Fig 2: GFL regulation of glutamine metabolism by the NF-?B pathway. (A) Glutamate content in the liver. mRNA expression of (B) GLS1 and (C) GLS2 in the liver. Representative (D) GLS1 and (E) GLS2 immunohistochemical images of liver tissue sections (×200 magnification). (F) Protein expression of GLS1 and GLS2 in the liver. (G) Protein expression statistics of GLS1 and GLS2. (H) Protein expression of the NF-?B pathway in the liver. (I) Protein expression statistics of the NF-?B pathway. Data are expressed as the mean ± SD, n = 3. Data were analyzed using one-way ANOVA. #p < 0.05, ##p < 0.01 compared to the sham group. *p < 0.05, **p < 0.01 compared to the model group.

Fig 3: ATL III affects ECM synthesis through the PI3K/AKT signaling pathway, regulates glutamine metabolism to inhibit GLS1, and improves metabolic disorders, thereby ameliorating liver fibrosis.

Fig 4: Inhibition of glutaminase by ATL III in BDL-induced liver fibrosis. (A) Molecular docking of ATL III with the protein GLS1. (B) ATL III binding to the GLS1. (C) Glutamate content in the liver. (D) Representative GLS1 and GLS2 immunohistochemical images of liver tissue sections. (E) Protein expression of GLS1 and GLS2 in the liver. Protein expression statistics of (F) GLS1 and (G) GLS2. Results are expressed as mean ± SD, n = 3. ## p < 0.01 compared with the sham group. * p < 0.05, ** p < 0.01 compared with the model group.