Second Affiliated Hospital of Wenzhou Medical University

Biejia-Ruangan (BRG) has been approved in China as an antifibrotic traditional Chinese medicine for patients with chronic liver diseases; however, data on the reversal of hepatitis B-related cirrhosis by BRG are still limited.

To investigate the reversal effect of BRG in patients with hepatitis B-related cirrhosis.

Hepatitis B-related cirrhotic patients who received either entecavir (ETV) monotherapy or combination therapy with ETV and BRG for 7 years, were analysed. The primary endpoints included the regression of liver cirrhosis, liver histological improvement, and a significant reduction in the LSM value.

In total, 153 cirrhotic patients were enrolled, of whom 63 received ETV alone and 90 received both ETV and BRG. Ninety-four patients, of whom 39 received ETV monotherapy and 55 received both ETV and BRG, underwent liver biopsies at both the second and seventh years of treatment. Although the rate of liver cirrhosis regression did not significantly increase after two years of antifibrotic therapy in patients who received ETV and BRG combination therapy (43.3 % vs. 38.1 %, P = 0.217), the median LSM decreased significantly (8.3 kPa vs. 11.2 kPa, P = 0.041); after seven years of treatment, a significantly greater rate of liver cirrhosis regression was achieved (55.6 % vs. 38.1 %, P = 0.033), and the LSM value further decreased significantly (6.4 kPa vs. 11.0 kPa, P = 0.036).

BRG enhances the efficacy of ETV in reversing liver cirrhosis in patients with chronic HBV infection, but this reversal takes a longer time.

Impaired postural control, attributed to abnormal function of motor-related cortices, has been proven as one of the potential mechanisms of chronic low back pain (CLBP). Based on available evidence, anodal transcranial direct current stimulation over the primary motor cortex (M1-tDCS) can significantly enhance cortical activation and improve postural control. However, the neuromechanism underlying the effect of anodal M1-tDCS on patients with CLBP remains unclear.

Twenty-six participants with CLBP were randomly assigned to the active tDCS group or sham group. A 20-minute session of anodal M1-tDCS or sham intervention was applied. Before and after the intervention, postural control performance and cortical activity during unipedal standing were assessed by center of pressure displacement and functional near-infrared spectroscopy (fNIRS), respectively. Regions of interest (ROIs) included bilateral primary motor cortex (M1), dorsolateral prefrontal cortex (DLPFC), frontopolar area (FpA), and supplementary motor area (SMA). Functional connectivity (FC) among these ROIs was also analyzed.

Significant interactions (Group × Time) were observed in anterior-posterior (AP) velocity, sway length, left M1 activation, and FC between left M1 and right DLPFC, as well as between the left M1 and bilateral FpA (ps<0.05). Post-hoc comparisons demonstrated that AP velocity and sway length significantly decreased after the anodal M1-tDCS intervention (p_FDR<0.001, effect size (d)= 2.060). Additionally, participants in the active tDCS group exhibited significantly reduced left M1 activation (p_FDR<0.001, d=1.894), FC between the left M1 and right DLPFC (p_FDR=0.008, d=1.420), and FC between the left M1 and bilateral FpA (left: p_FDR=0.006, d=1.461; right: p_FDR=0.027, d=1.227) after the intervention.

The improvement in postural control of patients with CLBP following anodal M1-tDCS, accompanied by reduced cortical activation and functional connectivity, suggests enhanced neural efficiency (more efficient neural processing) and reduced compensatory demands within sensorimotor networks.

CXCR7, an alternative receptor for the inflammatory chemokine SDF-1, is involved in cell proliferation and migration. Recent studies have reported that CXCR7 also plays a role in adipose tissue. However, evidence regarding the role of CXCR7 and its ligands in adipocyte differentiation is limited. In this study, we aimed to elucidate changes in CXCR7 expression during adipocyte differentiation and the role of the SDF-1/CXCR7/CXCR4 axis in adipogenesis using recombinant SDF-1, the CXCR7 ligand CCX771, and small interfering RNAs. The results indicated that the levels of SDF-1 and its receptors, CXCR7 and CXCR4, decreased during the early stages of adipogenesis. Treatment with recombinant SDF-1 and CCX771 inhibited adipogenesis and lipid accumulation by inducing β-arrestin2, Wnt expression, and AKT phosphorylation and downregulating C/EBPα, PPARγ, and FABP4 expression. In contrast, knockdown of SDF-1 and CXCR7 in preadipocytes downregulated the β-arrestin2/Wnt and AKT pathway, leading to the induction of adipogenesis. Meanwhile, knockdown of CXCR4 had no significant effect. In mice, basal gene expression levels of SDF-1 and CXCR7 were higher in the stromal vascular fraction compared to mature adipocytes and were significantly upregulated by a high-fat diet. Our results provide new insights into the local role of the SDF-1-CXCR7 axis in adipocytes and offer additional benefits for the prevention of obesity-related metabolic disorders.