Abstract
Aim To investigate the mechanisms of Fuzheng Huayu (FZHY) Capsule in the treatment of hepatitis B (HBV)- associated fibrosis, HBV patients were divided into two groups, 50 cases were in the nucleotide analogues (NAs) group, while additional 50 cases were in the NAs + FZHY group. Methods We assessed the curative effects of antifibrosis through liver function, FibroScan test, and liver biopsy and detected the ratio of lymphocyte subsets by flow cytometry. Peripheral blood lymphocyte and CD8+T, CD4+T, and natural killer cell subsets collected from patients were cocultured with LX-2 cells. Activation of LX-2 cells, production of the extracellular matrix, apoptosis, and proliferation of LX-2 cells were determined. Chronic liver injury models were established by ConA treatment. Results It is evident that FZHY treatment significantly increased the percentage of NK cells, the rate of death, and apoptosis of LX-2 cells and decreased the FibroScan liver stiffness measurement value. The expressions of α-SMA and procollagen type I mRNA in LX-2 cells of the FZHY treatment group as downregulated when they were cocultured with lymphocytes compared to those from the NAs group. The proliferation of LX-2 cells in the FZHY treatment group was inhibited compared to that in the NAs group. In a mouse model of hepatic fibrosis, PBLs and IHLs from ConA exposure plus FZHY treatment inhibited the ability of JS-1 cells to express α-SMA. Conclusions FZHY Capsule improved the disordered cellular immunity and postponed liver fibrosis possibly through inhibiting the interaction between lymphocyte and hepatic stellate cells.
Highlights
It is well known that various chronic liver diseases may be accompanied by hepatic fibrosis
Serum Alb content was increased to some extent in both nucleotide analogues (NAs) + Fuzheng Huayu (FZHY) and NAs groups compared to the levels prior to the treatment
E FibroScan LSM value was 22.56 ± 10.14 kPa and 23.34 ± 13.91 kPa in NAs and NAs + FZHY groups before treatment, and it was significantly decreased to 19.14 ± 7.66 and 14.98 ± 7.28 kPa I (P < 0.01) in both groups after treatment (Figure 1(a)), suggesting that the addition of FZHY Capsule significantly improved fibrotic extent in HBV-infection patients while antiviral therapy was successful as indicated by the fact that HBV viral DNA load was dramatically decreased by 5 logs (Figure 1(b))
Summary
It is well known that various chronic liver diseases may be accompanied by hepatic fibrosis. Hepatic fibrosis (fibrosis of the liver) mainly results from hepatitis virus infection or alcoholism. It has been estimated that 350 million and 180 million individuals carry hepatitis B (HBV) and C (HCV) viruses in the world, respectively [1]. Hepatic fibrosis may develop into cirrhosis and eventually progress to death due to its complications. In the initiation and progression of hepatic fibrosis, hepatic stellate cells (HSCs) play a critical role. HSCs proliferate massively, express various growth factors and receptors, and cause an imbalance between synthesis and degradation of collagen-based extracellular matrices (ECMs), leading to excessive deposit of ECM components in the liver, and result in the progression from hepatic fibrosis to cirrhosis [2, 3]
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