Abstract
The present study was aimed to investigate the regulatory effect of Nitric oxide donor andrographolide (Q-1) on cellular immunity in patients with chronic hepatitis B. Peripheral blood mononuclear cells (PBMCs) were isolated from patients with chronic hepatitis B. Cell viability was assessed using 3‑(4,5‑dimethyl‑thiazol‑2‑yl)‑2,5‑diphenyl‑2H‑tetrazolium bromide (MTT) assay. The levels of expression of interferon gamma (IFN-γ), interleukin 4 (IL-4), interleukin 10 (IL-10) and tumor necrosis factor α (TFN-α) in PBMCs of patients with chronic hepatitis B were determined using real-time quantitative polymerase chain reaction (qRT-PCR). Anti-HBV effect of isolated HBV DNA was also assessed in vitro. Q-1 had no significant effect on the viability of Vero and isolated PBMCs (p > 0.05). The expression of IFN-γ in PBMCs of control patients significantly and time-dependently increased after treatment with Q-1, but the expressions of IL-4 and IL-10 in PBMCs of patients with chronic hepatitis B were decreased significantly and time-dependently (p < 0.05). The function of Th1 cells was significantly enhanced by Q-1 treatment (p < 0.05). The mean replication of HBV DNA in HepG2cells at the three concentrations of Q-1 and adefovir were 3.96 × 106, 4.13 × 106 and 4.53 × 106 copies/mL, respectively. There was no significant difference in the expression of HBV DNA among the concentration levels. These results indicate that andrographolide enhances the function of HBV-specific T cells in patients with chronic hepatitis B.
Highlights
Chronic hepatitis B is caused by persistent HBV infection
Q-1 had no significant effect on the viability of Vero and isolated Peripheral blood mononuclear cells (PBMCs) (p > 0.05)
The expression levels of IFN-γ and interleukin 10 (IL-10) in PBMCs of patients with chronic hepatitis B were not significantly different from those of control group (p > 0.05), but the corresponding interleukin 4 (IL-4) expression level was significantly higher in PBMCs of patients with chronic hepatitis B than in control group (p < 0.05; Figure 2)
Summary
Chronic hepatitis B is caused by persistent HBV infection. It is caused by decline in antigen-specific cell function, leading to persistent infection [1, 2]. Nucleoside analogues and interferons are employed in antiviral therapy for the treatment of chronic hepatitis B [3, 4]. Interferons play an antiviral role via the regulation of cellular immunity, while nucleotide analogues directly inhibit viral replication. Studies have shown that activation of HBV antigen-specific T-cell in patients with chronic hepatitis B after antiviral therapy is due mainly to enhancement in T helper 1 cells (Th1 cells) and balance in Th1/Th2. Antiviral therapy is limited by several factors [5, 6]
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