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. The gene discussed is ACTA1; the disease is metabolic dysfunction-associated steatotic liver disease.