Current Treatments for Hepatitis

Fleming, J. Clifton

doi:10.1097/00129804-200211000-00006

Cited by 9 publications

(3 citation statements)

References 4 publications

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“…Hepatitis B virus (HBV) causes acute and chronic hepatitis and remains a major problem to public health (Fleming, 2002). HBV plays a critical role in the development of liver fibrosis, cirrhosis and hepatocellular carcinoma (Seeger et al, 2000;Kelleher et al, 2006), with over 350 million people worldwide chronically infected and at risk of these severe diseases (Liaw et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Anti-Hepatitis B Virus Effects of Dehydrocheilanthifoline fromCorydalis saxicola

et al. 2013

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In this report, the anti-hepatitis B virus (HBV) activity of dehydrocheilanthifoline (DHCH), a quaternary ammonium alkaloid isolated from the traditional Chinese medicine Corydalis saxicola Bunting (Papaveraceae), was determined in vitro. Following six days of treatment, DHCH efficiently suppressed the secretions of HBsAg and HBeAg in HepG2.2.15 cell cultures, with a half-maximal inhibitory concentration (IC(50)) of 15.84 and 17.12 μM, and with a therapeutic index (TI) of 7.32 and 6.77, respectively. Further studies revealed that DHCH reduced the levels of extracellular DNA, intracellular DNA and covalently closed circular DNA (cccDNA) of HBV in a dose-dependent and time-dependent manner, with IC(50) values of 15.08, 7.62 and 8.25 μM, respectively after six days of treatment. In contrast, the level of viral pre-genomic RNA (pgRNA) increased 6.13-fold after treatment with DHCH. Together, it was demonstrated for the first time that DHCH could significantly inhibit the replication of HBV, which warrants further studies on the antiviral mechanisms of DHCH, and suggests that it may be a promising candidate in the therapy of HBV infection.

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Section: Introductionmentioning

confidence: 99%

Anti-Hepatitis B Virus Effects of Dehydrocheilanthifoline fromCorydalis saxicola

et al. 2013

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“…Hepatitis B virus (HBV) infection remains a major public health problem worldwide [1][2][3][4] . HBV causes transient and chronic infection of liver.…”

Section: Introductionmentioning

confidence: 99%

Anti-HBV activity of TRL mediated by recombinant adenovirus

Gong¹

2005

WJG

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AIM: To investigate the inhibitive effect of hepatitis B virus (HBV)-TRL on HBV replication. METHODS:Based on previously constructed pcDNA3.1 (-)/TRL, TR, TRmut, HBV core protein (HBVc) and hEDN, interest gene sequences TRL, TR, HBVc and hEDN were inserted into adenovirus shuttle plasmid pDC316 respectively and co-transfected HEK293 cells with rescue plasmid pBHGlox(delta)E1,3Cre to acquire RAd/TRL, TR, HBVc and hEDN. And then RAds were identified, amplified and the titers in HEK293 cells were determined. RAd/TRL and TR were named as the experimental groups, and others were control ones. After HepG2.2.15 cells were infected, RAd/TRL expression was identified by indirect immunofluorescence staining. Supernatant HBV-DNA content was determined by fluorescent quantification PCR. Meanwhile, metabolism of HepG2.2.15 cells was evaluated by MTT colorimetry. RESULTS:RAd vectors with distinct interest gene sequence were successfully constructed. Effective expression of RAd/TRL in HepG2.2.15 cells resulted in a significant decrease of supernatant HBV-DNA content compared to RAd/TR (0.63±0.14 vs 1.60±0.47, P = 0.0266, <0.05) and other control groups (0.63±0.14 vs 8.50±2.78, 8.25±2.26, 8.25±2.29, 8.50±1.51, 8.57±1.63, P<0.01). MTT assay suggested that there were no significant differences in cell metabolic activity between groups (P>0.05). CONCLUSION:The construction and expression of RAd/TRL has been achieved and it could inhibit HBV replication successfully, which has laid the foundation for further research on anti-HBV activity in vivo.

