Humans ; Liver Neoplasms ; metabolism ; pathology

Endotoxemia ; metabolism ; pathology ; HMGB1 Protein ; Humans ; Liver ; metabolism ; pathology

Hepatocytes ; metabolism ; pathology ; Liver Diseases ; genetics ; metabolism ; pathology

OBJECTIVETo observe the change in the amount of sialic acids on hepatocellular carcinoma (HCC) cell membrane.

METHODSSurgical specimens of HCC and liver cirrhosis tissues were obtained from 28 patients to prepare carcinoma cell and hepatocyte suspensions by collagenase digestion. For assay of α2, 3 and α2, 6-sialic acids, the cells were suspended in the staining buffer containing either fluorescein isothiocyanate-Maackia amurensis lectin (FITC-MAL) or fluorescein isothiocyanate-Sambucus nigra bark lectin (FITC-SNA) and incubated for 1 h, respectively. Flow cytometric analysis was carried out to measure the mean fluorescence intensity (MFI) on the cell surface.

RESULTSIn both FITC-MAL- and FITC-SNA-incubated HCC cells, the MFI on the cell surface was greater than that of the hepatocytes.

CONCLUSIONBoth of α2, 3 and α2, 6- sialic acids increases significantly on the hepatocyte membrane after the carcinomatous change.

Carcinoma, Hepatocellular ; metabolism ; pathology ; Cell Membrane ; metabolism ; Humans ; Liver Cirrhosis ; metabolism ; pathology ; Liver Neoplasms ; metabolism ; pathology ; Sialic Acids ; metabolism

OBJECTIVETo investigate the changes of osteopontin (OPN) in the liver tissues during nonalcoholic fatty liver fibrosis in rats and to explore the effect of OPN in the development of nonalcoholic fatty liver fibrosis.

METHODSFifty-six male Wistar rats were randomly divided into a control group (8 rats) and a high-fat diet group. The high-fat diet group was divided into 6 subgroups (8 rats in each subgroup) with high-fat feedings for 4, 8, 12, 16, 20 or 24 weeks. Conventional histochemical, HE, Masson-trichrome and immunohistochemical staining for alpha-smooth muscle actin (a-SMA) were performed with the liver histological preparations. The expression of OPN was detected with reverse transcription and polymerase chain reactions and Western blot.

RESULTSLevels of OPN in liver tissues in rat nonalcoholic fatty liver fibrosis induced by high-fat diet were significantly increased over those in the control group (F=7.15, P less than 0.01). OPN expressions were closely correlated with a-SMA and nonalcoholic fatty liver fibrosis, and correlation coefficients of the two groups were 0.94 and 0.82, and both P values were less than 0.01.

CONCLUSIONExpression of OPN increases dramatically in the livers during the development of nonalcoholic fatty liver fibrosis, and OPN may play an important role in this event.

Animals ; Fatty Liver ; metabolism ; pathology ; Liver ; pathology ; Liver Cirrhosis ; metabolism ; pathology ; Male ; Osteopontin ; metabolism ; Rats ; Rats, Wistar

Carcinoma, Hepatocellular ; metabolism ; pathology ; Hepatocytes ; metabolism ; pathology ; Humans ; Liver Neoplasms ; metabolism ; pathology ; NF-kappa B ; metabolism

Collagen ; biosynthesis ; Liver Cirrhosis ; metabolism ; pathology

Hepatitis ; metabolism ; pathology ; Humans ; Liver Regeneration

Objective To study the effect and mechanism of pearl hydrolysate on hepatic sinusoidal capillarization in liver fibrosis. Methods Hepatic sinusoidal endothelial cells (HSEC) and hepatic stellate cells (HSC-LX2) were incubated with Hepu pearl hydrolysate.The proliferation of HSEC and HSC-LX2 was examined by MTT colorimetry.The cell cycle and apoptosis of HSC-LX2 were measured by flow cytometry.The changes of the microstructures such as fenestra and basement membrane of HSEC were observed by transmission electron microscopy. Results The intervention with leptin increased the viability of HSC-LX2 (P=0.041),decreased the viability of HSEC (P=0.004),and caused capillarization signs such as decreased number and diameter of fenestrae and formation of continuous basement membrane.The treatment with pearl hydrolysate at different doses increased and expanded the fenestrae of HSEC (low dose:P=0.020;medium dose:P=0.028;high dose:P=0.032),disintegrated the extracellular basement membrane of HSEC (low dose:P=0.020;medium dose:P=0.028;high dose:P=0.032),decreased the viability of HSC-LX2 (low dose:P=0.018;medium dose:P=0.013;high dose:P=0.009),and induced the apoptosis of HSC-LX2 (low dose:P=0.012;medium dose:P=0.006;high dose:P=0.005).Pearl hydrolysate exerted therapeutic effect on capillarization in a dose-dependent manner (low dose:P=0.020;medium dose:P=0.028;high dose:P=0.032).Moreover,high-dose pearl hydrolysate showed stronger effect on capillarization of hepatic sinuses than colchicine (P=0.034) and salvianolic acid B (P=0.038). Conclusion Hepu pearl hydrolysate can increase the viability of HSEC,restore the area of fenestrae,disintegrate the basement membrane,and decrease the viability and induce the apoptosis of HSC-LX2,demonstrating significant pharmacological effects on the capillarization of HSEC and HSC-LX2.
Humans ; Endothelial Cells/metabolism* ; Liver Cirrhosis ; Liver/pathology*

