Carbohydrate antigen 125 and carcinoembryonic antigen in the differentiation of tuberculous peritonitis and peritonitis carcinomatosa.

Tumor markers could increase in both tuberculous peritonitis and peritonitis carcinomatosa, confusing the differentiation of these diseases. This study aimed to better understand the extent of elevation and diagnostic efficacies of carbohydrate antigen 125 (CA 125), carcinoembryonic antigen (CEA) and combinative use of them in tuberculous peritonitis and peritonitis carcinomatosa. Of 2998 patients reviewed, 101, 120 and 71 patients were assigned to TBP group (tuberculous peritonitis), non-OCA group (non-ovarian carcinoma-related peritonitis carcinomatosa) and OCA group (ovarian carcinoma-related peritonitis carcinomatosa), respectively. The composite index was calculated by CA 125 multiplying CEA. Receiver operator characteristic curves for CA 125, CEA and composite index were acquired. As a result, CA 125 value in OCA group was higher than other two groups (serum CA 125: P < 0.001; ascites CA 125: P < 0.001). On the other hand, non-OCA group had the highest CEA value among three groups (serum CEA: P < 0.001; ascites CEA: P < 0.001). Area under curves of serum/ascites composite index and serum/ascites CEA were larger than those of serum/ascites CA 125. Furthermore, ascites and serum composite index displayed the best sensitivity (0.907) and specificity (0.989), respectively. In conclusion, CA 125 increases in tuberculous peritonitis and non-ovarian carcinoma-related peritonitis carcinomatosa, but it elevates more in ovarian carcinoma-related peritonitis carcinomatosa. CEA is found to increase more significantly in non-ovarian carcinoma-related peritonitis carcinomatosa. CEA and composite index are helpful in distinguishing peritonitis carcinomatosa from tuberculous peritonitis, but composite index is slightly superior to CEA in the differential diagnosis.

Expression of cyclooxygenase-2 is correlated with lncRNA-COX-2 in cirrhotic mice induced by carbon tetrachloride.

Multiple long non-coding RNAs (lncRNAs) have been demonstrated to be involved in liver disease. Increased cyclooxygenase-2 (COX­2) levels have also been reported to be involved in the progression of liver cirrhosis. In the present study, the correlations between lncRNA­COX­2 RNA expression levels, COX­2 mRNA expression levels and liver fibrosis were examined. Liver fibrosis was induced by intraperitoneal injection of carbon tetrachloride (CCl4) in mice for 2 months (CCl4­2M) or 3 months (CCl4­3M). Liver histopathological evaluation was conducted using hematoxylin and eosin and Masson trichrome staining. Hepatic expression of COX­2 and lncRNA­COX­2 was evaluated by reverse transcription­quantitative polymerase chain reaction and immunohistochemical staining. Compared with the control group, fibrotic areas were increased four and nine times in the CCl4­2M group and the CCl4­3M group, respectively. LncRNA-COX-2 and COX­2 upregulation were observed in the cirrhotic liver. COX­2 mRNA expression levels and lncRNA-COX-2 RNA expression levels were significantly positively correlated with the fibrotic area. In addition, COX­2 mRNA expression was significantly positively correlated with lncRNA­COX­2 expression. These results suggest that expression of COX­2 and lncRNA­COX­2 increased with the progression of liver fibrosis. LncRNA-COX-2 may potentially be considered as a novel therapeutic target for liver fibrosis.

Collapsed Reticular Network and its Possible Mechanism during the Initiation and/or Progression of Hepatic Fibrosis.

Among the researches on hepatic fibrosis, great attention was paid to both hepatocytes and extracellular matrix (ECM). However, little focus was drawn on reticular fibrous network, which is important for demarcation and support of hepatocytes. The aim of this study was to investigate the change pattern of reticular fibers in hepatic fibrosis/cirrhosis and its underlying mechanism. In this study, thioacetamide (TAA) and bile duct ligation (BDL) were utilized to induce rat hepatic fibrosis respectively, and Human liver cirrhotic microassay was analyzed with IHC to confirm the results in animal experiment and to detect the metalloproteinases (MMPs) expressions. As a result, the reticular fibers decreased markedly after 1 week in TAA and 1 day in BDL treated rats. Multiple representative regulators of MMPs and MMPs increased significantly in their expressions and activities. Further more, in human liver cirrhotic microassay, MMPs expressions also showed similar patterns as that of animal experiment. In Conclusions: Degradation or collapse of reticular fibers in hepatic sinusoid can be considered as a pathological feature during the initiation and/or progression of hepatic fibrosis. Moreover, such degradation is associated with and probably caused by the over/dysregulated expression of MMPs.

Inhibition of cyclooxygenase-2 alleviates liver cirrhosis via improvement of the dysfunctional gut-liver axis in rats.

