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Can L(+)-lactate be used as a marker of experimentally induced inflammation in rats?
Anja Finn1, Sandra Claudine Oerther
1Disease Biology, Local Discovery Research Area CNS and Pain Control, AstraZeneca R&D Södertälje, Södertälje, Sweden. anja.finn@astrazeneca.com
Objective:
The purpose of this study was to investigate if L(+)-lactate (lactate) can be used as a marker of progression of joint inflammation in comparison with a reference marker, prostaglandin E2 (PGE(2)), and to analyse implications for drug treatments.
Materials And Methods:
The assessment of the inflammation time course and the treatment efficacy studies were performed on two occasions. At specific time points, synovial fluid was extracted from Sprague-Dawley rats (n = 87) challenged with either carrageenan (Cg) or Freund's complete adjuvant (FCA) or from six non-inflamed rats. Naproxen (7.5 or 30 micromol/kg) or rofecoxib (30 micromol/kg) was administered per os 2 h post Cg or at 48 h post FCA. Levels of PGE(2) and lactate were assessed either by immuno-assay or by colorimetric assay.
Results:
Increased levels of both markers were detected following Cg or FCA injection. Pharmacological treatments resulted in lower concentrations of PGE(2) whereas levels of lactate remained unaffected compared to the vehicle-treated group.
Conclusion:
Our results suggest that lactate may be useful as an additional biomarker of inflammatory processes, especially for monitoring the non-cox-inhibitor sensitive cascade.
