Oxidative stress is important factor underlying in a variety of diseases. Antioxidative
enzymes such as
superoxide dismutase (SOD) and
glutathione peroxidase (GSH-PX) are part of the physiological defenses against oxidative stress.
Malondialdehyde (MDA) is a lipid peroxidation
biomarker and its elevated level in various diseases is related to
free radical damage.
Cysteamine is a
cytotoxic agent, acting through generation of
reactive oxygen species (ROS) and may decrease defense activity of antioxidative
enzymes against ROS and induce
duodenal ulcer.
Captopril, acts as
free radical scavengers and protect against
injuries from oxidative damage to tissues.The aim of this study was the evaluation of the effect of
captopril against
cysteamine-induced
duodenal ulcer by determining duodenal damage, duodenal tissue SOD and GSH-PX activities and plasma MAD level. This study was performed on 3 groups of 7 rats each: saline,
cysteamine and
cysteamine plus
captopril treated groups. The effect of
captopril against
cysteamine-induced
duodenal ulcer is determined by evaluating the duodenal damage, duodenal tissue SOD and GSH-PX activities and plasma MDA level. All animals were euthanized 24h after the last treatment and 2 ml blood and duodena samples were collected for calculation of
ulcer index, histopathological assessment and measurement of tissue SOD, GSH-PX activities and plasma MDA level.
Cysteamine produced severe duodenal damage, decreased the activity of duodenal tissue SOD and GSH-PX and increased the plasma MDA level compared with saline pretreated rats. Pretreatment with
captopril decreased the
cysteamine-induced duodenal damage and plasma level of MDA and increased the activities of SOD and GSH-PX in duodenal tissue compared with
cysteamine pretreated animal. Our results suggest that
captopril protects against
cysteamine-induced
duodenal ulcer and inhibits the decrease in SOD and GSH-PX activities and lipid peroxidation by increasing
antioxidant defenses.