April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
Benfotiamine Prevents Endotoxin-Induced Uveitis in Lewis Rats
Author Affiliations & Notes
  • U. C. Yadav
    Biochemistry & Molecular Biology, Univ Texas Medical Branch, Galveston, Texas
  • S. Subramanyam
    Biochemistry & Molecular Biology, Univ Texas Medical Branch, Galveston, Texas
  • K. V. Ramana
    Biochemistry & Molecular Biology, Univ Texas Medical Branch, Galveston, Texas
  • Footnotes
    Commercial Relationships  U.C. Yadav, None; S. Subramanyam, None; K.V. Ramana, None.
  • Footnotes
    Support  GM71036
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 2651. doi:
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      U. C. Yadav, S. Subramanyam, K. V. Ramana; Benfotiamine Prevents Endotoxin-Induced Uveitis in Lewis Rats. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2651.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : To investigate the anti-inflammatory effect of a Vitamin B1 analogue, benfotiamine, on ocular inflammation caused by endotoxin in rats.

Methods: : Endotoxin-induced uveitis (EIU) in Lewis rats was developed by subcutaneous injection of lipopolysaccharide (LPS) followed by the treatment with benfotiamine. The rats were sacrificed 24 h after LPS injection, aqueous humor (AqH) was collected from enucleated eyes, and the number of infiltrating cells, protein concentration, and the levels of inflammatory markers were determined. Immunohistochemical analysis of eye sections was performed to determine the expression of iNOS and Cox-2, and transcription factor NF-ΚB. Macrophages were used to investigate the molecular mechanism of benfotiamine action.

Results: : Endotoxin-induced increase in infiltrating leukocytes, protein concentration and inflammatory cytokines and chemokines in rat AqH was significantly prevented by benfotiamine supplementation. In addition, benfotiamine prevented the increased expression of inflammatory marker proteins iNOS and Cox-2 in ciliary body and retinal wall of rat eyes. Incubation of benfotiamine with macrophages prevented LPS -induced generation of ROS, activation of PKC, IKK, MAPK, and activation of NF-ΚB and expression of inflammatory cytokines.

Conclusions: : Our results indicate that benfotiamine suppresses oxidative stress-induced NF-ΚB signals which cause ocular inflammation indicating that benfotiamine supplementation could be used for the treatment of ocular inflammation, especially uveitis.

Keywords: antioxidants • inflammation • signal transduction: pharmacology/physiology 

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