It has been shown that estrogens have anti-inflammatory effects in different experimental inflammation models, however the effect of estrogen on acute pancreatitis was not investigated. In the study it is aimed to determine the potential role of estrogen receptor agonists on acute pancreatitis model induced by pancreaticobiliary ligation. In the study both sexes of Sprague-Dawley rats (n= 88, 250-300 g) were used. Animals were divided into two groups as pancreaticobiliary duct ligated group and pancreaticobiliary duct ligation with bilateral ovariectomy group. The rats were anesthetized by intraperitoneal ketamine (100mg/kg) and chlorpromazine (10mg/kg) before surgeries. Laparoscopic surgery was made to the animals in the sham group. ER-α agonist propyl-pyrazole-triol (PPT;1mg/kg/day), ER-β agonist diarylpropionitrile (DPN;1mg/kg/day) and 17-beta östradiol (10mg/kg/day) were dissolved in olive oil and administered intraperitonally to the groups for 3 days. At 3th day, the animals were decapitated, and the trunk blood was collected, lung and pancreas tissues were taken. Serum TNF-α, IL-1β, IL-6 and IL-10 levels were measured. Malondialdehyde (MDA), glutathione (GSH), myeloperoxidase (MPO) activity, superoxide dismutase (SOD) and catalase levels were measured and histological analyzes were made in pancreas and lung tissues. In both tissues of male and female acute pancreatitis groups MPO, MDA, SOD levels were significantly increased (p<0.05-0.01) and the antioxidant GSH levels were decreased (p<0.05) compared to sham group. Pancreas MDA and SOD levels were elevated in DPN and 17-beta- estradiol treated male rats with acute pancreatitis compared to sham group (p<0,05-0,001). After acute pancreatitis MDA and SOD levels in female rats were decreased (p<0.01-0.001). The increased MPO levels in pancreatitis group were decreased with PPT (p<0,05-0.001) application. IL-1β, IL-6, and TNF-α levels of female rats and IL-1β, IL-6 levels of male rats with acute pancreatitis increased compared to sham group (p<0,05-0,001). The estrogen receptor agonists decreased the variant IL levels. These results suggest that the increased inflammatory status by experimental pancreatitis induction was alleviated by estrogen receptor agonists via alpha and beta receptor subtypes in lung and pancreas tissues.