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Early inflammatory changes in radiation-induced oral mucositis : Effect of pentoxifylline in a mouse model
Verfasser / VerfasserinGruber, Sylvia ; Bozsaky, Eva ; Roitinger, Eva ; Schwarz, Karoline ; Schmidt, Margret ; Dörr, Wolfgang
Erschienen in
Strahlentherapie und Onkologie, 2017, Jg. 193, H. 6, S. 499-507
ErschienenSpringer, 2017
DokumenttypAufsatz in einer Zeitschrift
Schlagwörter (EN)Fractionated irradiation / Oral mucositis / Head and neck cancer / Radiation protection / Animal model
URNurn:nbn:at:at-ubmuw:3-3386 Persistent Identifier (URN)
 Das Werk ist frei verfügbar
Early inflammatory changes in radiation-induced oral mucositis [1.47 mb]
Zusammenfassung (Englisch)


Early inflammation is a major factor of mucosal reactions to radiotherapy. Pentoxifylline administration resulted in a significant amelioration of radiation-induced oral mucositis in the mouse tongue model. The underlying mechanisms may be related to the immunomodulatory properties of the drug. The present study hence focuses on the manifestation of early inflammatory changes in mouse tongue during daily fractionated irradiation and their potential modulation by pentoxifylline.

Materials and methods

Daily fractionated irradiation with 5 fractions of 3 Gy/week (days 04, 711) was given to the snouts of mice. Groups of 3 animals per day were euthanized every second day between day 0 and 14. Pentoxifylline (15mg/kg, s.c.) was administered daily from day 5 to the day before sacrifice. The expression of the inflammatory proteins TNF, NF-B, and IL-1 were analysed.


Fractionated irradiation increased the expression of all inflammatory markers. Pentoxifylline significantly reduced the expression of TNF and IL-1, but not NF-B.


Early inflammation, as indicated by the expression of the inflammatory markers TNF, NF-B, and IL-1, is an essential component of early radiogenic oral mucositis. Pentoxifylline differentially modulated the expression of different inflammatory markers. The mucoprotective effect of pentoxifylline does not appear to be based on modulation of NF-B-associated inflammation.

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