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“…Viral hepatitis remains a worldwide public health problem [1][2][3][4] and is reported by the Chinese Ministry of Public Health as an infectious disease with the highest morbidity and mortality in China. Many complications are considered to be involved in viral hepatitis [5][6][7][8][9][10][11][12][13][14][15][16][17] .…”

Section: Introductionmentioning

confidence: 99%

Effects of autoantibodies against β₁-adrenoceptor in hepatitis virus myocarditis on action potential and L-type Ca²⁺currents

Liu¹,

Liao²,

Wang³

et al. 2004

WJG

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AIM:To investigate the effects of autoantibodies against β 1 -adrenoceptor in hepatitis virus myocarditis on action potential and L-type Ca 2+ currents. METHODS:Fifteen samples of autoantibodies against β 1 -adrenoceptor positive sera of patients with hepatitis virus myocarditis were obtained and IgGs were purified by octanoic acid extraction. Binding of autoantibodies against β 1 -adrenoceptor to guinea pig cardiac myocytes was examined by immunofluorescence. Using the patch clamp technique, the effects on the action potential and I Ca-L of guinea pig cardiac myocytes caused by autoantibodies against β 1 -adrenoceptor in the absence and presence of metoprolol were investigated. Cell toxicity was examined by observing cell morphology and permeability of cardiac myocytes to trypan blue. RESULTS:The specific binding of autoantibodies against β 1 -adrenoceptor to guinea pig cardiomyocytes was observed. Autoantibodies against β 1 -adrenoceptor diluted at 1:80 prolonged APD 20 , APD 50 and APD 90 by 39.2%, 29.1% and 15.2% respectively, and only by 7.2%, 5.3% and 4.1% correspondingly in the presence of 1 µmol/L metoprolol. Autoantibodies against β 1 -adrenoceptor diluted at 1:80, 1:100 and 1:120 significantly increased the I Ca-L peak current amplitude at 0 mV by 55.87±4.39%, 46.33±5.01% and 29.29±4.97% in a concentration-dependent manner. In contrast, after blocking of β 1 -adrenoceptors (1 µmol/L metoprolol), autoantibodies against β 1 -adrenoceptor diluted at 1:80 induced a slight increase of I Ca-L peak amplitude only by 6.81±1.61%. A large number of cardiac myocytes exposed to high concentrations of autoantibodies against β 1 -adrenoceptor (1:80 and 1:100) were turned into rounded cells highly permeable to trypan blue. CONCLUSION:Autoantibodies against β 1 -adrenoceptor may result in arrhythmias and/or impairment of myocardiums in HVM, which would be mediated by the enhancement of I Ca-L .

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Current Treatments for Hepatitis

Cited by 9 publications

References 4 publications

Anti-Hepatitis B Virus Effects of Dehydrocheilanthifoline fromCorydalis saxicola

Anti-Hepatitis B Virus Effects of Dehydrocheilanthifoline fromCorydalis saxicola

Anti-HBV activity of TRL mediated by recombinant adenovirus

Effects of autoantibodies against β₁-adrenoceptor in hepatitis virus myocarditis on action potential and L-type Ca²⁺currents

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Current Treatments for Hepatitis

Cited by 9 publications

References 4 publications

Anti-Hepatitis B Virus Effects of Dehydrocheilanthifoline fromCorydalis saxicola

Anti-Hepatitis B Virus Effects of Dehydrocheilanthifoline fromCorydalis saxicola

Anti-HBV activity of TRL mediated by recombinant adenovirus

Effects of autoantibodies against β1-adrenoceptor in hepatitis virus myocarditis on action potential and L-type Ca2+currents

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Product

Resources

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Effects of autoantibodies against β₁-adrenoceptor in hepatitis virus myocarditis on action potential and L-type Ca²⁺currents