Basic Research
Copyright ©2005 Baishideng Publishing Group Inc.
World J Gastroenterol. Nov 7, 2005; 11(41): 6477-6482
Published online Nov 7, 2005. doi: 10.3748/wjg.v11.i41.6477
Figure 1
Figure 1 The histological structure of intestine in sham-operated control group (A), 6 h after ischemia-reperfusion in R group (B) and 6 h after ischemia-reperfusion in A group (C) (100×). Anatomic structures of villi and crypts of intestine in control group were intact. In R group, at 6 h after reperfusion, the crypt-villus structure was seriously spoiled, accompanied by inflammatory cells infiltrating into the intestinal wall. In A group, the structures of crypt and villi were both protected, with less damage of the intestinal mucosa.
Figure 2
Figure 2 The cellular apoptotic rates in sham-operated control group (A), 6 h after ischemia-reperfusion in R group (B) and 6 h after ischemia-reperfusion in A group (C) (200×). Cellular apoptotic rates were less in sham-operated control group and were significantly increased in villi and crypts at 6 h after reperfusion. The augmentation of the cellular apoptotic rates was evident along the length of jejunal crypt-villus units. The cellular apoptotic rates both decreased remarkably at 6 h after reperfusion in villi and crypts of A group vs those of R group.
Figure 3
Figure 3 The expression of PCNA protein in sham-operated control group (A), 6 h after ischemia-reperfusion in R group (B) and 6 h after ischemia-reperfusion in A group (C) (200×). PCNA was weakly expressed in sham-operated control group, with positive particles mostly distributing in the nuclei of the lower third of crypt cells. Protein contents of PCNA were significantly increased in villi and crypts at 6 h after reperfusion compared with control group. The contents of PCNA increased remarkably in villi and crypts at 6 h after reperfusion in A group vs R group.