AIM: To investigate the effect of rhubarb on MAPK activation in sodium taurocholate-induced pancreatitis in rats. METHODS: All rats were randomly divided into three groups: control, acute pancreatitis (AP) and rhubarb treatment groups. The MAPK activation was detected by western blotting. The levels of TNFα and IL6 in serum were estimated by ELISA. The pathological changes of the pancreas were examined microscopically. RESULTS: It was found that hemorrhage, exudates and infiltration of inflammatory cells in the pancreas were significantly less in the rhubarb group than in the AP group. In the AP group, the activation of MAPKs in pancreatic tissues was enhanced significantly at every time point compared with the control group and the levels of TNFα and IL6 were also increased. Rhubarb treatment markedly inhibited activation of MAPKs concomitantly with inhibition of TNFα and IL6 expression. CONCLUSION: We suggest that rhubarb probably attenuates AP by inhibiting activation of MAPKs and expression of inflammatory mediators.
AIM: To investigate the effect of rhubarb on MAPK activation in sodium taurocholate-induced pancreatitis in rats. METHODS: All rats were randomly divided into three groups: control, acute pancreatitis (AP) and rhubarb treatment groups. The MAPK activation was detected by western blotting. The levels of TNFα and IL6 in serum were estimated by ELISA. The pathological changes of the pancreas were examined microscopically. RESULTS: It was found that hemorrhage, exudates and infiltration of inflammatory cells in the pancreas were significantly less in the rhubarb group than in the AP group. In the AP group, the activation of MAPKs in pancreatic tissues was enhanced significantly at every time point compared with the control group and the levels of TNFα and IL6 were also increased. Rhubarb treatment markedly inhibited activation of MAPKs concomitantly with inhibition of TNFα and IL6 expression. CONCLUSION: We suggest that rhubarb probably attenuates AP by inhibiting activation of MAPKs and expression of inflammatory mediators.