title: Relationship between carbachol hyperstimulation-induced pancreatic intracellular trypsinogen and NF-kappa B activation in rats in vitro.
abstract: The relationship between intracellular trypsinogen activation and NF-kappa B 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-kappa B inhibitor (PDTC) in vitro. Intracellular trypsin activity was measured by using a fluorogenic substrate. The activity of NF-kappa B 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-kappa B in pancreatic acinar cells treated with high concentrations 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-kappa B activities in pancreatic acinar cells after treated with high concentrations of carbachol (10(-3) mol/L) in vitro, but the intracellular trypsinogen activity was not obviously inhibited (P>0.05). It was concluded that intracellular trypsinogen activation is likely involved in the regulation of high concentrations of carbachol-induced NF-kappa B activation in pancreatic acinar cells in vitro. NF-kappa B activation is likely not necessary for high concentrations of carbachol-induced trypsinogen activation in pancreatic acinar cells in vitro.
authors.affiliation: Department of Emergency Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. jiangcfang@126.com
authors.forename: Chunfang
authors.initials: C
authors.lastname: Jiang
authors.forename: Hai
authors.initials: H
authors.lastname: Zheng
authors.forename: Sunan
authors.initials: S
authors.lastname: Liu
authors.forename: Kaifeng
authors.initials: K
authors.lastname: Fang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D002217:Carbachol / Q000378:metabolism* / Q000494:pharmacology; D002467:Cell Nucleus / Q000378:metabolism; D018679:Cholinergic Agonists / Q000494:pharmacology; D066298:In Vitro Techniques; D016328:NF-kappa B / Q000378:metabolism*; D009841:Oligonucleotides / Q000737:chemistry; D010179:Pancreas / Q000166:cytology / Q000378:metabolism*; D011392:Proline / Q000031:analogs & derivatives / Q000494:pharmacology; D051381:Rats; D013450:Sulfones / Q000494:pharmacology; D013859:Thiocarbamates / Q000494:pharmacology; D014357:Trypsin / Q000737:chemistry / Q000378:metabolism; D014361:Trypsin Inhibitors / Q000494:pharmacology; D014362:Trypsinogen / Q000737:chemistry* / Q000378:metabolism
chemical_list: D000975:Antioxidants; D018679:Cholinergic Agonists; D016328:NF-kappa B; D009841:Oligonucleotides; D013450:Sulfones; D013859:Thiocarbamates; D014361:Trypsin Inhibitors; C066229:prolinedithiocarbamate; C002010:4-(2-aminoethyl)benzenesulfonylfluoride; D002217:Carbachol; D014362:Trypsinogen; D011392:Proline; D014357:Trypsin