Fig. 8: Graphical abstract of the study. | Cell Death & Disease

Fig. 8: Graphical abstract of the study.

From: Estrogen-dependent activation of TRX2 reverses oxidative stress and metabolic dysfunction associated with steatotic disease

Fig. 8

(1) Human embryonic stem cells (hESC) were differentiated into hepatocyte-like cells (HLC) using an 18-day differentiation protocol; (2) HLC and hepatic immortalized cell lines (AML12, HepG2) were then treated with sodium L lactate (L), sodium pyruvate (P) and octanoic acid (O), a protocol of induction called LPO. LPO administration induces distinct steatotic traits, such as the increase of lipid droplets and reactive oxygen species (ROS) levels. (3) Treatment with 17-β estradiol (E2) results in a reduction of the distinctive traits of MASLD through the activation of the mitochondrial antioxidant mechanism of thioredoxin 2 (TRX2), which is inhibited by the administration of auranofin.

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