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Abstract
The aim of this study was to investigate whether resolvin E1 (RvE1) protects against hepatic fibrosis in a murine model of liver fibrosis induced by Schistosoma japonicum infection. A total of 30 pathogen-free Kunming mice were randomly and equally divided into three groups: Control (uninfected, untreated), model (infected, untreated) and RvE1 intervention (infected, RvE1-treated; 100 ng daily). The mice were infected with Schistosoma japonicum by inoculating the abdominal skin with 20±2 cercariae to induce models of liver fibrosis. The area and numbers of the granulomas in the livers were assessed through histopathology after 70 days of treatment. The levels of tumor necrosis factor (TNF)-α and interferon (IFN)-γ were evaluated in the serum by enzyme-linked immunosorbent assay (ELISA). The expression levels of TNF-α were detected in the hepatic tissue by reverse transcription-polymerase chain reaction and western blot analysis. The activity levels of alanine aminotransferase and aspartate aminotransferase were determined in the serum by ELISA. The expression levels of laminin (LN), hyaluronic acid (HA), procollagen type III (PC-III) and type IV collagen (IV-C) were detected in the serum by radioimmunoassays. The results revealed that the mean area of the granulomas was smaller in the RvE1 intervention group compared with that in the model group. Following RvE1 treatment, the serum levels of TNF-α were lower than those in the model group, while the serum levels of IFN-γ were higher compared with those in the model group. The expression levels of TNF-α were lower in the hepatic tissue following RvE1 treatment compared with those in the model group. The indicators of liver fibrosis, the levels of LN, HA, PC-III and IV-C in the serum, were lower following RvE1 treatment than those in the model group. In conclusion, RvE1 treatment may reduce the growth of granulomas, thereby slowing the process of hepatic fibrosis, and this effect may be the result of anti-inflammatory and immune system adjustment.
Highlights
Schistosomiasis is a type of zoonotic parasitic disease that is distributed globally and causes serious harm to human health [1]
Schistosome eggs are an important source of antigens to which the host is exposed during Schistosoma japonicum infection and these cells induce an imbalance in T‐cell immunity, which is considered to be a trigger of liver fibrosis [11]
These fibroblasts increase the levels of collagen formation and suppress its decomposition, which eventually results in matrix protein deposition and fibrosis [12]
Summary
Schistosomiasis is a type of zoonotic parasitic disease that is distributed globally and causes serious harm to human health [1]. The main pathological changes caused by Schistosoma japonicum infection are the formation of granulomas and hepatic fibrosis [3]. Hepatic fibrosis is the principal cause of serious complications and mortality due to Schistosoma japonicum infection [4]. Hepatic fibrosis is a compensatory response that is secondary to the process of tissue repair following liver inflammation or damage caused by Schistosoma japonicum infection [5]. The lack of an endogenous anti‐inflammatory and pro‐resolving mediator leads to persistent inflammation and causes liver fibrosis [6]. The effects of RvE1 on liver fibrosis in schistosome‐infected mice were investigated
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