Figure 3.

The alterations in APE1, p53 mRNA and protein levels as well as the expression profile of cirrhosis-related versus anti-cirrhosis genes in cirrhotic versus human MNCs-treated rats. RT-PCR analysis of p53, p21, APE1 and SOD levels of TAA-administered rats indicated pathological hepatocytes damage with reduced level of p53 protein and mRNA up to week 20. MNCs induced HSCs apoptosis with significant elevation in p53 mRNA level at weeks 22 (b). Change in p21 mRNA level was used as positive control for p53 activation. APE1 mRNA and protein levels were significantly reduced during the time course of HSCs activation. MNCs-treatment induced HSCs inhibition and up-regulation of APE1 expression as shown in Figures a & b. Alterations in SOD mRNA level were used to assess the general decline in the hepatocytes total antioxidant capacity. Moreover, SOD gene expression has been reported to be down-regulated by p53 protein. GAPDH was used as an internal control. β-actin level was used as internal control in western blotting analysis. c) Real time-PCR analysis of APE1 levels indicated significant reduction during TAA-induced cirrhosis development versus control and siginfcant elevation in its level in treated versus self-recovery weeks. e) Immunohistochemical analysis of APE1 in treated liver at week 22 indicated marked cytoplasmic expression. MNCs treatment induced elevation in APE1 level at week 24. * represent the statistical difference from control and ** represents the statistical significance between groups.