GPX4-Regulated Ferroptosis Mediates S100-Induced Experimental Autoimmune Hepatitis Associated with the Nrf2/HO-1 Signaling Pathway

Figure 3

Exacerbation of S100-induced autoimmune hepatitis after GPX4 knockdown. (a) Experimental protocol for the transfection of AAV8-m-GPX4 and the establishment of the mouse AIH model; (b)–(d) ALT, AST, and IgG levels in the NC + AAV8-m-GPX4, AIH + AAV8-m-GPX4, NC + AAV8-EGFP, and AIH + AAV8-EGFP groups. (e) Representative H&E staining of liver tissue sections. The black arrow indicates lymphocytic infiltration (original magnification 20×); (f) TNF-α, IFNγ, IL-17, IL-10, and TGF-β levels in liver; (g) and (h) Western blot showing protein expression of COX2, ACSL4, GPX4, and FTH1 in the NC + AAV8-m-GPX4, AIH + AAV8-m-GPX4, NC + AAV8-EGFP, and AIH + AAV8-EGFP groups; GAPDH was used as a loading control. (i) IHC images of COX2 and GPX4 in liver sections (original magnification 20×). (j) Semiquantitative IHC results. (k) Detection of lipid peroxidation by measuring malondialdehyde (MDA) levels. (l) Fe²⁺ levels in liver; , compared with the NC + AAV8-EGFP group; ^#, compared with the AIH + AAV8-EGFP group.

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