Effect of transforming growth factor beta 1 (TGF-beta 1) on nitric oxide production and lipid peroxidation in oral mucosal wound healing


COŞKUN CEVHER Ş. , Peker E. G. G. , Balabanli B., Ahiska S., ACARTÜRK F.

MEDICINAL CHEMISTRY RESEARCH, vol.20, no.1, pp.23-28, 2011 (Journal Indexed in SCI) identifier identifier

  • Publication Type: Article / Article
  • Volume: 20 Issue: 1
  • Publication Date: 2011
  • Doi Number: 10.1007/s00044-009-9276-7
  • Title of Journal : MEDICINAL CHEMISTRY RESEARCH
  • Page Numbers: pp.23-28
  • Keywords: TGF-beta 1, Nitric oxide, Lipid peroxidation, Oral wound healing, EXPRESSION, GROWTH-FACTOR-BETA-1, INHIBITION, SYNTHASE, FORMULATION, SECRETION, PATTERNS, COLLAGEN, TISSUES, STRESS

Abstract

Wound healing is a highly orchestrated process including complex and coordinated interactions involving peptide growth factors of which transforming growth factor-beta (TGF-beta) is one of the most important modulators. Exogenous TGF-beta treatment has been shown to accelerate wound healing in normal and impaired animal models. Nitric oxide (NO) also plays a key role in wound healing. The objective of this study is to examine the effects of exogenous TGF-beta 1 treatment on NO and lipid peroxidation levels in the process of oral wound healing on different days. In this study, we used 5-month-old New Zealand albino male rabbits. After a standard surgical incision in the diestema region, the rabbits were divided into controls and TGF-beta 1 implanted groups. NO levels and malondialdeyhde (MDA) levels which are indicators of lipid peroxidation were determined by spectrophotometry. In the TGF-beta 1 implanted groups, both NO and MDA levels significantly increased only on the third day after wounding when compared to control groups. We found decreased MDA levels parallel to NO levels on the fifth day after wounding. These findings suggest that TGF-beta 1 affects mucosal wound healing by altering NO production on different days of wounding. TGF-beta 1 may regulate NO production by its dual effect in as both an activator and inhibitor an in oral mucosal healing.