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Copyright ©2008 The WJG Press and Baishideng.
World J Gastroenterol. Nov 14, 2008; 14(42): 6551-6559
Published online Nov 14, 2008. doi: 10.3748/wjg.14.6551
Figure 1
Figure 1 Pathological changes of liver under light microscope. A: Lamellar hemorrhagic necrosis, model control group (6 h); B: Massive hemorrhagic necrosis, model control group (12 h); C: Spotty necrosis of liver cell, Baicalin treated group (12 h); D: Piecemeal necrosis, Octreotide treated group (12 h); E: Normal liver, sham-operated group (12 h). (HE, × 200).
Figure 2
Figure 2 TMA of liver was prepared and immunohistochemical staining. A: Bax protein expression level was “++”, model control group (3 h); B: Bcl-2 protein expression level was “+++”, model control group (6 h); C: Caspase 3 protein expression level was “++”, Octreotide treated group (6 h). (× 200).
Figure 3
Figure 3 TMA of liver was prepared and conduced TUNEL staining, observing the changes of apoptotic indexes. A: model control group (3 h), there was no apoptotic cell; B: Baicalin treated group (3 h), several hepatic apoptotic cells appeared; C: Baicalin treated group (6 h), several apoptotic hepatic Kupffer cells; D: Baicalin treated group (12 h), several apoptotic hepatic Kupffer's cells; E: Octreotide treated group (3 h), several apoptotic hepatic Kupffer's cells. (TUNEL, × 400).