[Apoptosis of pathological tissues and expression of apoptosis-related genes in hepatic venous stricture Budd-Chiari syndrome].
OBJECTIVE
To investigate the pathogenesis of hepatic venous stricture Budd-Chiari syndrome from the point of view of hepatic venous intimal proliferation, apoptosis and apoptosis-related genes.


METHODS
Thirty samples resected from patients with hepatic venous stricture Budd-Chiari syndrome and 21 samples of normal hepatic vein and vena cava obtained from necropsy of fresh corps as controls were examined. The paraffin sections of the samples were stained with hematoxyline and eosin and diaminobenzidine respectively and observed under light microscope to examine the pathology and calculate the apoptotic cells. SP immunohistochemistry was used to detect the expression of Bcl-2 and Bax. Proliferating cell nuclear antigen (PCNA) expression was detected by SABC immunohistochemistry.


RESULTS
Light microscopy showed irregular proliferation in the tunica intima and tunica media, especially in the former. Incomplete elastic fiber, spotted smooth muscle cells, proliferation of fibrous connective tissue, and degeneration of partial tissues, and infiltration of inflammatory cells, etc. were observed. In the endothelial tissue TUNEL positive cells was 1.94 +/- 0.64 in the Budd-Chiari syndrome patients, significantly higher than that in the controls (0.56 +/- 0.21, P < 0.002); and PCNA positive cells was 3.46 +/- 0.51 in the Budd-Chiari syndrome patients, significantly higher than that in the controls (0.78 +/- 0.16, P < 0.0005). The bcl-2 expression rate was 8.56 +/- 1.17 in the Budd-Chiari syndrome patients, significantly higher than that in the normal controls (4.34 +/- 1.28, P < 0.0005); Bax expression was 3.95 +/- 1.31 in the Budd-Chiari syndrome patients, significantly lower than that in the normal controls (5.06 +/- 1.21, P < 0.001); and the bcl/Bax ratio of the cells in the tunicae intima and media of the normal hepatic veins was 0.914 +/- 0.334, significantly lower than that in the Budd-Chiari syndrome patients (2.402 +/- 1.021, P < 0.01). Electron microscopy showed that in comparison with the normal tissues the pathological tissues had more synthesized smooth muscle cells and lacked normal myoendothelial structure.


CONCLUSIONS
Irregular proliferation of tunica intima of hepatic vein and apoptosis may be one of the mechanisms of hepatic venous stricture Budd-Chiari syndrome.
Wang
Chun-xi
CX
Department of General Surgery, General Hospital of Chinese People's Liberation Army, Beijing 100853, China.
Huang
Zhi-qiang
ZQ
Liang
Fa-qi
FQ
Li
Rong
R
Peng
Zheng
Z
D000328:Adult; D017209:Apoptosis / Q000502:physiology*; D006502:Budd-Chiari Syndrome / Q000235:genetics* / Q000473:pathology*; D005260:Female; D006503:Hepatic Veins / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D018809:Proliferating Cell Nuclear Antigen / Q000096:biosynthesis / Q000235:genetics; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis / Q000235:genetics; D017539:Tunica Intima / Q000737:chemistry / Q000473:pathology*; D051028:bcl-2-Associated X Protein / Q000096:biosynthesis / Q000235:genetics
D018809:Proliferating Cell Nuclear Antigen; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein