Intraperitoneal gardiquimod protects against hepatotoxicity through inhibition of oxidative stress and inflammation in mice with sepsis.

Many reports recapitulate the contribution of reactive oxygen species (ROS) over-accumulation to the organ damage; it is of significance to strictly target ROS production. In this study, we evaluated the potential role of TLR7 agonist gardiquimod (GDQ) in oxidative stress (OS) in liver injury induced by sepsis. Here, we observed that intraperitoneal pretreatment with GDQ dramatically elevated the septic survival rate and effectively attenuated the septic liver injury. Interestingly, the increased ROS and inflammatory factor IL-6 levels were reversed after GDQ intervention. Subsequently, Western blot was employed to determine the definite mechanism. As expected, it was showed that the upregulation of c-Jun N-terminal kinase (JNK)/c-Jun pathway in liver of septic animals was considerably suppressed by GDQ pre-exposure. Our current result highlight that pre-administration of GDQ ameliorated sepsis induced hepatotoxicity and reduced the generation of IL-6 and OS responses, which was associated with downregulation of JNK/c-Jun pathway. Our strategies might be ultimately beneficial in mitigating liver injury symptom.