PMID- 9609097
OWN - NLM
STAT- MEDLINE
DCOM- 19980616
LR  - 20151119
IS  - 0899-1987 (Print)
IS  - 0899-1987 (Linking)
VI  - 22
IP  - 1
DP  - 1998 May
TI  - Inhibitory effects of pentoxifylline on ultraviolet B light-induced cutaneous 
      inflammation.
PG  - 16-25
AB  - It is now recognized that ultraviolet (UV) radiation is a potent environmental 
      insult capable of interfering with immunity to skin cancers and modifying certain 
      immunologic reactions within both locally irradiated skin and distant, unexposed 
      sites. Exposure to UVB light (290-320 nm) induces a potent cutaneous inflammatory 
      response that involves the infiltration of leukocytes into the dermis as well as 
      the production of proinflammatory cytokines by both resident epidermal 
      keratinocytes and dermal cells. Tumor necrosis factor-alpha (TNF-alpha) is a 
      proinflammatory cytokine that has been shown to be a major mediator of UVB light 
      effects on cutaneous immunity. Recent studies have demonstrated that 
      pentoxifylline (PTX), a xanthine-derived phosphodiesterase inhibitor, has the 
      ability to inhibit synthesis of TNF-alpha. To examine the effects of PTX on 
      UVB-mediated cutaneous inflammation, Skh/hr hairless mice were injected 
      intraperitoneally with either phosphate-buffered saline or 50 microg/g PTX 1 h 
      before exposure to 2240 J/m2 UVB. Reverse transcription-polymerase chain reaction 
      and immunohistochemical techniques were used to demonstrate that 24 h to 1 wk 
      after UVB-light irradiation, PTX inhibited UVB-induced TNF-alpha gene expression, 
      inhibited the increase in epidermal TNF-alpha protein synthesis, blocked the 
      increase in epidermal proliferation observed after exposure to UVB light, and 
      decreased production of myeloperoxidase by neutrophils infiltrating into the 
      dermis. These studies demonstrated that PTX modifies epidermal responses after 
      acute UVB light exposure and suggest that PTX treatment may be used clinically to 
      modulate the deleterious effects of long-term UVB-light irradiation.
FAU - Oberyszyn, T M
AU  - Oberyszyn TM
AD  - Department of Medical Microbiology/Immunology, The College of Medicine, The Ohio 
      State University, Columbus, USA.
FAU - Tober, K L
AU  - Tober KL
FAU - Ross, M S
AU  - Ross MS
FAU - Robertson, F M
AU  - Robertson FM
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Mol Carcinog
JT  - Molecular carcinogenesis
JID - 8811105
RN  - 0 (Biomarkers)
RN  - 0 (Proliferating Cell Nuclear Antigen)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 1.11.1.7 (Peroxidase)
RN  - SD6QCT3TSU (Pentoxifylline)
SB  - IM
MH  - Animals
MH  - Biomarkers/analysis
MH  - Cell Division/drug effects/radiation effects
MH  - Inflammation/prevention & control
MH  - Mice
MH  - Mice, Hairless
MH  - Neutrophils/drug effects/physiology/radiation effects
MH  - Pentoxifylline/*pharmacology/therapeutic use
MH  - Peroxidase/analysis
MH  - Proliferating Cell Nuclear Antigen/analysis
MH  - Radiation Injuries, Experimental/*prevention & control
MH  - Skin/drug effects/pathology/*radiation effects
MH  - Tumor Necrosis Factor-alpha/analysis/biosynthesis
MH  - *Ultraviolet Rays
EDAT- 1998/06/03 00:00
MHDA- 1998/06/03 00:01
CRDT- 1998/06/03 00:00
PHST- 1998/06/03 00:00 [pubmed]
PHST- 1998/06/03 00:01 [medline]
PHST- 1998/06/03 00:00 [entrez]
AID - 10.1002/(SICI)1098-2744(199805)22:1<16::AID-MC3>3.0.CO;2-J [pii]
PST - ppublish
SO  - Mol Carcinog. 1998 May;22(1):16-25.