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The Korean journal of physiology & pharmacology : ... 14건

  1. [국내논문]   Mechanism of Action of Pancreatic Polypeptide (PP) on Pancreatic Exocrine Secretion in Isolated Rat Pancreas  

    Lee, Yun-Lyul (Department of Physiology, College of Medicine, Hallym University ) , Kwon, Hyeok-Yil (Department of Physiology, College of Medicine, Hallym University ) , Park, Hyung-Seo (Department of Physiology, College of Medicine, Hallym University ) , Park, Hyoung-Jin (Department of Physiology, College of Medicine, Hallym University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 83 - 90 , 1997 , 1226-4512 ,

    초록

    Aim of this study was to investigate if pancreatic polypeptide (PP) reduced the insulin action via the intra-pancreatic cholinergic nerves in the isolated rat pancreas. The pancreas was isolated from rats and perfused with intra-arterial infusion of modified Krebs-Henseleit solution containing 2.5 mM glucose at a flow rate of 1.2 ml/min. Simultaneous intra-arterial infusion of insulin (100 nM) resulted inpotentiation of the pancreatic flow rate and amylase output which were stimulated by cholecystokinin (CCK, 14 pM). These potentiating actions of insulin on the CCK -stimulated pancreatic exocrine secretion were completely abolished by administration of rat PP. Vesamicol, a potent inhibitor of vesicular acetylcholine storage, and tetrodotoxin (TTX) also significantly reduced the combined actions of insulin and CCK. Administration of carbamylcholine, an acetylcholine agonist, completely restored the vesamicol- or TTX-induced inhibition of the potentiation between insulin and CCK. Also rat PP failed to attenuate the restoring effect of carbamylcholine. Electrical field stimulation (15-30 V, 2 msec and 8 Hz) resulted in a significant increase in the pancreatic flow rate and amylase output in voltage-dependent manner. Effects of electrical field stimulation were augmented by endogenous insulin. Rat PP also suppressed the pancreatic exocrine secretion stimulated by electrical field stimulation. These observations strongly suggest that PP inhibits the potentiating actions of insulin on CCK -stimulated pancreatic exocrine secretion by suppression of the intra-pancreatic cholinergic activity in the isolated rat pancreas.

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  2. [국내논문]   Lipocortin 1 Mediates the Suppressive Effects of Dexamethasone on ConA-induced Proliferative Response and Nitric Oxide Production in Rat Splenic Leukocytes  

    Jang, Yeon-Jin (Departments of Physiology, University of Ulsan College of Medicine ) , Park, Hyoung-Sup (Departments of Pharmacology, University of Ulsan College of Medicine ) , Kang, Soon-A (Departments of Pharmacology, University of Ulsan College of Medicine ) , Yang, Sus-Jung (Departments of Physiology, University of Ulsan College of Medicine ) , Na, Doe-Sun (Departments of Biochemistry, University of Ulsan College of Medicine)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 91 - 96 , 1997 , 1226-4512 ,

    초록

    Lipocortin 1 has been proposed as a putative mediator of anti-inflammatory actions of glucocorticoids. We investigated the role of lipocortin 1 in the effect of dexamethasone using rat splenic leukocytes. Concanavalin A(ConA; 1 ${\mu}g/ml$ ) increased the leukocyte proliferation and nitric oxide(NO) generation, which were measured as $[^3H]-thymidine$ uptake by the cells and nitrite accumulation in the culture media, respectively. Dexamethasone suppressed ConA-induced cell proliferation, in a concentration-dependent manner with $EC_{50}$ around 50nM. The addition of anti-lipocortin l(Anti-LCl) reversed dexamethasone effects: 0.24, 1.2, 6 ${\mu}g/ml$ of Anti-LC1 reversed dexamethasone(50 nM)-induced suppression of thymidine uptake by $9{\pm}3%$ , $16{\pm}3%$ , $36{\pm}5%$ , respectively; 0.24, 1.2, and 6 ${\mu}g/ml$ of Anti-LCI reversed dexa-methasone-induced decrease of nitrite concentration by $49{\pm}16%$ , $61{\pm}20%$ , $77{\pm}19%$ , respectively. The present data indicate that lipocortin 1 mediates, at least in part, glucocorticoids-induced suppression of leukocyte proliferation and blockade of NO generation.

