ObjectiveTo investigate the correlation of quality of life (QOL) with aspartate aminotransferase-to-platelet ratio index (APRI), liver stiffness measurement (LSM), and histopathology after entecavir antiviral therapy for patients with chronic hepatitis B liver fibrosis. MethodsA total of 95 patients who were diagnosed with chronic hepatitis B and liver fibrosis in The Affiliated Hospital of Yanbian University from October 2013 to March 2015 were enrolled, and all patients underwent entecavir antiviral therapy. Before treatment and at weeks 26, 52, and 78 of treatment, SF-36 scale was used to assess QOL, transient elastography was used to measure LSM, and serum APRI was measured. Among these patients, 31 underwent liver biopsy before treatment and at week 78 of treatment to observe the degree of inflammation and fibrosis, and QOL, APRI, LSM, and histopathology were analyzed before and after antiviral therapy. The Kruskal-Wallis H test was used for comparison of non-normally distributed continuous data at different time points, and a Spearman correlation analysis was performed. ResultsThere was a tendency of increase in QOL after antiviral treatment, and there were significant differences in general health, role-physical, role-motional, bodily pain, social functioning, and vitality at different time points (H=25.084, 8.699, 12.293, 22.874, 12.079, and 10.403, all P＜0.05). There was a tendency of reduction in APRI, with a significant change after treatment (H=60.030, P＜0.01), and there was also a significant reduction in LSM after treatment (H=35.744, P＜0.01). APRI and LSM were negatively correlated with QOL (all P＜0.05). Among the patients who underwent liver biopsy, 22 achieved the improvement in histological inflammation after antiviral therapy, 15 achieved the improvement in fibrosis, 14 achieved the improvement in both inflammation and QOL, and 8 achieved the improvement in both fibrosis and QOL. ConclusionEntecavir antiviral therapy can improve the QOL of patients with chronic hepatitis B liver fibrosis, and reductions in APRI and LSM can predict the improvement in QOL in patients with chronic hepatitis B liver fibrosis. Improvement in histological inflammation and fibrosis have a certain effect on the improvement in QOL in patients with chronic hepatitis B liver fibrosis.

ObjectiveTo investigate the effect of 1，25（OH）₂D₃ on the level of peroxisome proliferator-activated receptor-γ （PPAR-γ） in the liver， the phenotype of hepatic macrophages， and liver inflammation in a rat model of nonalcoholic steatohepatitis （NASH）， as well as the mechanism of 1，25（OH）₂D₃ improving liver inflammation. MethodsAfter 1 week of adaptive feeding， 24 specific pathogen-free Wistar rats were randomly divided into normal group ［choline-supplemented L-amino acid-defined （CSAA） diet］， normal+1，25（OH）₂D₃ group ［CSAA diet+1，25（OH）₂D₃］， model group ［choline-deficient L-amino acid-defined diet （CDAA） diet］， and model+1，25（OH）₂D₃ group ［CDAA diet+1，25（OH）₂D₃］， with 6 rats in each group. The dose of 1，25（OH）₂D₃ was 5 μg/kg for intraperitoneal injection twice a week for 12 weeks. The serum levels of aspartate aminotransferase （AST） and alanine aminotransferase （ALT） were measured， liver histopathology was observed， and SAF score was assessed. M1 hepatic macrophages and M2 hepatic macrophages were measured to analyze in the change in the phenotype of hepatic macrophages， and ELISA was used to measure the levels of tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， interleukin-4 （IL-4）， and interleukin-10 （IL-10） in liver tissue， and qPCR was used to measure the mRNA level of PPAR-γ. The two-factor analysis of variance was use for comparison between groups， and the least significant difference t-test was used for further comparison； the Pearson method was used for correlation analysis. ResultsCompared with the normal group， the model rats with CDAA diet-induced NASH had significant increases in the serum levels of AST and ALT （P=0.019 and P<0.001）， the SAF score of liver histopathology （P<0.001）， the level of M1 hepatic macrophages （P<0.001）， and the ratio of M1 and M2 hepatic macrophages （P<0.001）， as well as a significant increase in the level of TNF-α （P<0.001） and a significant reduction in the level of IL-4 in liver tissue （P=0.025）. The 1，25（OH）₂D₃ group had significant reductions in the serum levels of ALT （P<0.001）， the SAF score of liver histopathology （P<0.001）， the level of M1 hepatic macrophages （P<0.001）， and the ratio of M1 and M2 hepatic macrophages （P=0.001）， the level of IL-1β （P<0.001） and a significant increase in the level of M2 hepatic macrophages （P=0.017）， the level of IL-10 （P=0.039）， the level of IL-4 （P<0.001）， the level of PPAR-γ （P=0.016）. There were significant interactions between CDAA diet-induced NASH model and 1，25（OH）₂D₃ in serum the levels of AST and ALT （P=0.007 and P=0.008）， the SAF scores of liver histopathology （P<0.001）， the level of M1 hepatic macrophages （P<0.001）， the level of M2 hepatic macrophages （P=0.008）， the ratio of M1 and M2 of hepatic macrophages （P=0.005）， the level of TNF-α （P<0.001）， the level of IL-10 （P=0.038）， the level of IL-4 （P<0.001） and the level of PPAR-γ （P=0.009）. The correlation analysis showed that PPAR-γ was negatively correlated with the ratio of M1 and M2 hepatic macrophages （r=-0.415， P=0.044） and was positively correlated with M2 hepatic macrophages （r=0.435， P=0.033）， IL-10 （r=0.433， P=0.035）， and IL-4 （r=0.532， P=0.007）. ConclusionThis study shows that 1，25（OH）₂D₃ improves liver inflammation in NASH by activating PPAR-γ to regulate the phenotypic transformation of hepatic macrophages.