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1.
Chinese Journal of Pancreatology ; (6): 176-178, 2008.
Artigo em Chinês | WPRIM | ID: wpr-399747

RESUMO

Objective To investigate the effect of prebiotics supplement on intestinal epithelial tight junctions and barrier function of the rats with acute pancreatitis (AP). Methods The AP model in Wistar rat was established by intraperitoneal injection of L-arginine. The rats were randomly divided into 3 groups: control group, AP group, GOS group. GOS was given 4g·kg-1·d-1at 7d before ANP induced. Twelve hours after modeling, the AP rats in each group were sacrificed. 2 ml of blood sample was taken from heart for the analysis of plasma diamine oxidase (DAO) activity. Jejunum was taken for histological examination. The transmembrane binding proteins (occludin) were measured with immunohistochemistry. Results The plasma DAO level in AP group was (7.29±0.68) U/L, and significantly higher than (2.01±0.34) U/L of control group (P<0.01). The DAO level in GOS group was (3.44±0.59) U/L, and significantly lower than that of AP group. The occludin protein level in AP group was 95.1±9.2, and significantly lower than 44.7±8.2 of control group and 59.7±7.8 of GOS group (P<0.01). The occludin protein level in COS group was significantly higher than that of control group (P<0.05). Conclusions The prebiotics may increase the expression of occludin protein, enhance the intestinal epithelial tight junction, maintain the intestinal permeability, and protect the intestinal barrier function.

2.
Chinese Journal of Hepatology ; (12): 818-822, 2008.
Artigo em Chinês | WPRIM | ID: wpr-250109

RESUMO

<p><b>OBJECTIVE</b>To evaluate the causes of alanine aminotransferase (ALT) level elevation in HBsAg-positive chronic hepatitis B (CHB) patients with low HBV DNA loads.</p><p><b>METHODS</b>One hundred nineteen HBsAg positive CHB patients with both serum HBV DNA loads less than 1000 copies/ml and ALT more than 1.25 upper limits of normal (ULN) lasting for at least 6 months were enrolled in this study. Patients co-infected with hepatitis C virus or HIV or suffering from other liver diseases were not included. HBV DNA loads were assayed by PCR. Serological biochemistry and liver biopsy histopathological changes and clinical characteristics of the patients were analyzed.</p><p><b>RESULTS</b>Of the 119 patients 102 were males and 17 were females. The mean age of the patients was (33.9+/-9.7) years and their body mass index (BMI) was (23.4+/-3.7) kg/m2. Mean ALT levels were (150.0+/-166.6) U/L and AST levels were (102.4+/-193.2) U/L. Liver biopsies showed hepatic steatosis in 26.9 % (32/119) of the cases, chronic hepatitis in 53.8% (64/119), non-specific changes in 12.6% (15/119), and 1 without any change. However, hepatic steatosis was more frequently seen in patients taking nucleoside analogs (56.7%), x2=10.394, Probability value less than 0.01. BMI, apolipoprotein B (APO-B), triglyceride, cholesterol and uric acid were all significantly higher in patients with hepatic steatosis than those without (t values were 5.369, 4.276, 3.216, 4.223 and 2.438 respectively, all P less than 0.05) while ALT, AST and apolipoprotein A were much lower in those with steatosis than those without (t values were -2.234, -3.877 and -2.956 respectively, all P less than 0.05). Obesity, dyslipidemia and hyperuricemia were more frequently seen in patients with steatosis than in patients without it (x2 value 3.829, 7.659, 13.389, 0.549, all P less than 0.05). The severity of inflammation and fibrosis were also more significant in patients with steatosis (x2 value 20.978, 17.550, all P less than 0.05). As compared to those patients without specific changes, serum levels of ALT, AST, GGT in patients with chronic hepatitis were obviously higher, all P less than 0.05. In contrast, there were no significant differences in mean age, BMI, male preference, obesity, diabetes, dyslipidemia or hyperuricemia, and the levels of triglyceride, cholesterol, and fasting plasma glucose between the two groups.</p><p><b>CONCLUSION</b>Our data indicate that hepatic steatosis might be a factor associated with elevated ALT levels in HBsAg-positive CHB patients with low HBV DNA loads, especially in patients treated with nucleoside analogs.</p>


Assuntos
Adulto , Feminino , Humanos , Masculino , Adulto Jovem , Alanina Transaminase , Sangue , Portador Sadio , Fígado Gorduroso , Virologia , Antígenos de Superfície da Hepatite B , Sangue , Vírus da Hepatite B , Hepatite B Crônica , Sangue , Virologia , Hepatócitos , Patologia , Carga Viral
3.
Chinese Journal of Hepatology ; (12): 73-76, 2003.
Artigo em Chinês | WPRIM | ID: wpr-276492

RESUMO

<p><b>OBJECTIVE</b>To explore the role of endotoxin in the pathogenesis of nonalcoholic steatohepatitis (NASH).</p><p><b>METHODS</b>Rat models of NASH were established by giving a fat-riched diet. These rats were sacrificed at the 4th, 8th, 12th, 16th and 24th weeks during the study. The other rats fed with normal diet were taken as normal controls at the same stage during the study. The blood of abdominal aorta was obtained and the levels of serum endotoxin, tumor necrosis factor-alpha (TNF-a), and interleukin-1 beta (IL-1 b) were measured. The expression of CD(14) and lysozyme in rats' livers were detected by immunohistochemistry.</p><p><b>RESULTS</b>Rat models of NASH with liver fibrosis were established successfully. The levels of endotoxin in aorta blood of NASH rats increased significantly at the 24th week (0.23 EU/L 0.06 EU/L vs 0.15 EU/L 0.03 EU/L, t>2.179, p <0.05) while the expression of CD(14) increased from the 4th week, and the Kupffer cells expressing lysozyme were activated, then kept increasing activation through the study. In NASH rats, the levels of serum TNF-a increased from the 8th week (26.39 pg/ml 24.21 pg/ml vs 9.82 pg/ml 9.29 pg/ml, t>2.145, p < 0.05) and serum IL-1beta increased from the 16th week (23.76 pg/ml 21.81 pg/ml vs 6.25 pg/ml 2.98 pg/ml, t>2.145, p<0.05).</p><p><b>CONCLUSION</b>Liver injury results from endotoxin existing in NASH rats which may play an important role in the pathogenesis of NASH by activating Kupffer cells and inducing the production of cytokines, such as TNF-a.</p>


Assuntos
Animais , Masculino , Ratos , Citocinas , Sangue , Modelos Animais de Doenças , Progressão da Doença , Endotoxinas , Sangue , Fígado Gorduroso , Sangue , Imuno-Histoquímica , Receptores de Lipopolissacarídeos , Ratos Sprague-Dawley
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