AI Article Synopsis
- TRAIL plays a significant role in hepatitis B virus (HBV) infection, and a study investigated the effects of a recombinant human soluble death receptor 5 (sDR5) in a mouse model of HBV-induced acute hepatitis.
- The researchers found that administering sDR5 before HBV infection reduced liver damage by inhibiting TRAIL-induced apoptosis in HBV-infected liver cells, with a dosage of 16 mg/kg proving to be the most effective.
- Importantly, sDR5 demonstrated comparable effectiveness in protecting against liver injury as the established drug Stronger Neo-Minophagen C (SNMC), suggesting it could be a new treatment option for patients with severe hepatitis.
Article Abstract
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) may play important roles during hepatitis B virus (HBV) infection. In this study, we used a recombinant human soluble death receptor 5 (sDR5) to explore its effect in a mouse model of HBV-induced acute hepatitis. By measuring blood transaminase activity and hepatocyte apoptosis, we found that sDR5 could alleviate liver damage by blocking TRAIL-induced apoptosis of HBV-transfected hepatocytes. sDR5 injection at 16 mg/kg 24h before HBV transfection was the most effective. Additionally, we showed that sDR5 was equally effective in protecting liver injury as the Stronger Neo-Minophagen C (SNMC), a commonly used drug for patients with liver diseases. Thus, sDR5 represents a potential novel therapeutic drug for patients with fulminant hepatitis.
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| http://dx.doi.org/10.1016/j.bbrc.2006.11.024 | DOI Listing |
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