AIM: To study the beneficial effects of triterpene alpha,beta-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 x 2.5 g/kg, intraperitoneal, 1 h apart) and 1 h later, they received a single oral dose of alpha,beta-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)-alpha 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-alpha and inducible nitric oxide synthetase (iNOS) were performed. RESULTS: alpha,beta-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-alpha 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-alpha and iNOS immunostaining further confirmed the amelioration of pancreatic injury by alpha,beta-amyrin. CONCLUSION: alpha,beta-amyrin has the potential to combat acute pancreatitis by acting as an anti-inflammatory and antioxidant agent.
AIM: To study the beneficial effects of triterpenealpha,beta-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 x 2.5 g/kg, intraperitoneal, 1 h apart) and 1 h later, they received a single oral dose of alpha,beta-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)-alpha 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-alpha and inducible nitric oxide synthetase (iNOS) were performed. RESULTS:alpha,beta-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-alpha 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-alpha and iNOS immunostaining further confirmed the amelioration of pancreatic injury by alpha,beta-amyrin. CONCLUSION:alpha,beta-amyrin has the potential to combat acute pancreatitis by acting as an anti-inflammatory and antioxidant agent.
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