA-stimulated group treated with DMSO. ##p < 0.01 versus the LPA-stimulated group treated with E2. (B) E2 (100 pM) inhibited LPA-induced p38 phosphorylation at Thr180/Tyr182. HepG2 cells were treated and western blot was conducted as described above. (C) Schematic diagram illustrates BBR restrained liver tumorigenesis through antagonizing the ATX-LPA-LPAR2-p38-leptin axis, and reducing LPA-stimulated abnormal leptin transcription in hepatoma cells.