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Comparative Viability Studies on Isolated Gastric Mucosal Mixed Cells and Hepatoma and Myeloma Cell Lines with Ethanol, Indomethacin and Their Combination

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Biochemical Pharmacology as an Approach to Gastrointestinal Disorders
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Abstract

The toxic effects of ethanol (EtOH), indomethacin (IND) and their combination were studied in vitro. The experiments were performed on freshly isolated gastric mucosal mixed cells and two types of stable cultured cells: Sp2/0-Ag14, which is a non-secreting mouse myeloma cell line, and Нер G2, which is a human hepatocellular carcinoma cell line. EtOH decreased the viability of all types of cells in a concentration-dependent manner. At all concentrations, the EtOH caused a greater decrease in the viability of gastric mucosal cells than in the viability of Sp2/0-Ag14 cells. IND had no effect on the viability of the cultured cells, when this was employed without any other aggressive factor, such as EtOH. When used in combination, IND aggravated the EtOH-induced cell injury. These results show that the endogenous prostaglandins may play a role in the maintenance of cell integrity in all three types of cells.

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References

  1. Robert A, Nezamis JE, Lancaster C, Hancher AJ. Cytoprotection by prostaglandins in rats. Gastroenterology. 1979; 77: 433–43.

    PubMed  CAS  Google Scholar 

  2. Robert A. Cytoprotection by prostaglandins. Gastroenterology. 1979; 77: 761–7.

    PubMed  CAS  Google Scholar 

  3. Grijalva CV, Novin D. The role of the hypothalamus and dorsal vagal complex in the gastrointestinal function and pathophysiology. Ann NY Acad Sci. 1990; 597: 207–22.

    Article  PubMed  CAS  Google Scholar 

  4. Mózsik Gy, Karádi O, Király Á et al. Vagal nerve and the gastric mucosal defence. J Physiol (Paris). 1993; 87: 59–64.

    Article  Google Scholar 

  5. Mózsik Gy, Király Á, Garamszegi M et al. Mechanism of vagal nerve in gastric mucosal defence: unchanged gastric emptying and increased vascular permeability. J Clin Gastroenterol. 1992; 14 (suppl 1): 5140–4.

    Google Scholar 

  6. Szabo S, Trier JS, Broown A, Schoor J. Early vascular injury and increased vascular permeability in the gastric mucosal injury caused by ethanol in the rat. Gastroenterology. 1985;88:228–36.

    Google Scholar 

  7. Guth PH, Paulsen G, Nagata H. Histologic and microcirculatory changes in alcohol-induced gastric lesions in the rat: effects of prostaglandin cytoprotection. Gastroenterology. 1984; 87: 1083–90.

    PubMed  CAS  Google Scholar 

  8. Lacy ER, Ito S. Rapid epithelial restitution of the rat gastric mucosa after ethanol injury. J Lab Invest. 1984; 51: 573–83.

    CAS  Google Scholar 

  9. Nagy L, Szabo S, Morales RE, Plebani M, Jenkins JM. Identification of subcellular targets and sensitive tests of ethanol-induced damage in isolated gastric mucosal cells. Gastroenterology. 1994; 107: 907–14.

    PubMed  CAS  Google Scholar 

  10. Djahanguiri В. The production of acute gastric ulceration by indomethacin in the rat. Scand J Gastroenterol. 1969; 17: 265–7.

    Google Scholar 

  11. Brodie DA, Cook PG, Bauer BJ. Indomethacin-induced intestinal lesions in the rat. Toxicol Appi Pharmacol. 1970; 17: 615–24.

    Article  CAS  Google Scholar 

  12. Karádi O, Bbdis B, Király Á et al. Surgical vagotomy enhances the indomethacin-induced gastrointestinal mucosal damage in rats. Inflammophaгmacology. 1994; 2: 389–99.

    Article  Google Scholar 

  13. Lacy ER, Ito S. Microscopic analysis of ethanol damage to rat gastric mucosa after treatment with a prostaglandin. Gastroenterology. 1982; 83: 619–25.

    PubMed  CAS  Google Scholar 

  14. Rainsford KD. Mechanism of NSAID-induced ulcerogenesis: structural properties of drugs, focus on the microvascular factors, and novel approaches for gastro-intestinal protection. Acta Physiol Hung. 1992; 80: 23–38

    PubMed  CAS  Google Scholar 

  15. Rainsford KD. Prevention of indomethacin induced gastro-intestinal ulceration in the rat by glucose-citrate formulations: Role of ATP in mucosal defences. Br J Rheumatol. 1987; 26 (suppl): 81.

    Google Scholar 

  16. Prostaglandin protection of human isolated gastric glands against indomethacin and ethanol injury. J Clin Invest. 1988; 81: 1081–9.

    Article  PubMed  CAS  Google Scholar 

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© 1997 Springer Science+Business Media Dordrecht

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Szabó, I., Bódis, B., Németh, P., Mózsik, G. (1997). Comparative Viability Studies on Isolated Gastric Mucosal Mixed Cells and Hepatoma and Myeloma Cell Lines with Ethanol, Indomethacin and Their Combination. In: Gaginella, T.S., Mózsik, G., Rainsford, K.D. (eds) Biochemical Pharmacology as an Approach to Gastrointestinal Disorders. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5390-4_31

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  • DOI: https://doi.org/10.1007/978-94-011-5390-4_31

  • Publisher Name: Springer, Dordrecht

  • Print ISBN: 978-94-010-6267-1

  • Online ISBN: 978-94-011-5390-4

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