Published online Sep 14, 2010. doi: 10.3748/wjg.v16.i34.4272
Revised: May 25, 2010
Accepted: June 1, 2010
Published online: September 14, 2010
AIM: To study the beneficial effects of triterpene α,β-amyrin and the underlying mechanisms in an experimental pancreatitis model.
METHODS: Acute pancreatitis was induced in five groups of rats (n = 8) by L-arginine (2 × 2.5 g/kg, intraperitoneal, 1 h apart) and 1 h later, they received a single oral dose of α,β-amyrin (10, 30 and 100 mg/kg), methylprednisolone (30 mg/kg) and vehicle (3% Tween 80). A saline (0.9% NaCl) treated group served as a normal control. Efficacy was assessed at 24 h by determination of serum levels of amylase, lipase and pro-inflammatory cytokines [tumor necrosis factor (TNF)-α and interleukin (IL)-6], pancreatic myeloperoxidase (MPO) activity, lipid peroxidation [thiobarbituric acid reactive substances (TBARS)], nitrate/nitrite levels, and the wet weight/body weight ratio. Tissue histology and the immunoreactivity for TNF-α and inducible nitric oxide synthetase (iNOS) were performed.
RESULTS: α,β-amyrin and methylprednisolone treatments significantly (P < 0.05) attenuated the L-arginine-induced increases in pancreatic wet weight/body weight ratio, and decreased the serum levels of amylase and lipase, and TNF-α and IL-6, as compared to the vehicle control. Also, pancreatic levels of MPO activity, TBARS, and nitrate/nitrite were significantly lower. Histological findings and TNF-α and iNOS immunostaining further confirmed the amelioration of pancreatic injury by α,β-amyrin.
CONCLUSION: α,β-amyrin has the potential to combat acute pancreatitis by acting as an anti-inflammatory and antioxidant agent.