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. Consequently, our study explored miR-155 modulation of HBV replication and investigated the potential mechanism involved. miR-155 was inhibited on HBV infection. miR-155 transfection remarkably reinforced HBV replication, antigen expression, and progeny secretion in HepG2215 cells. Moreover, miR-155 impaired the inhibition of the cytokine signalling 1 (SOCS1)/Akt/ mTOR axis and reinforced HepG2215 autophagy. Additionally, the autophagy inhibitor (3-MA) eliminated HBsAg secretion triggered by miR-155. Taken together, miR-155 reinforced HBV replication by reinforcing SOCS1-triggered autophagy.Significance of the study: The research studied the potential mechanism involved in HBV replication and miR-155 that miR-155 reinforces HBV replication by reinforcing the SOCS1/Akt/mTOR axis-stimulated autophagy, and therefore, it can provide medical practitioners with the inspiration that chronic HBV might be cured or improved by regulating the activation of miR-155 in cells. In the study, the experiments show that autophagy inhibitors (3-MA) counteracted miR-155 contribution to HBV replication, and it might be a practicable way to improve HBV through some therapies that can repress the autophagy in related cells. K E Y W O R D S autophagy, HBV replication, infection, miR-155, SOCS1

SNMC can effectively protect liver against FHF induced by LPS/D-Gal N. SNMC can prevent hepatocyte apoptosis by inhibiting inflammatory reaction and stabilizing mitochondria membrane to suppress the release of Cyt-C and sequent activation of caspase-3.

Cathepsin B plays an essential role in the pathogenesis of fulminant hepatic failure, and the cathepsin B inhibitor CA-074me can attenuate apoptosis and liver injury.

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ABSTRACT.We investigated the effect of atorvastatin on vascular endothelial growth inhibitor (VEGI) expression in rats with diabetic retinopathy. Wistar rats were divided into a blank group and diabetic model group, which was further randomly divided into treatment and control groups. Rats in the treatment group received 10 mg/kg atorvastatin daily, while rats in the blank and control groups received normal saline. Rats were randomly euthanized at 3 or 6 months. Immunohistochemical staining was used to determine changes in VEGI and vascular endothelial growth factor, interleukin-4, and tumor necrosis factor α levels in rats with diabetic retinopathy. Survival rate in the treatment group was 84% (63/75) after 6 months, which was significantly higher than that in the control group (P < 0.05); rats in the control group showed the lowest survival rate. Survival in the treatment group was higher than that in the control group but not significant compared with the blank group after 3 months. VEGI, vascular endothelial growth factor, tumor necrosis factor α, and interluekin-4 expression was lower than that in the control group, but higher than the blank group after 3 months. The (2015) expression of each factor decreased to the blank group level in the treatment group and was significantly lower than that in the control group after 6 months (P < 0.05). Expression in control and blank groups was similar at 3 and 6 months. Atorvastatin can inhibit VEGI and vascular endothelial growth factor expression to protect rats from diabetic retinopathy.