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Bulletin of Experimental Biology and Medicine

, Volume 168, Issue 1, pp 14–17 | Cite as

Hepatic Mast Cells in Mice with Experimental Amyloidosis

  • L. Yu. IlynaEmail author
  • V. A. Kozlov
  • S. P. Sapozhnikov
Article
  • 11 Downloads

We studied the response of mast cells in mouse liver to experimental amyloidosis modeled by administration of aqueous solution of soy cream substitute and its correction by spontaneous dry red wine intake per os. Mast cells in mice with amyloidosis and intact mice were presented by α-ortho- and β1-metachromatic non-degranulating forms. In mice with amyloidosis, the relative content of β1-metachromatic mast cells in the capsule and parenchyma of the liver was by 1.8 and 1.5 times higher than in intact animals, respectively. In mice with amyloidosis receiving dry red wine, the proportions of mast cells with different degrees of metachromasy and degranulation were similar to those in intact mice, but the relative content of β1-metachromatic mast cells in the liver parenchyma in these animals was by 1.6 times higher than in intact mice. Therefore, mast cells respond to amyloidosis development by changes in both the metachromasy and degranulation degree; dry red wine can be considered as a factor of amyloidosis prevention.

Key Words

mice red wine liver mast cells experimental amyloidosis 

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References

  1. 1.
    Baglay EO, Dubikov AI. Mast cells are key participants in thepathogenesis of immunoinflammatory diseases. Nauch.-Prakt. Revmat. 2015;53(2):182-189. Russian.Google Scholar
  2. 2.
    Gordon DS. Tinctorial parallels of mast cells. Macro- and Microstructure of Tissues in the Norm, Pathology, and Experiment. Cheboksary, 1981. P. 97-101. Russian.Google Scholar
  3. 3.
    Kozlov VA, Busova OS. Mast cell migration in kidney. Vestn. Chuvash. Gos. Ped. Univer. im. I.Ya.Yakovleva. 2010;(1):40-45. Russian.Google Scholar
  4. 4.
    Kozlov VA, Sapozhnikov SP, Karyshev PB, Sheptukhina AI, Nikolaeva OV. Systemic Amyloidosis Model on Young Mice. Bull. Exp Biol. Med. 2017;162(4):520-523. doi:  https://doi.org/10.1007/s10517-017-3652-y CrossRefGoogle Scholar
  5. 5.
    Lindner DP, Poberin IA, Rozkin MYa, Efimov VS. Morphometric analysis of populations of mast cells. Arkh. Patol. 1980;42(6):60-64. Russian.Google Scholar
  6. 6.
    Piruzyan LA, Leksina LA. Transition from physiological to pathophysiological indices as exemplified by amyloidosis in periodic disease, non-insulin-dependent diabetes mellitus, and Alzheimer’s disease. Human Physiology. 2009;35(1):96-107.CrossRefGoogle Scholar
  7. 7.
    Anekonda TS. Resveratrol--a boon for treating Alzheimer’s disease? Brain Res. Rev. 2006;52(2):316-326.CrossRefGoogle Scholar
  8. 8.
    Bartolini M, Andrisano V. Strategies for the inhibition of protein aggregation in human diseases. Chembiochem. 2010;11(8):1018-1035.CrossRefGoogle Scholar
  9. 9.
    Danilewicz M, Wagrowska-Danilewicz M. Quantitative analysis of interstitial mast cells in AA and AL renal amyloidosis. Pathol. Res. Pract. 2002;198(6):413-419.CrossRefGoogle Scholar
  10. 10.
    Harcha PA, Vargas A, Yi C, Koulakoff AA, Giaume C, Sáez JC. Hemichannels Are Required for Amyloid β-Peptide-Induced Degranulation and Are Activated in Brain Mast Cells of APPswe/PS1dE9 Mice. J. Neurosci. 2015;35(25):9526-9538.CrossRefGoogle Scholar
  11. 11.
    So M, Hata Y, Naiki H, Goto Y. Heparin-induced amyloid fibrillation of β2-microglobulin explained by solubility and a supersaturation-dependent conformational phase diagram. Protein Sci. 2017;26(5):1024-1036.CrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • L. Yu. Ilyna
    • 1
    Email author
  • V. A. Kozlov
    • 1
  • S. P. Sapozhnikov
    • 1
  1. 1.I. N. Ulyanov Chuvash State UniversityCheboksaryRussia

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