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1.
Chinese Journal of Experimental and Clinical Virology ; (6): 340-343, 2013.
Article in Chinese | WPRIM | ID: wpr-318026

ABSTRACT

<p><b>OBJECTIVE</b>To study the impact of IFN-gamma on liver fibrosis and its possible mechanism. Thirty healthy male SD rats were randomly divided into two groups: fibrosis model group, IFN-gamma treatment group. Experimental liver fibrosis was induced by subcutaneous injection of CCl4. After 12-week-treatment, serum hyalurnic acid and TGF-beta1 was examined, histopathological changes and degrees of fibrosis were observed by optical microscopy. Meanwhile, the expression of TGF-beta1, TbetaR- I and Smad2/3 proteins was detected by immunohistochemistry and quantified by using computerized image analysis.</p><p><b>RESULTS</b>(1) Pathological observation of hepatic specimens: histological examination showed that there were significant difference between normal group and fibrosis model group by comparing with the degrees of inflammation and fibrosis (P < 0.05). And the difference between fibrosis model group and IFN-gamma treatment group was significant (P < 0.05). (2) Changes of the hepatic fibrosis index (serum HA and TGF-beta1): the levels of serum HA, TGF-beta1 in fibrosis model group were higher than IFN-gamma treatment groups (P < 0.05). (3) Changes of gene protein levels about TGF-beta1/Smad: the expressions of TGF-beta1, TbetaR- I and Smad2/3 in rat hepatic tissue were detected with immunohistochemistry techniques. The expressions of the three items in model group were higher than normal group (P < 0.01). The difference between model group and IFN-gamma treatment group was significant (P < 0.05);</p><p><b>CONCLUSION</b>IFN-gamma treatment group had significant results on treating experimental hepatic fibrosis. By the way of inhibiting expressions of TGF-beta1, TbetaR- I, Smad2/3, IFN-gamma treatment group exerted its anti-fibrosis effect.</p>


Subject(s)
Animals , Humans , Male , Rats , Disease Models, Animal , Interferon-gamma , Therapeutic Uses , Liver , Metabolism , Liver Cirrhosis , Drug Therapy , Genetics , Metabolism , Rats, Sprague-Dawley , Smad2 Protein , Genetics , Metabolism , Smad3 Protein , Genetics , Metabolism , Transforming Growth Factor beta1 , Genetics , Metabolism
2.
Chinese Journal of Experimental and Clinical Virology ; (6): 366-369, 2012.
Article in Chinese | WPRIM | ID: wpr-305033

ABSTRACT

<p><b>OBJECTIVE</b>To study the effects of acetylcysteine magnesium on the vasoactive substances and hepatic fibrosis indexes in liver cirrhosis and portal hypertension of rats.</p><p><b>METHODS</b>The rat liver cirrhosis model was made with 12 microg/kg dimethylnitrosamines. Then acetylcysteine magnesium was injected respectively with 25, 50, and 100 mg x kg(-1) dose daily into abdominal cavity. After 8 weeks treatment, pathological section, TGF-beta1, NO, TNOS and iNOS of hepatic tissue were detected to assess the effect of acetylcysteine magnesium against cirrhosis portal hypertension.</p><p><b>RESULTS</b>After the DMNA modeling was completed, the HE and Sweet reticulocyte staining of liver pathological section showed that cirrhosis of the liver was in the III-IV phase, the infiltration of lymphocytes and formation of pseudolobuli in liver were alleviated in three acetylcysteine magnesium treatment groups (low, medium, and high dose), and the degree of liver fiber sclerosis in three groups was significantly lower than control group. Compared with control group, TGF-beta1, NO, TNOS and iNOS were significantly reduced in all treatment groups (P < 0.05).</p><p><b>CONCLUSION</b>Acetylcysteine magnesium is probably a distinctive antioxidant which can remove various free radical in body and modulate ligand-dependent signal transduction and the growth of cell. It also have protection in the liver cirrhosis and portal hypertension of rats induced by dimethylnitrosamine.</p>


Subject(s)
Animals , Male , Rats , Acetylcysteine , Therapeutic Uses , Hypertension, Portal , Metabolism , Pathology , Liver Cirrhosis, Experimental , Metabolism , Pathology , Nitric Oxide , Physiology , Rats, Sprague-Dawley , Transforming Growth Factor beta1
3.
Chinese Journal of Experimental and Clinical Virology ; (6): 331-333, 2011.
Article in Chinese | WPRIM | ID: wpr-246248

