Saikosaponin a attenuates hyperlipidemic pancreatitis in rats via the PPAR-γ/NF-κB signaling pathway

The therapeutic effect of saikosaponin a (SSa) on hyperlipidemic pancreatitis (HP) is not completely understood. The aim of the present study was to investigate the therapeutic effect and the underlying mechanism of SSa using a rat model of HP. Following successful establishment of the HP rat model, different doses of SSa (low dose group, 10 mg/kg or high dose group, 20 mg/kg) were administrated. Histopathological examination, the wet/dry (W/D) ratio and myeloperoxidase (MPO) activity of the pancreatic tissues were assessed. The lipid, amylase (AMY), Lipase and proinflammatory cytokine profiles in serum, as well as the expression of Peroxisome Proliferator-activated Receptor (PPAR)-γ and the NF-κB signaling pathway-related proteins in pancreatic tissues were evaluated. The results showed that SSa effectively attenuated pancreatic pathological injury and reduced both the W/D ratio and MPO activity compared to the HP model rats. SSa also improved lipid metabolism by significantly decreasing the serum levels of total Cholesterol and triglycerides (P<0.05). Following the administration of SSa, the activity of AMY and Lipase, as well as the levels of the proinflammatory cytokines tumor necrosis factor-α, interleukin (IL)-1β and IL-6 were reduced, particularly in the high dosage group (P<0.05). Furthermore, SSa activated PPAR-γ expression and suppressed the NF-κB signaling pathway in pancreatic tissues. The present study suggested that SSa attenuated HP in rats by increasing lipid metabolism and inhibiting the release of proinflammatory cytokines via the NF-κB inflammatory pathway. The results from the present study indicated that SSa might be a promising therapeutic agent for the treatment of HP.

NF-κB; hyperlipidemia; pancreatitis; peroxisome proliferator-activated receptor-γ; saikosaponin a.