Protective effects of melatonin against caustic esophageal burn injury in rats

Abstract

Caustic ingestion is one of the most life-threatening events in the pediatric age group, which requires the immediate management and subsequent treatment of its most significant complication, i.e. alterations in esophageal structure. We investigated whether melatonin could reduce the esophageal burn damage induced by sodium hydroxide. It was assumed that melatonin could be effective because of its function as a direct free radical scavenger, its antioxidative actions and its ability to diminish tissue hydroxyproline (HP) levels. Esophageal burns were induced in male rats by the administration of 10% sodium hydroxide. Lipid peroxidation (LPO) products were then measured at the following times: 0, 1, 6, 24, 48 and 72 hr after treatment. Tissue HP concentrations in the injured area were assessed at 14 days after the administration of sodium hydroxide. The groups received either systemic melatonin or normal saline. There were two, non-ischemic, sham control groups treated with or without melatonin. LPO products, malondialdehyde (MDA) and 4-hydroxyalkenal (4-HDA), increased immediately after the administration of sodium hydroxide; this indicates the participation of free radicals in the development of damage. Melatonin diminished the oxidative response and the amount of HP in the late phase of the lesion. Melatonin reduced oxidative damage in the early phase of the esophageal burns induced by sodium hydroxide.

A novel approach for preventing esophageal stricture formation: olmesartan prevented apoptosis

“…The latter suggests that the anti-fibrotic and anti-apoptotic effects of OLM administration in esophageal caustic burn observed in our study could be also attributed to the suppression of oxidative stress by AT1R antagonism. This hypothesis is in agreement with the results of previous studies which demonstrated partially successful treatment of caustic esophageal burns by increasing the antioxidant capacity of the tissue [25][26][27][28][29][30][31][32][33][34][35]. The present study provides new evidence that the renin-angiotensin system can be a promising target for the treatment of esophageal burns caused by corrosive agents.…”

Mercaptoethylguanidine attenuates caustic esophageal injury in rats: a role for scavenging of peroxynitrite

“…Our previous works and other studies with more rigorous investigation revealed that oxidative stress has a significant role in the affected site of the injured esophageal wall [13][14][15]20]. A variety of antioxidant agents may help to prevent stricture formation in a caustic esophageal burn model in rats [19,[35][36][37]. These observations strongly suggest that caustic esophageal injury is associated with decreased antioxidant activity resulting in increased tissue damage.…”

“…Studies with more rigorous investigation revealed that oxidative stress has a significant role in the affected site of the esophageal wall [14,15]. In addition, studies displayed that a variety of antioxidant agents may help to prevent stricture formation in a caustic esophageal burn model in rats [19,[35][36][37]. The development of dense scar tissue at the injury site is a later consequence of caustic esophageal injury [3,6].…”

Pirfenidone prevents rat esophageal stricture formation

“…Although several treatment protocols have been devised and used to accomplish anti-inflammatory and anti-fibrogenic actions, the benefit and standardization of these treatment methods are still controversial [3]. Nowadays, the effects of many therapeutic agents in preventing esophageal stricture formation continue to be investigated in experimental caustic esophageal burn injury models [4,5].…”