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1.
Chinese Journal of Experimental and Clinical Virology ; (6): 99-101, 2011.
Article in Chinese | WPRIM | ID: wpr-231182

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effect of IL-10 and the methylation of its promoter in acute on chronic liver failure (ACLF).</p><p><b>METHODS</b>Patients were divided into three groups: 25 with ACLF, 25 with CHB, 10 healthy controls. Respectively detect the serum level of IL-10 via ELISA, and the methylation of IL-10 promoter via MSP, to analyze the difference among the three groups.</p><p><b>RESULTS</b>Both the ACLF group and the CHB group have significant increase in serum level of IL-10 compared with the control group (P < 0.05); the ACLF group's level is higher than the CHB group, however without statistical significance (P > 0.05). The serum level of IL-10 in ACLF group has no significant relativity with ALT and HBV-DNA( r = -0.022, r = 0.033, respectively; P > 0.05); has positive relativity with TBIL and MELD ( r = 0.566, r = 0.443, respectively; P < 0.05); and negative relativity with PTA (r = -0.581, P < 0.05). The distribution of the methylation of IL-10 promoter in ACLF group is significantly different from the other two.</p><p><b>CONCLUSION</b>The serum level of IL-10 in hepatitis patients is significantly higher and increases with the degree of liver failure. The promoter methylation may be important in the gene inactivation.</p>


Subject(s)
Adolescent , Adult , Female , Humans , Male , Middle Aged , Young Adult , Chronic Disease , DNA Methylation , Interleukin-10 , Blood , Genetics , Metabolism , Liver Failure, Acute , Blood , Genetics , Metabolism , Methylation , Promoter Regions, Genetic
2.
Chinese Journal of Experimental and Clinical Virology ; (6): 131-133, 2010.
Article in Chinese | WPRIM | ID: wpr-316943

ABSTRACT

<p><b>OBJECTIVE</b>To investigate oxidative stress in chronic hepatitis B (CHB) patients with elevated serum total bilirubin (TBIL).</p><p><b>METHODS</b>75 CHB patients with elevated serum TBIL were enrolled in the present study. A, B, C, D and E group were defined. Serum Malondialdehyde (MDA), Xanthine Oxidase (XOD), Vitamin C (V(C)) and Vitamin E (V(E)) were determined. The control group contained 11 healthy donors and the carrier group contained 16 Hepatitis B surface antigen (HBsAg) carriers.</p><p><b>RESULTS</b>The concentrations of MDA and XOD were significantly higher in each group of patients than in the control (P < 0.05), while V(C) and V(E) were significantly lower (P < 0.05). The concentration of XOD was significantly higher in the carrier group than in the control (P < 0.05), while MDA, V(C) and V(E) were not significantly different (P > 0.05). The concentrations of MDA and XOD were significantly positively correlated with TBIL (r = 0.670, P < 0.01; r = 0.737, P < 0.01, respectively) in the patients, while V(C) and V(E) were significantly negatively correlated with TBIL (r = -0.463, P < 0.01; r = -0.247, P < 0.05, respectively). The concentration of MDA was significantly different among all the groups in the patients except the comparison between group A and group B. The concentration of XOD was significantly different between group A, B, C and group D, E (P < 0.05). The concentration of V(C) was significantly different between group A and group D, E and between group B, C, D and group E (P < 0.05). The concentration of V(E) was significantly different between group A, B and group E (P < 0.05).</p><p><b>CONCLUSION</b>There was a disturbance between oxidative stress and anti-oxidative ability in CHB patients with elevated serum TBIL. Oxidative stress became more serious along with the increasing of serum TBIL. In HBsAg carriers, oxidative stress level was low. The results suggest antioxidant treatment for CHB patients with elevated serum TBIL may help to improve the effect of therapy.</p>


Subject(s)
Adolescent , Adult , Female , Humans , Male , Middle Aged , Young Adult , Bilirubin , Blood , Hepatitis B, Chronic , Blood , Metabolism , Malondialdehyde , Metabolism , Oxidative Stress , Physiology , Reactive Oxygen Species , Metabolism , Vitamin E , Metabolism
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