Protective effect of trapidil against oxidative organ damage in burn injury

Abstract 

Animal models of thermal injury indicate reactive oxygen species and inflammatory cytokines as causative agents in tissue injury on various organs distant from the original wound. Trapidil has various properties, such as inhibition of platelet aggregation and lipid peroxidation as well as reduction of the inflammatory response to injury. This study was designed to determine the possible protective effect of trapidil treatment against oxidative organ damage in lung, intestine and kidney induced by cutaneous thermal injury.

Thirty Wistar rats were randomly divided into five groups. Sham group (n=6) was exposed to 21°C water while burn-3h group (n=6) and burn+trap-3h group (n=6), burn-24h (n=6) and burn+trap-24h groups were exposed to boiling water for 12s to produce a full thickness burn in 35–40% of total body surface area. In both burn+trap-3h and burn–trap-24h group, 8mg/kg trapidil was given intravenously immediately after thermal injury. Three and 24h later, tissue samples were taken for biochemical analysis from lung, intestine and kidney and blood samples were obtained to determinate serum TNF-α levels. Cutaneous thermal injury caused a significant increase in myeloperoxidase (MPO) activity and malondialdehyde (MDA) and 3-nitrotyrozine (3-NT) levels in all tissues and elevated serum TNF-α levels at post-burn 3 and 24h. Trapidil treatment significantly reduced in biochemical parameters, as well as serum TNF-α levels. These data suggest that trapidil has a protective effect against oxidative organ damage in burn injury.

Keywords: Burn injury, Trapidil, Nitric oxide, TNF-α, Lipid peroxidation, 3-Nitrotyrosine