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15LO1 increases intracellular oxidative potential by lowering GSH and increasing extracellular GSSG To confirm that 15LO1-PEBP1 complex activity alters IL-13induced intracellular GSH levels, we modeled these relationships in vitro by stimulating cultured HAECs (at ALI) with IL-13 for 710 days in the presence and absence of 15LO1 protein (dicer siRNA knockdown [KD] of ALOX15 gene) or enzymatic activity (specific 15LO1 inhibitor BLX2477) (14, 15)

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As these transcriptional alterations suggest a reduction in hepatic fibrosis in response to lowering oxalate via AGXT overexpression, we next evaluated hepatic fibrosis through histopathological and immunofluorescence analyses coupled with biochemical verification