OBJECTIVETo study the expression and significance of GPC3, CD10 and CD34 in hepatocellular carcinoma (HCC), dysplastic nodules (DN), cirrhotic regenerative nodules (CRN), focal nodular hyperplasia (FNH) and hepatocellular adenoma (HA).

METHODSImmunohistochemical study for GPC3, CD10, CD34 and AFP was performed on 80 cases of HCC (30 cases of well-differentiated HCC and 50 cases of advanced HCC), 30 cases of DN (18 cases of high-grade DN and 12 cases of low-grade DN), 36 cases of CRN, 20 cases of FNH and 20 cases of HA.

RESULTS(1) The positive expression rate of GPC3 was 92% (46/50) in advanced HCC, 66.7% (20/30) in well-differentiated HCC, 2/18 in high-grade DN, and 0 in low-grade DN, CRN, FNH and HA. The expression rate of GPC3 in well-differentiated HCC was lower than that in advanced HCC and higher than that in high-grade DN (P < 0.05). (2) The negative expression rate of CD10 was 78% (39/50) in advanced HCC, 43.3% (13/30) in well-differentiated HCC, 20% (4/20 and 4/20) in both FNH and HA, 2.8% (1/36) in CRN and 0 in both high-grade DN and low-grade DN. The occurrence of CD10-strongly positive cells was 2% (1/50) in advanced HCC, 16.7% (5/30) in well-differentiated HCC, 15/18 in high-grade DN, 11/12 in low-grade DN, 80.6% (29/36) in CRN and 60% (12/20 and 12/20) in both FNH and HA. The positive expression rate of CD10 in well-differentiated HCC was higher than that in advanced HCC and lower than that in high-grade DN, low-grade DN, CRN, FNH and HA (P < 0.05). (3) The positive expression rates of CD34 in advanced HCC and well-differentiated HCC ranged from 25% to 100% [and strongly positive in 76% (38/50) and 70% (21/30), respectively]. The rates in high-grade DN and low-grade DN ranged from 5% to 25% (and weakly positive in 16/18 and 10/12, respectively). In CRN, the rate ranged from 0 to 5% [and weakly positive in 27.8% (10/36)]. In FNH and HA, the positive rates ranged from 25% to 50%. The positive expression rate of CD34 in well-differentiated HCC was significantly higher than that in high-grade DN, low-grade DN, CRN, FNH and HA (P < 0.05). (4) The positive expression rate of AFP was 44% (22/50) in advanced HCC, 20% (6/30) in well-differentiated HCC, no expression in DN, LCN, LCN, FNH and HA. The positive expression rate of AFP in well-differentiated HCC was lower than that in advanced HCC and higher than that in LCN, FNH and HA. The different expression had statistical significance (P < 0.05).

CONCLUSIONSGPC3 is a relatively sensitive and specific marker in pathologic diagnosis of HCC. When coupled with immunohistochemical results of CD34, CD10 and AFP, GPC3 is useful in differentiating HCC from DN, LCN, FNH and HA.

Adenoma, Liver Cell ; metabolism ; pathology ; Antigens, CD34 ; metabolism ; Biomarkers, Tumor ; metabolism ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Diagnosis, Differential ; Focal Nodular Hyperplasia ; metabolism ; pathology ; Glypicans ; metabolism ; Humans ; Immunohistochemistry ; Liver Cirrhosis ; metabolism ; pathology ; Liver Neoplasms ; metabolism ; pathology ; Neprilysin ; metabolism ; alpha-Fetoproteins ; metabolism