In addition, the results of immunohistochemistry also showed that the protein expression level of fibrosis markers (α-SMA, collagen I, collagen IV, and fibronectin) was significantly up-regulated in the NAFLD rat model, and up-regulation of these protein were reversed by SSJZF or PC treatment (Figure 2(E,F)), suggesting that SSJZF ameliorated liver fibrosis in rats with NAFLD. This evidence concerns the gene FN1 and metabolic dysfunction-associated steatotic liver disease.