The inhibitory effect of 15-R-LXA4 on experimental endometriosis

Eur J Obstet Gynecol Reprod Biol. 2009 Aug;145(2):200-4. doi: 10.1016/j.ejogrb.2009.05.015. Epub 2009 Jun 11.

Abstract

Objective: To determine the pro-resolution actions of 15-R-LXA(4) (LXA(4)) on endometriotic lesions and on the expression of interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) in the murine endometriosis model.

Study design: In a prospective, placebo-controlled experimental study, endometriosis was induced in thirty BALB/c mice, and fifteen sham-operated mice served as negative controls. Among the thirty mice with induced endometriosis, fifteen were administered 15-R-LXA(4) and acted as study group (LXA(4) group) and the other fifteen were used as positive controls (EM group). Then all the mice were sacrificed and the endometriotic lesions were weighed. The mRNA and protein levels of IL-1beta and TNF-alpha in the peritoneal fluid were quantified by using real-time polymerase chain reaction (PCR) and enzyme-linked immunoabsorbent assay (ELISA).

Result(s): Compared with the positive controls, 15-R-LXA(4) reduced the weight of the endometriotic lesions, decreased the concentrations of IL-1beta and TNF-alpha, and lowered the mRNA levels of IL-1beta and TNF-alpha in peritoneal fluid cells.

Conclusion(s): These findings suggest that 15-R-LXA(4) inhibits the progression of endometriosis possibly by suppressing the gene and protein expression of IL-1beta and TNF-alpha.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Ascitic Fluid / metabolism
  • Endometriosis / drug therapy*
  • Estrous Cycle / drug effects
  • Female
  • Interleukin-1beta / genetics
  • Interleukin-1beta / metabolism
  • Lipoxins / therapeutic use*
  • Mice
  • Mice, Inbred BALB C
  • Prospective Studies
  • RNA, Messenger / metabolism
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukin-1beta
  • Lipoxins
  • RNA, Messenger
  • Tumor Necrosis Factor-alpha
  • lipoxin A4