Salidroside protects against caerulein with the LPS-induced severe acute pancreatitis through suppression of oxidative stress and inflammation in mice

Abstract

• Salidroside attenuated caerulein with LPS-induced pancreatic injury in a mouse model of SAP. • Salidroside significantly ameliorated oxidative stress and inflammation responses in the pancreas of SAP mice. • Depletion of Nrf2 weakened the therapeutic effect of salidroside and reduced the anti-oxidative stress and anti-inflammatory effects in salidroside treated SAP mice. • Molecular mechanism studies showed that salidroside mediated anti-oxidant stress and anti-inflammatory responses in SAP mice partially through the Nrf2/NF-κB p65 pathway. Severe acute pancreatitis (SAP) is a fatal inflammation with no effective treatment. Salidroside, a monomer isolated from the traditional Chinese medicine Rhodiola, has been shown cytoprotective roles in many inflammation-related diseases. However, whether salidroside plays a protective role in an acute inflammation like SAP in mice is unknown. In this study, we aimed to investigate the molecular mechanism underlying the pancreatic protection of salidroside. The results showed that salidroside attenuated caerulein with the LPS-induced pancreatic injury in a mouse model of SAP. Also, we found that salidroside ameliorated oxidative stress and inflammation responses in SAP mice. Furthermore, SAP mice treated with salidroside were associated with higher phosphorylation levels of Nrf2 and less nuclear accumulation of NF-κB p65. We further found that depletion of Nrf2 weakened the protective effect of salidroside in SAP mice. Collectively, salidroside mediated anti-oxidant stress and anti-inflammation in SAP mice partially through the Nrf2/NF-κB p65 pathway.