CK19和PCNA在肝纤维化大鼠部分肝切除后再生肝中的表达
方方, 刘前进, 岳学强, 李娜娜, 刘恒兴
中国临床解剖学杂志 ›› 2012, Vol. 30 ›› Issue (5) : 552-555.
CK19和PCNA在肝纤维化大鼠部分肝切除后再生肝中的表达
Expression of CK19 and PCNA in fibrosis rat regenerating liver after partial hepatectomy
目的 检测肝纤维化大鼠部分肝切除后不同时点CK19及PCNA的表达，了解胆管再生情况。 方法 雄性SD大鼠，对照组和实验组各42只，实验组腹腔注射CCl4制备肝纤维化模型，两组均进行部分肝切除术，在不同时点取材后利用HE、免疫组化及免疫荧光双标染色等方法检测CK19和PCNA的表达情况。 结果 实验组和对照组术后随时间延长CK19表达均呈增强趋势，且实验组术后各时间点CK19的表达均高于对照组同时间点。两组PCNA的表达量都随时间推移逐步升高，但实验组大鼠明显上升缓慢，持续时间延长，表达高峰晚于对照组出现。 结论 （1）肝纤维化大鼠部分肝切除能刺激肝卵圆细胞增殖和向胆管细胞的分化，而正常大鼠部分肝切除后再生肝中的胆管上皮细胞主要来源于原有细胞的代偿性增生。（2）术前肝纤维化大鼠的肝脏细胞就出现了增殖修复，术后由于肝纤维化大鼠本身肝脏受到伤害，因此肝脏的有效再生细胞数低于正常肝脏。
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.
新乡医学院重点学科开放课题(ZD200949)
京ICP备08002354号-3/
| 〈 |
|
〉 |