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the influence of the individual genotype differences of DC-SIGN and DC-SIGNR on the mother-to-neonate intrauterine infection of HBV.</p><p><b>METHODS</b>The genotypes of the gene DC-SIGN and DC-SIGNR in the pregnant women with HBV positive were detected by PCR and agarose gel electrophoresis. The significant difference of gene diversity of DC-SIGN and DC-SIGNR was analyzed by chi-square test.</p><p><b>RESULTS</b>(1) All of 29 cases in intrauterine infection group were 7/7 DC-SIGN genotype. In the non-intrauterine infection group, 7/5 genotype were observed in 2 of 54 cases, and the other 52 cases were 7/7 genotype. The two groups was no significant difference (P = 0.54). (2) 29 cases of intrauterine infection group was observed 4 genotypes of DC-SIGNR such as 7/7, 7/5, 9/7 and 6/5, the genotype frequencies were 0.3793, 0.3448, 0.2414 and 0.0345 respectively. 54 cases of non-intrauterine infection group was found 6 genotypes such as 7/7, 7/5, 9/5, 9/7, 7/6 and 6/5, genotype frequencies were 0.5186, 0.1481, 0.0926, 0.1852, 0.0370 and 0.0185 respectively. The distribution of 7/5 genotype in the intrauterine infection group (29 cases) and the non-intrauterine infection group (54 cases) was statistically significant (P = 0.038) , and no significant difference was found in other genotypes between the two groups (P > 0.05).</p><p><b>CONCLUSION</b>The gene DC-SIGN showed relatively little variation in the pregnant women infected with HBV. On the countrary, there were multiple genotypes of the gene DC-SIGNR in these women, and the genotype "7/5" of DC-SIGNR might be one of the susceptibility genes associated with intrauterine infection.</p>


Subject(s)
Female , Humans , Infant, Newborn , Male , Pregnancy , Cell Adhesion Molecules , Genetics , Metabolism , Genetic Predisposition to Disease , Genetic Variation , Hepatitis B , Genetics , Virology , Hepatitis B virus , Genetics , Infectious Disease Transmission, Vertical , Lectins, C-Type , Genetics , Metabolism , Polymorphism, Genetic , Pregnancy Complications, Infectious , Genetics , Virology , Receptors, Cell Surface , Genetics , Metabolism
4.
Chinese Journal of Experimental and Clinical Virology ; (6): 126-128, 2007.
Article in Chinese | WPRIM | ID: wpr-248827

ABSTRACT

<p><b>OBJECTIVE</b>To investigate if glutamine (Gln) reduces intestinal bacterial translocation in acute hepatic failure (AHF) in rats and its mechanisms.</p><p><b>METHODS</b>Acute hepatic failure model in rat was established by intraperitoneal injection of galatosamine. The rats were randomly divided into 4 groups: the normal control group (A), prevention and treatment group (B), treatment group (C), and model group (D). The rats in groups A and D were fed with normal saline. Two days before intraperitoneal injection, the rats in group B were fed with Gln and those in group C were fed with Gln 24 hours after injection. After 4 days of treatment, the rats were sacrificed and pathological scores of liver were assessed. The percentage of intestinal bacterial transloaction and bacteria in mesenteric lymph nodes (MLN) were measured. The villus height, crypt depth of ileum mucosa were analyzed. The levels of serum diamine oxidase (DAO) were measured.</p><p><b>RESULTS</b>The liver pathological scores of groups B and C were significantly lower than those of group D. The frequency of the bacteria found in MLN was significantly lower in group B compared with group D. The levels of DAO in blood were significantly lower in groups B and C than that of group D, and the level was significantly lower in group B than in group C. The villus height and crypt depth of the mucosa were significantly greater in group B and group C than in group D, and greater in group B than in group C.</p><p><b>CONCLUSION</b>The results of the present study show that Gln can reduce the occurrence of the intestinal bacterial translocation in AHF in rats by improving the function of intestinal barrier.</p>


Subject(s)
Animals , Male , Rats , Bacterial Physiological Phenomena , Bacterial Translocation , Glutamine , Metabolism , Intestines , Metabolism , Microbiology , Liver Failure, Acute , Microbiology , Random Allocation , Rats, Sprague-Dawley
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