Figure 4.

Acute histopathological changes in a rat female HE model induced by TAA alone versus TAA plus EtOH. (A) The normal parenchymal liver architecture. (B) A 6-week-old rat that received TAA alone; there is mild hepatocyte congestion (yellow arrow) and hemosiderin disposition with fibroblast cells. (C) A 6-week-old rat receiving both TAA + EtOH; there is a notable severity of the changes (black arrow), extending from the portal area to hepatic parenchyma between the degenerated hepatocytes. (D) Rats after 5 months of receiving TAA alone; the liver displays fatty changes and mild congestion (yellow arrows) with some apoptotic hepatocytes. However, adding alcohol (E) to those rats unveiled more steatosis (black asterisk) and fibroblast accumulation and worsened the congestion. There was mild–moderate fat and hemosiderin accumulation and congestion in (F) in 12-month-old rats, whereas adding alcohol to those rats illustrated worsening hepatocyte changes (black arrow) (G). The livers of rats treated with TAA alone at 24 months exhibited moderate steatosis, fibroblast localization, apoptotic alteration, and congestion (H). Furthermore, when EtOH was added to TAA in those rats (I), there was remarkable steatosis (black asterisk) around the portal vein with worsening hepatocyte degeneration, more fibroblast recruited, and an increased level of congestion, as well as some fibrotic changes and inflammatory cells being recruited. Scale bar = 50 μm.