Inflammatory transport through the gut-liver axis may facilitate liver cirrhosis. Cyclooxygenase-2 (COX-2) has been considered as one of the important molecules that regulates intestinal epithelial barrier function. This study was aimed to test the hypothesis that inhibition of COX-2 by celecoxib might alleviate liver cirrhosis via reduction of intestinal inflammatory transport in thiacetamide (TAA) rat model. COX-2/prostaglandin E2 (PGE2)/EP-2/p-ERK integrated signal pathways regulated the expressions of intestinal zonula occludens-1 (ZO-1) and E-cadherin, which maintain the function of intestinal epithelial barrier. Celecoxib not only decreased the intestinal permeability to a 4-kDa FITC-dextran but also significantly increased expressions of ZO-1 and E-cadherin. When celecoxib greatly decreased intestinal levels of LPS, TNF-α, and IL-6, it significantly enhanced T cell subsets reduced by TAA. As a result, liver fibrosis induced by TAA was significantly alleviated in the celecoxib group. These data indicated that celecoxib improved the integrity of intestinal epithelial barrier, blocked inflammatory transport through the dysfunctional gut-liver axis, and ameliorated the progress of liver cirrhosis.

[Correlation study of rhubarb and expression changes of antimicrobial peptides in the small intestine of mice].

OBJECTIVE: To study the correlation between rhubarb and expressions of antimicrobial peptides (AP) in the small intestine of mice by observing the effect of rhubarb on it. METHODS: Thirty healthy ICR mice were randomly divided into the test group and the control group, fifteen in each. Ten percent rhubarb decoction and equal volume of normal saline solution was respectively given to mice of the two groups by gastrogavage. Mice were sacrificed 24 h later. The small intestines from the ligament of Treitz to the ileocecal junction were removed by ventrotomy. The lumen of each resected intestine was rinsed with 10% acetic acid solution and the perfusate was collected. The small intestine homogenate was prepared using 30% acetic acid solution. The equivalent samples were electrophoresed on 12.5% AU-PAGE and Tricine-16.5% SDS-PAGE, and peptide bands were visualized with Coomassie brilliant blue R-250 or ammoniacal silver-stained respectively. And then analysis of gel imaging and gel overlay assay were performed. The bactericidal activity and expressions of AP in the small intestine of samples in the two groups were compared. The molecular weight of AP in the small intestine was measured. RESULTS: After gastrogavaged with rhubarb decoction, changes of AP contents in the small intestine homogenate of mice were not obvious, but the molecular weights of AP were different. But the AP contents in the small intestine perfusate obviously increased, with the molecular weights being 14.3 to 18.4 kDa. But its bactericidal capacity showed no statistical difference when compared with that of the control group (P>0.05). CONCLUSION: Rhubarb enhanced the expressions of partial APs in the small intestine, which might possibly be one of its mechanisms of protecting and strengthening the intestinal barrier.

Analysis of gene expression in the tumor-associated macrophage.

INTRODUCTION: The tumor-associated macrophage (TAM) is at the front line of the host's defense against malignancy and provides an attractive target for immune-modulatory therapy. However, factors present within the tumor microenvironment can alter macrophage phenotype, preventing its cytotoxic activity and reducing its susceptibility to interferon-gamma and lipopolysaccharide-mediated stimulation. METHODS: Macrophages were isolated from subcutaneous B16 melanoma tumors implanted in C57 BL/6 mice. Wound macrophages were harvested from subcutaneously-implanted PVA sponges, and resting peritoneal macrophages were harvested by peritoneal lavage. Gene expression was analyzed using an Atlas cDNA array (Clontech, Mountain View, CA). RESULTS: TAM demonstrated a pattern of gene expression distinct from both wound and peritoneal macrophage. There is an increase in proliferation-associated genes and in genes encoding the ultrastructural proteins cofillin, zyxin, and vimentin more commonly associated with fibroblast-like cells. In addition, an observed decrease in expression of the CD14 gene, and increase in inhibitory pathways including osteopontin and its receptor CD44, the inositol 1,4,5-triphosphate receptor, and the receptors for interleukin-4 and granulocyte monocyte-colony stimulating factor could explain the resistance of TAM to lipopolysaccharide-mediated stimulation. There was also a significant decrease in the expression of the interferon-gamma second messenger, IRF-1. CONCLUSIONS: This study has identified a number of pathways involved in the suppression of TAM function. Targeting of these pathways may allow for the generation of more effective immune-modulatory anti-neoplastic therapy.

[Study on the mechanism by which Rhubarb protects the mucosal barrier of intestine of mouse].

OBJECTIVE: To observe the influence of Rhubarb on the the excretion of Type II PLA2 and lysozyme of small intestine of mouse. METHODS: Forty ICR mice were randomized to two groups. In the experiment group, the mice were gavaged with 0.3 ml 10% Rhubarb decoction every 8 hours; in the control group, the mice were given normal saline instead of Rhubarb decoction. After 24 hours, the mice were subjected to cervical dislocation, and their jejunum and ileum were taken out. The lumen of each resected intestine was rinsed with 100 g/L acetic acid, and the washed intestines from each mouse were cut into pieces 1-2 mm in length. Then the perfusate and homogenate were prepared, lyophilized, sealed, and stored at -20 degrees C. The Type II PLA2 activity and lysozyme were assayed respectively. RESULTS: The Type II PLA2 activities and lysozyme of homogenate in Rhubarb group were lower than those in Saline group (P<0.01). The type II PLA2 activities and lysozyme of perfusate in Rhubarb group were higher than those in Saline group (P<0.01). CONCLUSION: Rhubarb can stimulate the small intestine of mice to excrete Type II PLA2 and lysozyme, thus resulting in the increase of Type II PLA2 and lysozyme contents in the intestinal tract and enhancing the function of mucosal barrier of intestine.