Nimbolide inhibits tumor growth by restoring hepatic tight junction protein expression and reduced inflammation in an experimental hepatocarcinogenesis

Figure 3 Effect of nimbolide on liver function parameters and tumor and cell proliferation markers in diethylnitrosamine and N-nitrosomorpholine induced hepatocellular carcinoma mice. A: Plasma aspartate aminotransferase level in naïve and experimental groups; B: Plasma alanine aminotransferase level in naïve and experimental groups; C: Plasma alkaline phosphatase level in naïve and experimental groups; D: Plasma alpha-fetoprotein level in naïve and experimental groups; E: Representative images of glypican-3 immunostaining of mice liver from naive and experimental groups (200 × magnification); F: Quantification of glypican-3 positive cells in experimental groups by counting five 400 × fields of each liver section; G: Representative images of proliferating hepatocytes by proliferating cell nuclear antigen (PCNA) immunostaining of mice liver from naive and experimental groups (200 × magnification); H: Quantification of PCNA positive nuclei in experimental groups by counting five 400 × fields of each liver section. Scale bar: 200 μm; all the data are expressed as mean ± SEM (n = 3-6). The comparison between the groups was analyzed by one-way ANOVA followed by Tukey’s multiple comparison post-hoc test or Kruskal-Wallis followed by Dunn’s multiple comparison post-hoc test. ^cP < 0.0001 compared to naïve group; ^dP < 0.05, ^eP < 0.01 compared to hepatocellular carcinoma group. AST: Aspartate aminotransferase; ALT: Alanine aminotransferase; ALP: Alkaline phosphatase; AFP: Alpha-fetoprotein; PCNA: Proliferating cell nuclear antigen; HPF: High-power fields; HCC: Hepatocellular carcinoma.