May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Cyclooxygenase–2 inhibitor suppresses the expression of PGE2 stimulated by IL–1ß in human lens epithelial cells.
Author Affiliations & Notes
  • Y. Goto
    Ophthalmology, Chiba Hokusoh Hospital,Nippon Medical School, Inba–Gun,Inba Village, Japan
  • K. Tanemoto
    Ophthalmology, Chiba Hokusoh Hospital,Nippon Medical School, Inba–Gun,Inba Village, Japan
  • N. Ibaraki
    Ophthalmology, Chiba Hokusoh Hospital,Nippon Medical School, Inba–Gun,Inba Village, Japan
  • Footnotes
    Commercial Relationships  Y. Goto, None; K. Tanemoto, None; N. Ibaraki, None.
  • Footnotes
    Support  none
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 2634. doi:
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      Y. Goto, K. Tanemoto, N. Ibaraki; Cyclooxygenase–2 inhibitor suppresses the expression of PGE2 stimulated by IL–1ß in human lens epithelial cells. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2634.

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

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Abstract

Abstract: : Purpose: To study the effect of cyclooxygenase–2(COX2) inhibitor(Meloxicam) on the expression of prostaglandin E2(PGE2) in human lens epithelial cells. Methods: Human lens epithelial cell line (SRA01/04) cells were cultured in the presence of 0–1000ng/5ml of IL–1ß for one week.The expression of COX2 in SRA01/04 cells was detected by RT–PCR.PGE2 concentrations in the culture medium were measured by ELISA. PGE2 expressed by the cells cultured with 100ng/5ml of IL–1ß and 0–1000ng/5ml of Meloxicam was also measured. Results: The expression of COX2 in the cells was stimulated by IL–1ß ,and the concentrations of PGE2 were 59,51,51,303and 405 pg/ml in the prsence of 0,1,10,100,1000ng/5ml of IL–1ß ,repectively. The expressions of PGE2 were suppressed to 673,409,521,299 and179 pg/ml with 0,1,10,100,1000ng/5ml of Meloxicam,respectively. Conclusions: IL–1ß stimulated the expression of COX2 and PGE2 in SRA01/04 in a dose dependent manner. Meloxicam suppressed the expression of PGE2 stimulated by IL–1ß.

Keywords: eicosanoids • enzymes/enzyme inhibitors • cytokines/chemokines 
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