Expression of CK19 and PCNA in fibrosis rat regenerating liver after partial hepatectomy
FANG Fang, LIU Jian-Jin, YUE Hua-Jiang, LI Na-Na, LIU Heng-Xin
Chinese Journal of Clinical Anatomy ›› 2012, Vol. 30 ›› Issue (5) : 552-555.
Expression of CK19 and PCNA in fibrosis rat regenerating liver after partial hepatectomy
Objective To detect the expressions of CK19 and PCNA in fibrosis rat regenerating liver after partial hepatectomy (PH) at the different time phase, for evaluating the bile duct regeneration in fibrotic liver. Methods Male SD rats were divided into two groups: the control group (42 rats) and the experimental group (42 rats). The rats of experimental group were injected CCl4 to establish the hepatic fibrosis model, and then the two groups was endured PH operation. HE, immunohistochemical and double-label immunofluorescence were used to detect and analyze expressions of CK19 and PCNA in regenerating liver. Results The expression of CK19 increased gradually after PH in both groups, however, expression intensity in experimental animals was significantly higher than control ones at the same time point. As well, the expression of PCNA increased gradually after PH in both groups, however, expression level in experimental groups rose slowly, extended and the peak appeared later than the control. Conclusions (1) PH process of fibrotic rat liver can stimulate proliferation of OCs and the differentiation to BECs, which mainly originate from compensatory hyperplasia in normal rats regenerating liver. (2) Before PH, liver cells in fibrosis rats have already proliferated, after PH, the effective regenerating cells are lower than the other liver injury.
Rat / Hepatic fibrosis / Bile duct / CK19 / PCNA
[1] Hosui A, Kimura A, Yamaji D, et al. Loss of stat5 causes liver fibrosis and cancer development through increased and stat3 activation
[J]. J Exp Med, 2009, 206(4): 819-831.
[2] Kuhlmann WD, Peschke P. Hepatic progenitor cells, stem cells, and afp expression in models of liver injury
[J]. Int J Exp Pathol, 2006, 87(5): 343-359.
[3] Higgins G.M, Anderson RM. Experimental pathology of the liver: Restoration of the liver of the white rat following partial surgical removal
[J]. Arch Patho, 1931, 12: 186-102.
[4] Fausto N, Campbell JS, Riehle KJ. Liver regeneration
[J]. Hepatology, 2006, 43(2 Suppl 1): S45-53.
[5] Michalopoulos GK. Liver regeneration
[J]. J Cell Physiol, 2007, 213(2): 286-300.
[6] Piryaei A, Valojerdi MR, Shahsavani M, et al. Differentiation of bone marrow-derived mesenchymal stem cells into hepatocyte-like cells on nanofibers and their transplantation into a carbon tetrachloride-induced liver fibrosis model
[J]. Stem Cell Rev, 2011, 7(1): 103-118.
[7] Vessey CJ, de la Hall PM. Hepatic stem cells: A review
[J]. Pathology, 2001, 33(2): 130-141.
[8] Michalopoulos GK. Liver regeneration after partial hepatectomy: Critical analysis of mechanistic dilemmas
[J]. Am J Pathol, 2010, 176(1): 2-13.
[9] Pham Van T, Couchie D, Martin-Garcia N, et al. Expression of matrix metalloproteinase -2 and -9 and of tissue inhibitor of matrix metalloproteinase-1 in liver regeneration from oval cells in rat
[J]. Matrix Biol, 2008, 27(8): 674-681.
[10]岳学强, 施相空, 李娜娜, 等. CK19和TGF-α在大鼠肝纤维化部分肝切除后残肝中的表达
[J]. 中国临床解剖学杂志, 2011, 29(2): 208-212.
[11]Liu C, Schreiter T, Frilling A, et al. Cyclosporine a, rapamycin and mycophenolate mofetil inhibit proliferation of human intrahepatic biliary epithelial cells in vitro
[J]. World J Gastroenterol, 2005, 11(48): 7602-7605.
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