Serum and tissue expressions of galectin-3 in hepatocellular carcinoma and the clinical significances / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study the expression of Galectin-3 in human hepatocellular carcinoma (HCC) tissues and the clinical value of serum Galectin-3 in the diagnosis of hepatocellular carcinoma.</p><p><b>METHODS</b>Immunohistochemistry method was used to detect the expression of Galectin-3 in the 46 pairs of HCC tissues and their para cancerous tissues. The relationship between expression levels of Galectin-3 and clinical parameters was analyzed. Serum Galectin-3 in different liver diseases were measured with ELISA. The sensitivity and specificity of galectin-3, alpha fetoprotein (AFP) and gamma-glutamyltranspeptidase II (GGT-II) for diagnosis of HCC were compared and the complementary diagnostic values of Galectin-3 and AFP and GGT-II for HCC were studied.</p><p><b>RESULTS</b>(1) The positive rate of Galectin-3 in the tissue of HCC was 78.2%, dramatically higher than that in para cancerous tissues (15.2%) (P is less than 0.01). The expression levels were correlated with differentiation and with the high expression in poor differentiation tissues; (2) Based on ROC curve, the cut-off of serum Galectin-3 for HCC diagnosis was set as 0.62mug/L, the serum galectin-3 positive rate was 64.5% in HCC cases, which was apparently higher than that in liver cirrhosis, chronic hepatitis and healthy persons (P is less than 0.05); (3) Serum Galectin-3 was not correlated with AFP and GGT-II. Combined determination of the three markers had the complementary diagnostic value for HCC and might increase the diagnostic sensitivity to 94.7%.</p><p><b>CONCLUSION</b>Galectin-3 is overexpressed in HCC tissues and is correlated with the tumor differentiation, suggesting that Galectin-3 may be associated with the carcinogenesis and development of HCC. Serum galectin-3 increases in the HCC cases and combined determination of serum Galectin-3, AFP and GGT-II can increase the diagnostic efficiency for HCC. Galectin-3 could be a novel serum tumor marker for HCC.</p>

Effects of decreased leptin expression on liver fibrosis / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study the effects of decreased leptin expression on liver fibrosis.</p><p><b>METHODS</b>The small interfering RNA, targeting leptin gene, was designed according to the secondary structure of leptin gene. The recombinant plasmids were encapsulated with lipofectamine and then injected into carbon tetrachloride (CCl4) induced rat liver fibrosis models. Leptin and I, III collage were detected by immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>The mRNA and protein levels of leptin in the fibrotic liver transfected with leptin shRNA were significantly decreased compared with those in controls (P less than 0.01). The depositions of type I and type III collagens were also decreased (P less than 0.01).</p><p><b>CONCLUSION</b>Decreased leptin expression prevents liver fibrosis.</p>

Effects of antisense RNA of connective tissue growth factor expressing plasmid on rat liver fibrosis / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To observe the effects of antisense RNA of connective tissue growth factor (CTGF) on rat liver fibrosis.</p><p><b>METHODS</b>Gene recombinant techniques were used to construct a rat antisense RNA of CTGF recombinant plasmid which could be expressed in eukaryotic cells. The recombinant plasmids were encapsulated with lipofectamine and then transducted into a carbon tetrachloride (CCl4) induced rat liver fibrosis model. Expression of CTGF was assessed by RT-PCR, Western blot and immunohistochemistry. Immunohistochemistry was used to identify type I and III collagens. HE stained liver slides were used for pathological study.</p><p><b>RESULTS</b>The mRNA and protein expression of CTGF in the fibrotic liver transfected with antisense-CTGF were significantly decreased compared with those of the controls (P<0.01). The depositions of type I and type III collagens were also decreased (P<0.05). Antisense-CTGF also minimized the pathological fibrosis in the rat livers (P<0.01).</p><p><b>CONCLUSION</b>The results demonstrate that the antisense RNA of CTGF recombinant plasmid has certain effects in preventing liver fibrosis and makes it a possible candidate for use in future gene therapy.</p>

The expression of platelet-derived growth factor (PDGF) receptor-beta and its correlation with extracellular matrix in hepatic tissue in hepatic fibrosis rats / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the expression of PDGF receptor-beta and its correlation with extracellular matrix in hepatic tissue during hepatic fibrosis.</p><p><b>METHODS</b>The model of hepatic fibrosis in rats was induced by carbon tetrachloride. PDGF receptor-beta subunit, collagen I, collagen III and a-SMA in hepatic tissues of these rats were examined using immunohistochemistry. The correlation between PDGF receptor-beta subunit and collagen I, III was analyzed using SAS software after the results of immunohistochemistry were semi-quantified.</p><p><b>RESULTS</b>PDGF receptor-beta subunit and a-SMA were not detected in normal controls. Collagen I and III were distributed in the portal tracts and beneath the endothelia of the central veins and of the Disse spaces. Two weeks after CCl4 injection, the PDGF receptor-beta and a-SMA were detected, and the expression of collagen I and III increased. At the end of 4 and 6 weeks, the above four proteins were further increased. Two weeks after CCl4 injection, PDGF receptor-beta had no apparent correlation with collagen I and III. However, PDGF receptor-beta had a significant correlation with collagen I and III 2 weeks later, and the correlation coefficient was 0.74 and 0.60 respectively at 4 weeks, and 0.83 and 0.67 respectively at 6 weeks. PDGF receptor-beta had a significant correlation with a-SMA during the whole process of hepatic fibrosis and the correlation coefficient was 0.62, 0.69 and 0.81, respectively at the time of 2, 4 and 6 weeks after CCl4 injection.</p><p><b>CONCLUSION</b>The PDGF receptor-beta was overexpressed during the process of hepatic fibrosis development, and it significantly correlated with collagen I and collagen III.</p>