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 toinvestigate the response of liver oval cells (bipotent liver progenitors) to the epigenetic modifier trichostatin A (TSA), anHDAC1 inhibitor, and to develop a scoring system for assessing the response of these cells. Three groups of equally dividedrats (n=24) were selected: control (A, dimethyl sulfoxide treated); oval cell induction (B, acetylaminofluorene [2-AAF] toblock 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 responsewas measured by calculating the bile duct (BD) to portal vein (PV) ratio and the percentage of individual oval cells in liversections. The expression level of HDAC1 was also analyzed. The administration of TSA significantly enhanced oval cellproliferation and the ductular response (6.13±0.28). The control group exhibited limited immunoreactivity to OV-6, whilegroup B showed significant induction of ductular response with distinct morphology (4.13±0.28). The expression levels ofHDAC1 were elevated in both the oval cell induction group and the epigenetic modulation group compared to the controlgroup. This study developed a precise method for quantifying liver oval cells and analyzing their response to TSA. TSAadministration 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 theresponse of liver oval cells.