Liver oval cells in response to HDAC1 inhibitor trichostatin A: immunohistochemical characterization using OV-6 hepatic expression.

Liver regeneration is intricate, involves many cells, and necessitates extended research. This study aimed to investigate the response of liver oval cells (bipotent liver progenitors) to the epigenetic modifier trichostatin A (TSA), an HDAC1 inhibitor, and to develop a scoring system for assessing the response of these cells. Three groups of equally divided rats (n=24) were selected: control (A, dimethyl sulfoxide treated); oval cell induction (B, acetylaminofluorene [2-AAF] to block hepatocyes/carbon tetrachloride [CCL4] to induce oval cell response); and epigenetic modulation (C, TSA post 2-AAF/CCL4 injury). The oval cell response was quantified using immunoreactivity to the OV-6 antibody, and the ductular response was measured by calculating the bile duct (BD) to portal vein (PV) ratio and the percentage of individual oval cells in liver sections. The expression level of HDAC1 was also analyzed. The administration of TSA significantly enhanced oval cell proliferation and the ductular response (6.13±0.28). The control group exhibited limited immunoreactivity to OV-6, while group B showed significant induction of ductular response with distinct morphology (4.13±0.28). The expression levels of HDAC1 were elevated in both the oval cell induction group and the epigenetic modulation group compared to the control group. This study developed a precise method for quantifying liver oval cells and analyzing their response to TSA. TSA administration enhanced oval cell proliferation, suggesting its significance in regulating hepatic progenitor cell dynamics. The findings support the use of epigenetic modifiers in liver regeneration and propose a scoring system for assessing the response of liver oval cells.