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  3. [국내논문]   Comparision of Regulatory Action of cAMP and cGMP on the Activation of Neutrophil Responses  

    Han, Chang-Hwang (Department of Pharmacology, College of Medicine, Chung-Ang University ) , Yoon, Young-Chul (Department of Pharmacology, College of Medicine, Chung-Ang University ) , Shin, Yong-Kyoo (Department of Pharmacology, College of Medicine, Chung-Ang University ) , Han, Eun-Sook (Department of Pharmacology, College of Medicine, Chung-Ang University ) , Lee, Chung-Soo (Department of Pharmacology, College of Medicine, Chung-Ang University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 97 - 105 , 1997 , 1226-4512 ,

    초록

    The regulatory role of cyclic nucleotides in the expression of neutrophil responses has been examined. fMLP-stimulated superoxide production in neutrophils was inhibited by dibutyryl adenosine 3',5'-cyclic monophosphate (DBcAMP), histamine, adenosine + theophylline, cAMP elevating agents, and 8-bromoguanosine 3' ,5' -cyclic monophosphate (8-BrcGMP) and sodium nitroprusside, cGMP elevating agents. Staurosporine, a protein kinase C inhibitor, genistein, a protein tyrosine kinase inhibitor and chlorpromazine, a calmodulin inhibitor, inhibited superoxide production by fMLP, but they did not further affect the action of DBcAMP on the stimulatory action of fMLP. DBcAMP, histamine, adenosine+theophylline and genistein inhibited myeloperoxidease release evoked by fMLP, whereas BrcGMP, sodium nitroprusside and staurosporine did not affect it. The elevation of $[Ca^{2+}]_i$ evoked by fMLP was inhibited by genistein and chlorpromazine but was not affected by staurosporine. DBcAMP exerted little effect on the initial peak in $[Ca^{2+}]_i$ response to fMLP but effectively inhibited the sustained rise. On the other hand, BrcGMP significantly inhibited both phases. fMLP-induced $Mn^{2+}$ influx was inhibited by either DBcAMP or BrcGMP. These results suggest that fMLP-stimulated neutrophil responses may be regulated by cAMP more than cGMP. cAMP and cGMP appear not affect stimulated responses by direct protein kinase C activation. Their regulatory action on the stimulated neutrophil responses may be not influenced by other activation processes.

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  4. [국내논문]   Induction of Apoptosis by Bile Acids in HepG2 Human Hepatocellular Carcinoma Cells  

    Baek, Jin-Hyen (Department of Molecular Biology, Pusan National University ) , Kim, Jung-Ae (Department of Molecular Biology, Pusan National University ) , Kang, Chang-Mo (Department of Biology, Pusan National University ) , Lee, Yong-Soo (Department of Physiology, College of Medicine, Kwandong University ) , Kim, Kyu-Won (Department of Molecular Biology, Pusan National University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.1 ,pp. 107 - 115 , 1997 , 1226-4512 ,

    초록

    We studied the effects of bile acids on the induction ofapoptosis in HepG2 human hepatocellular carcinoma cells. Treatment with either ursodeoxycholic acid (UDCA) or lithocholic acid (LCA) resulted in a dose- and time-dependent decrease in cell viability assessed by MTT assay. Both UDCA and LCA also induced genomic DNA fragmentation, a hallmark of apoptosis, indicating that the mechanism by which these bile acids induce cell death was through apoptosis. Cycloheximide, a protein synthesis inhibitor, blocked the apoptosis induced by these bile acids, implying that new protein synthesis may be required for the apoptosis. Intracellular $Ca^{2+}$ release blockers (dantrolene and 3,4,5-trimethoxybenzoic acid-8-(diethylamino)octyl ester) inhibited decreased cell viability and DNA fragmentation induced by these bile acids. Treatment of HepG2 cells with calcium ionophore A23l87 induced DNA fragmentation. These results suggest that UDCA and LCA induce apoptosis in the HepG2 cells and that the activation of intracellular $Ca^{2+}$ signals may play an important role in the apoptosis induced by these bile acids.

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