To analyze miR-223-3p expression in patients with hepatitis B virus (HBV) live fibrosis and its effects on proliferation, activation, and apoptosis of human hepatic stellate cell line. One hundred patients with HBV-associated liver fibrosis were divided into S0 to 1, S2 to 3, and S4 groups according to Scheuer histological staging; healthy individuals during the same period were enrolled as healthy group. Relative expressions of miR-223-3p in healthy, S0 to 1, S2 to 3, and S4 groups were 0.56 ± 0.11, 1.08 ± 0.27, 2.16 ± 0.42, and 3.59 ± 1.06, respectively. Absorbance values of human hepatic stellate cell line cells at 24, 48, and 72 hours were higher in miR-223-3p-mimic group than in control group (CG) and NC-mimic group and were lower in miR-223-3p-inhibitor group than in CG and NC-inhibitor group (P < .05). mRNA miR-223-3p, α-smooth muscle actin, collagen 1A1, collagen 1A2, collagen 3A1, and transforming growth factor (TGF)-β1 levels were higher in miR-223-3p-mimic group than in CG and NC-mimic group and lower in miR-223-3p-inhibitor group than in CG and NC-inhibitor group (P < .05). Protein expressions of α-smooth muscle actin, transforming growth factor-β1, collagen I, collagen III, p-Smad3, p-Smad2, and B-cell lymphoma 2 were higher in miR-223-3p-mimic group than in CG and NC-mimic groups and lower in miR-223-3p-inhibitor group than in CG and NC-inhibitor group, whereas those of B-cell lymphoma 2-associated death promoter, B-cell lymphoma 2 associated X protein, cleaved caspase3, cleaved caspase9, poly ADP-ribose polymerase were lower in miR-223-3p-mimic group than in CG and NC-mimic group and higher in miR-223-3p-inhibitor group than in CG and NC-inhibitor group (P < .05). HBV liver fibrosis patients had elevated expression of miR-223-3p in plasma. Upregulation of miR-223-3p expression may be related to transforming growth factor-β1/Smad signaling pathway activation.

The hepatitis B virus (HBV) infection remains highly prevalent globally. The present study aimed to explore the possible therapeutic effect of notoginsenoside R1, which has attracted considerable attention due to its diverse pharmacological effects, on HBV infection. The HBV-containing hepatocellular carcinoma cell lines, HepG2 and MHCC97H, were used in this study. We first treated the two cell lines with different concentrations of notoginsenoside R1 and subsequently measured the relative levels of HBV DNA, HBV surface antigen, HBV core antigen, and sirtuin 1 (SIRT1) using reverse transcription-quantitative polymerase chain reaction and western blotting. Finally, an HBV hemodynamic replication model was created to test the effect of notoginsenoside R1 on HBV replication. Notoginsenoside R1 inhibited the replication of HBV. This inhibitory effect was mediated through the downregulation of SIRT1 activity. Additionally, the inhibition of SIRT1 activity by silencing its expression or treatment with the SIRT1 inhibitor, selisistat, suppressed HBV replication. Furthermore, our animal experiments demonstrated that notoginsenoside R1 was effective at suppressing HBV replication in vivo. Thus, notoginsenoside R1 suppresses HBV replication by downregulating SIRT1 activity in vitro and in vivo.