Relationship between Carbachol Hyperstimulation-induced Pancre-atic Intracelluar Trypsinogen and NF-κB Activation in Rats in vitro  

Relationship between Carbachol Hyperstimulation-induced Pancre-atic Intracelluar Trypsinogen and NF-κB Activation in Rats in vitro

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作  者:蒋春舫 郑海 刘苏南 方开峰 

机构地区:[1]Department of Emergency Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology

出  处:《Journal of Huazhong University of Science and Technology(Medical Sciences)》2008年第1期69-72,共4页华中科技大学学报(医学英德文版)

摘  要:The relationship between intracelluar trypsinogen activation and NF-κB activation in rat pancreatic acinar cells induced by M3 cholinergic receptor agonist (carbachol) hyperstimulation was studied. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active protease inhibitor (pefabloc) and NF-κB inhibitor (PDTC) in vitro. Intracelluar trypsin activity was measured by using a fluorogenic substrate. The activity of NF-κB was monitored by using electrophoretic mobility shift assay. The results showed that after pretreatment with 2 mmol/L pefabloc, the activities of trypsin and NF-κB in pancreatic acinar cells treated with high concertrations of carbachol (10^-3 mol/L) in vitro was significantly decreased as compared with control group (P〈0.01 ). The addition of 10^-2 mol/L PDTC resulted in a significant decrease of NF-κB activities in pancreatic acinar cells after treated with high concertrations of carbachol (10^-3 mol/L) in vitro, but the intracelluar trypsinogen activity was not obviously inhibited (P〉0.05). It was concluded that intracelluar trypsinogen activation is likely involved in the regulation of high concertrations of carbachol-induced NF-κB activation in pancreatic acinar cells in vitro. NF-κB activation is likely not necessary for high concertrations of carbachol-induced trypsinogen activation in pancreatic acinar cells in vitro.The relationship between intracelluar trypsinogen activation and NF-κB activation in rat pancreatic acinar cells induced by M3 cholinergic receptor agonist (carbachol) hyperstimulation was studied. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active protease inhibitor (pefabloc) and NF-κB inhibitor (PDTC) in vitro. Intracelluar trypsin activity was measured by using a fluorogenic substrate. The activity of NF-κB was monitored by using electrophoretic mobility shift assay. The results showed that after pretreatment with 2 mmol/L pefabloc, the activities of trypsin and NF-κB in pancreatic acinar cells treated with high concertrations of carbachol (10^-3 mol/L) in vitro was significantly decreased as compared with control group (P〈0.01 ). The addition of 10^-2 mol/L PDTC resulted in a significant decrease of NF-κB activities in pancreatic acinar cells after treated with high concertrations of carbachol (10^-3 mol/L) in vitro, but the intracelluar trypsinogen activity was not obviously inhibited (P〉0.05). It was concluded that intracelluar trypsinogen activation is likely involved in the regulation of high concertrations of carbachol-induced NF-κB activation in pancreatic acinar cells in vitro. NF-κB activation is likely not necessary for high concertrations of carbachol-induced trypsinogen activation in pancreatic acinar cells in vitro.

关 键 词:pancreatic acinar cell trypsinogen activation NF-κB activation 

分 类 号:R657.51[医药卫生—外科学]

 

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