Osthol attenuates hepatic steatosis via decreased triglyceride synthesis not by insulin resistance

Figure 1 Changes in body weight of control, non-alcoholic fatty liver disease and osthol groups. NAFLD: Non-alcoholic fatty liver disease.

Figure 2 Effect of osthol on serum aspartate transaminase/alanine transaminase and glucose levels. Changes in serum ASLT/ALT of control, non-alcoholic fatty liver disease (NAFLD) and osthol groups (A and B). Osthol treatment decreased serum glucose levels (C). AST: Aspartate aminotransferase; ALT: Alanine aminotransferase. ^aP < 0.05.

Figure 3 Changes in serum glucose levels following the oral glucose tolerance test. NAFLD: Non-alcoholic fatty liver disease.

Figure 4 Effect of osthol on liver histology. Hematoxylin and eosin staining showing the difference in periportal inflammation and fat content between control, NAFLD and osthol groups (A-E). ^aP < 0.05.

Figure 5 4-hydroxynonenal immunohistostaining comparing control, non-alcoholic fatty liver disease, and osthol groups (A-D). The NAFLD group shows increased 4-hydroxynonenal (4-HNE) immunohistostaining compared with the osthol group. NAFLD: Non-alcoholic fatty liver disease.

Figure 6 F4/80 immunohistostaining comparing control, non-alcoholic fatty liver disease, and osthol groups showing no significant difference between the groups (A-C). NAFLD: Non-alcoholic fatty liver disease.

Figure 7 Polymerase chain reaction expressions of SREBP1c, FAS, SCD-1, PPAR-α and CROT. Compared with the NAFLD group, osthol treatment decreased SREBP1c, FAS, and SCD-1 expression (A-C), and increased PPAR-α and CROT expression (D and E). ^aP < 0.05.

Figure 8 Polymerase chain reaction expressions of IRS-1, IRS-2, ATF6 and MCP-1 (A-D) showing no statistically significant differences between the groups.