The microRNA-155 mediates hepatitis B virus replication by reinforcing SOCS1 signalling-induced autophagy.

As small conserved RNAs without a coding function, microRNAs are expressed in multicellular organisms and contribute to the modulation of multiple cellular reactions, such as viral replication, as well as autophagy. microRNAs can regulate host gene expression and inhibit or reinforce hepatitis B virus (HBV) replication. Hepatic cells express miR-155 noticeably.

Hepatoprotective effects of cathepsin B inhibitor on acute hepatic failure induced by lipopolysaccharide/D-galactosamine in mice.

Background: Increasing evidence suggests that the inactivation of cathepsin B attenuates hepatocyte apoptosis and liver damage. This study aimed to investigate the protective effects of a cathepsin B inhibitor (CA-074me) on lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced acute hepatic failure (AHF) in mice.

Methods: Mice were intraperitoneally injected with a combination of LPS/D-GalN to induce AHF with or without CA-074me pretreatment.

Regulatory T-cell responses in chronic hepatitis B patients treated with nucleos(t)ide analogs compared with healthy subjects and untreated infected individuals.

Background/aims: The purpose of this prospective case-control study was to evaluate the clinical effects and host immune response in patients with chronic hepatitis B (CHB) treated with either entecavir (ETV)or adefovir dipivoxil (ADV).

Methodology: Forty-two patients diagnosed with CHB were recruited and randomly assigned to receive either ADV (n=19) or ETV(n=18) and were followed for a minimum of 96 weeks.Serum hepatitis B virus (HBV) DNA, hepatitis B e antigen and antibody (HBeAg, HBeAb), alanine amino-transferase (ALT) and aspartate aminotransferase(AST) were measured at baseline and every 24 weeks until study completion.

Role of cathepsin B-mediated apoptosis in fulminant hepatic failure in mice.

Aim: To investigate the pathogenic role of cathepsin B and the protective effect of a cathepsin B inhibitor (CA-074Me) in fulminant hepatic failure in mice.

Methods: LPS/D-Gal N was injected into mice of the model group to induce fulminant hepatic failure; the protected group was administered CA-074me for 30 min before LPS/D-Gal N treatment; the normal group was given isochoric physiologic saline. Liver tissue histopathology was determined with HE at 2, 4, 6 and 8 h after Lps/D-Gal injection.

Protective effect and mechanism of stronger neo-minophagen C against fulminant hepatic failure.

Aim: To investigate the protective effect of stronger neo-minophafen C (SNMC) on fulminant hepatic failure (FHF) and its underlying mechanism.

Methods: A mouse model of FHF was established by intraperitoneal injection of galactosamine (D-Gal N) and lipopolysaccharide (LPS). The survival rate, liver function, inflammatory factor and liver pathological change were obtained with and without SNMC treatment.

[Protective effect of SNMC on mice with fulminant liver failure].

Objective: To investigate the protective effect of stronger neo-minophagen C (SNMC) on fulminant liver failure (FLF).

Methods: D-Gal N and LPS were injected once into the abdominal cavity of rats to establish an experimental model of FLF. The level of plasma ALT, Alb, TBil, TNFalpha, NO, ET-1, IL-6 and liver histopathology of the rats were examined.

[Molecular mechanisms of the protection of SNMC in HepG2 cell apoptosis].

Objective: Apoptosis of the cells of liver cancer cell line HepG2 could be induced by TNF alpha and actinomycin D (Act D). In the current study, the molecular mechanism of the apoptosis protection of stronger neo-minophagen C (SNMC) to HepG2 cells was investigated.

Methods: SNMC was added to the HepG2 cell culture medium when the cell concentration reached 0, 2, 20, 100, 200, 800 microg/ml 30 min before their apoptosis were inducted with TNF alpha and Act D.