Basic Research
Copyright ©The Author(s) 2004.
World J Gastroenterol. Apr 1, 2004; 10(7): 1047-1051
Published online Apr 1, 2004. doi: 10.3748/wjg.v10.i7.1047
Figure 1
Figure 1 Liver tissue from control group showed normal lobular architecture and a normal distribution of collagen with a thin rim around central veins. Masson × 200.
Figure 2
Figure 2 A: Liver tissue from model group showed disorderly hepatocyte cords, severe fatty degeneration, spotty or focal necrosis and infiltration of inflammatory cells. HE × 200. B: Liver tissue from model group showed collagen deposition extending from central veins or portal tracts, with thick or thin fibrotic septa and pseudolobuli formation. Masson × 200.
Figure 3
Figure 3 Liver tissue from PII group showed apparent amelio-ration of hepatocyte degeneration, necrosis and infiltration of inflammatory cells. HE × 200.
Figure 4
Figure 4 Liver tissue from PII group showed marked reduction in collagen deposition with no obvious pseudolobuli formation. Masson × 100.