Fig. 3
Photomicrographs (100×) of the histopathological examinations of the liver samples of different groups. Even though the extract treated groups possessed injury marks however, the extent of signs of injury were much lower in the extract treated groups compared to CCl4 group. a Control group liver demonstrated normal liver architecture with normal sinusoids (NS), hepatocytes with intact nucleus (IN), un-inflamed portal vein (PV). b CCl4 group liver demonstrated significant loss of hepatocellular architecture with extensive fatty infiltration (FI) leading to steatosis, bile duct proliferation (BdP), vascular congestion (VC) and haemorrhagic necrosis (HN) around portal vein. Loss of hepatic nodular structure and disorganized hepatocytes marked the CCl4 induced liver damage. c Silymarin group demonstrated hepatoprotective activity by substantial amendment of proliferated bile duct (Bd) with normal sinusoids (NS) and intact portal veins (PV). d NOSE low group was marked by less leukocyte infiltrations (LI), sinusoidal dilations (SD) and bile duct proliferation (BdP). e NOSE high group reflected comparatively less haemorrhagic necrosis (HN) and fatty infiltrations (FI). f NORE low group also showed traces of sinusoidal dilations (SD), haemorrhagic necrosis (HN) and fatty infiltration (FI). g NORE high group demonstrated lowering of most of the injury signs however, leukocyte infiltrations (LI) could be identified in the liver samples