HBx gene is a multifunctional regulator,which has extensive trans-activating effects,and can activate transcription factors,inhibit DNA repair and regulate cell proliferation,differentiation and apoptosis.In recent years,the role of HBx gene in pathogenesis of hepatitis B virus-associated glomemlonephritis (HBV-GN) has been extensively studied,and the results show that HBx can promote glomerular mesangial cell proliferation,and induce damage or apoptosis of podocytes and renal tubular epithelial cells.This paper reviews the research progress on biological characteristics of HBx and its role in pathogenesis of HBV-GN.

Objective To determine whether mutation of Hepatitis B virus (HBV) X gene is associated with hepatitis B virus-associated glomerulonephritis (HBV-GN).Methods The venous blood was collected from 50 patients with HBV-GN and 60 patients with asymptomatic HBV carriers (control group).Serum HBV DNA was extracted to determine the serum titer of HBV-DNA and then polymerase chain reaction (PCR) was used to detect the HBV X gene mutation.Results (1)There were not statistical significance between age and gender in HBV-GN group and control group (P ＞0.05).There were not statistical significance of serum replication level of HBV DNA in HBV-GN with X gene mutation and control group (P ＞ 0.05).Urine protein excretion in HBV-GN group with or without X gene mutation was found with statistical significance (P ＜ 0.05).(2)Nucleotide mutations [84％ (42/50)] resulted in amino acid substitution in HBV-GN.Nucleotide mutations changed in transfunction control region of X gene,including position nt1653,nt1726,nt1727,nt1730,nt1753,nt1762 and nt1764.(3)Nucleotide mutations [8％(5/60)] resulted in amino acid substitution in control group.Nucleotide mutations changed in position nt1632 and nt1635,located in non-functional region.Conclusions HBV X gene mutations and the subsequent amino acid substitutions are found in HBV-GN.The urine protein excretion level increases in patients with X mutation,suggesting that these mutations may play an important role in the pathogenesis of HBV-GN.

Objective To investigate the correlation of HBV DNA level with clinicopathological characteristics and prognosis of HBV-associated glomerulonephritis ( HBV-GN ) .Methods One hundred and two patients with HBV-GN admitted in Affiliated Hospital of Qingdao University during January 2009 and October 2012 were successively enrolled.Fluorescence quantitative polymerase chain reaction was used to determine the serum titer of HBV DNA.According to HBV DNA levels the patients were divided into three groups:low-replication group (HBV DNA <103 copies/mL), moderate-replication group (103 copies/mL ≤HBV DNA≤105 copies/mL) and high-replication group ( HBV DNA >105 copies/mL) .Renal biopsy was performed to determine the pathological type, and immunofluorescence assay was used for quantitative detection of HBV related antigens ( HBsAg, HBcAg and HBeAg ) in kidney. All patients received lamivudine (100 mg/d) plus adefovir dipivoxil (10 mg/d) combination therapy and followed up for 18 months.The renal function, biochemical and immunological indexes before and after the treatment were measured.One-way ANOVA was used to analyze the differences of above parameters among patients in three groups.Spearman correlation coefficient was used for correlation analysis between HBV DNA level and pathological stages in kidney.Results There were 20 patients in low-replication group, 51 in moderate-replication group and 31 in high-replication group.With the increase of serum level of HBV DNA, 24-h urine protein excretion, plasma cholesterol, and triglycerides increased (F=34.64, 40.10 and 31.72, P<0.01), plasma level of albumin decreased (F=24.04, P<0.01), and the immune complexes of HBV related antigens ( HBsAg, HBcAg and HBeAg) in kidney increased ( F=41.49, 15.64 and 10.41, P<0.01).For 78 patients with HBV-membranous nephropathy ( HBV-MN), the pathological injury was aggravated with the increase of serum level of HBV DNA (r=0.38, P<0.01).The level of 24-h urine protein excretion declined after treatment in three groups ( t =7.86, 19.28 and 16.74, P <0.01 );complement C3 increased, but no statistical significance was observed ( t =1.05, 1.04 and 1.94, P >0.05);no change in creatinine was found (t =0.14, 0.52 and 0.57, P >0.05).After 18-month treatment, clinical remission rates in three groups were 95.0% ( 19/20 ) , 70.6% ( 36/51 ) and 54.8%(17/31), respectively.The clinical remission rate was significantly lower in the high-replication group as compared with that in low-replication group (χ2 =9.44, P<0.01).Conclusion Serum level of HBV DNA is closely correlated with renal function, renal pathology and clinical remission rate in HBV-GN patients, which may be used for the evaluation of kidney biopsy, treatment and prognosis in patients with HBV-GN.

Objective To investigate the change in NF-κB activity in astrocytes in spinal dorsal horn in a rat model of neuropathic pain and the underlying mechanism. Methods Sixteen male SD rats aged 2-3 months weighing 220-280 g were randomly divided into 2 groups ( n = 8 each) : sham operation group (group S) and CCI group. Neuropathic pain was induced by chronic constrictive injury (CCI) . Right sciatic nerve was exposed and 4 loose ligatures were placed on the sciatic nerve at 1 mm intervals with 4-0 chromic catgut. In group S the right sciatic nerve was exposed but not ligated. The paw withdrawal threshold (PWT) to von Frey filament stimulation and paw withdrawal latency (PWL) to radiant heat stimulation were measured at 1 d before (baseline) and 7 d after operation. The animals were then killed and the lumbar segment of the spinal cord (L_(4-6)) was removed. The expression of NF-κB in the astrocytes in spinal dorsal horn was determined by immuno-histochemistry. Results PWT and PWL to mechanical and thermal stimuli were significantly decreased after operation as compared with the baseline before operation in group CCI. The number of NF-κBp65 immunoreaction positive cells in the spinal dorsal horn on the operated side was significantly larger in group CCI than in group S. Conclusion NF-κB signal transduction pathway in the astrocytes in the spinal dorsal hom may be involved in neuropathic pain.

Biomarkers ; blood ; Female ; Humans ; Interleukins ; blood ; Male ; Myocardial Infarction ; blood ; Receptors, Cell Surface ; blood

Active Transport, Cell Nucleus ; Animals ; Cell Nucleus ; metabolism ; Forkhead Box Protein O3 ; metabolism ; Mice ; Mice, Knockout ; Muscle, Skeletal ; metabolism ; pathology ; Muscular Atrophy ; metabolism ; pathology ; Protein-Serine-Threonine Kinases ; deficiency ; metabolism