Display options
Share it on

Dermatol Res Pract. 2014;2014:736957. doi: 10.1155/2014/736957. Epub 2014 Sep 22.

The preliminary study of effects of tolfenamic Acid on cell proliferation, cell apoptosis, and intracellular collagen deposition in keloid fibroblasts in vitro.

Dermatology research and practice

Dan Yi, Ji Bihl, Mackenzie S Newman, Yanfang Chen, Richard Simman

Affiliations

  1. Department of Pharmacology and Toxicology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA.
  2. Department of Pharmacology and Toxicology, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA ; Department of Plastic and Reconstructive Surgery, Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA.

PMID: 25328513 PMCID: PMC4190122 DOI: 10.1155/2014/736957

Abstract

Keloid scarring is a fibroproliferative disorder due to the accumulation of collagen type I. Tolfenamic acid (TA), a nonsteroidal anti-inflammatory drug, has been found to potentially affect the synthesis of collagen in rats. In this preliminary study, we aimed to test the effects of TA on cell proliferation, cell apoptosis, and the deposition of intracellular collagen in keloid fibroblasts. Normal fibroblasts (NFs) and keloid fibroblasts (KFs) were obtained from human dermis tissue. Within the dose range 10(-3)-10(-6) M and exposure times 24 h, 48 h, and 72 h, we found that 0.55 × 10(-3) M TA at 48 h exposure exhibited significantly decreased cell proliferation in both NFs and KFs. Under these experimental conditions, we demonstrated that (1) TA treatment induced a remarkable apoptotic rate in KFs compared to NFs; (2) TA treatment reduced collagen production in KFs versus NFs; (3) TA treatment decreased collagen type I expression in KFs comparing to that of NFs. In summary, our data suggest that TA decreases cell proliferation, induces cell apoptosis, and inhibits collagen accumulation in KFs.

References

  1. Control Clin Trials. 1989 Mar;10(1):31-56 - PubMed
  2. Dan Med Bull. 1989 Sep;36(4):395-9 - PubMed
  3. J Invest Dermatol. 2013 Feb;133(2):386-93 - PubMed
  4. Mol Carcinog. 2013 May;52(5):377-86 - PubMed
  5. Am J Pathol. 2012 Nov;181(5):1642-58 - PubMed
  6. Plast Reconstr Surg. 2012 Sep;130(3):407e-417e - PubMed
  7. J Natl Cancer Inst. 2006 Jun 21;98(12):855-68 - PubMed
  8. PLoS One. 2012;7(4):e34988 - PubMed
  9. Cell Death Differ. 2000 Feb;7(2):166-76 - PubMed
  10. Wound Repair Regen. 2012 Sep-Oct;20(5):688-706 - PubMed
  11. J Clin Biochem Nutr. 2010 Jul;47(1):74-80 - PubMed
  12. J Biosci Bioeng. 2013 Apr;115(4):453-8 - PubMed
  13. J Burn Care Res. 2013 Jul-Aug;34(4):439-46 - PubMed
  14. Int J Dermatol. 2012 Apr;51(4):463-72 - PubMed
  15. Prostate. 2012 Nov;72(15):1648-58 - PubMed
  16. Dermatol Surg. 2006 Jul;32(7):907-15 - PubMed
  17. Dermatol Surg. 1996 Nov;22(11):955-9 - PubMed
  18. Arzneimittelforschung. 1987 Feb;37(2):177-80 - PubMed
  19. Mol Cancer Ther. 2008 Dec;7(12):3739-50 - PubMed
  20. Dan Med Bull. 1989 Oct;36(5):493-5 - PubMed
  21. Br J Dermatol. 2012 Sep;167(3):532-41 - PubMed
  22. J Pathol. 2005 Oct;207(2):232-42 - PubMed
  23. Cancer Res. 2007 Apr 1;67(7):3286-94 - PubMed
  24. Ann Plast Surg. 2003 Jan;50(1):71-6 - PubMed
  25. J Pathol. 2006 Jul;209(3):369-75 - PubMed
  26. Br J Dermatol. 2008 Nov;159(5):1103-15 - PubMed
  27. Ann Burns Fire Disasters. 2005 Jun 30;18(2):83-8 - PubMed
  28. Cancer Sci. 2011 Apr;102(4):742-8 - PubMed

Publication Types