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

Accidentally ingested corrosive substances can cause functional and structural damage to the esophageal tissue resulting in stricture formation. It has been reported that the administration of olmesartan (OLM) can have anti-inflammatory, antifibrotic and antiapoptotic effects on injured tissue. The aim of our study was to check if OLM could prevent formation of scars in the corrosive esophageal burn model. Fifty-one Wistar Albino rats were divided into six groups: Control, Sham, OLM, Sham + OLM, Burn, and Burn + OLM. Olmesartan (5 mg/kg) was given by gavage once per day for 21 consecutive days after injury. The morphology of the esophagus was assessed after Masson trichrome staining, and apoptosis was evaluated using the terminal deoxynucleotidyl transferased UTP nick end labeling (TUNEL) method. The serum nucleosomes (as an indicator of apoptosis), serum p53 protein, and esophageal tissue p53 protein levels of each group were measured by immunoassays. Muscularis mucosa damage, submucosal collagen deposition, and tunica muscularis injury in the Burn + OLM group decreased significantly compared with the Burn group (p < 0.05). Similarly, the number of apoptotic cells in the Burn + OLM group decreased compared with the Burn group (p < 0.05). Serum levels of nucleosomes and p53 and tissue of p53 protein did not differ between the groups. Exogenously administered OLM can effectively prevent the occurrence of esophageal strictures caused by corrosive esophageal burns.