Abstract
BackgroundLycopene is a robust antioxidant with significant antiulcer activity. Henceforth, the present study was ventured to elucidate the effect of lycopene on experimental esophagitis.MethodsGroups of rats were subjected to forestomach and pylorus ligation with subsequent treatment with lycopene (50 and 100 mg/kg, po) and pantoprazole (30 mg/kg, po).ResultsTreatment with lycopene evidenced sententious physiological protection when scrutinized for pH, acidity (total and free), volume of gastric juices and esophagitis index. Lycopene further embarked diminishing effect on oxidative stress through synchronising lipid and protein peroxidation along with regulating the enzymatic activity of SOD and catalase. Lycopene also modified the levels of immunoregulatory cytokines (IL- 1β and IL-6) favourably. The dose dependent efficacy of lycopene in the current experimental condition was also attested when exemplified morphologically through scanning electron microscopy.ConclusionFrom the current line of evidences, it was concluded that lycopene can impart momentous protection against experimental esophagitis by wrapping up the reactive oxygen species and through dual inhibition of the arachidonic acid pathway.
Highlights
Lycopene is a robust antioxidant with significant antiulcer activity
Inductive agents in the refluxate are mainly responsible for mucosal damage in Gastroesophageal reflux disease (GERD)
The experimental protocol was approved by Institutional Animal Ethics Committee (IAEC) (United Institute of Pharmacy, Naini, Allahabad, U.P, India) (Approval No.UIP/IAEC/2014/FEB/01)
Summary
Lycopene is a robust antioxidant with significant antiulcer activity. the present study was ventured to elucidate the effect of lycopene on experimental esophagitis. Gastroesophageal reflux disease (GERD) is a complex anarchy with the potential for developing esophagitis, esophageal strictures and baretts esophagitis [1]. Inductive agents in the refluxate are mainly responsible for mucosal damage in GERD. Abnormal antirefluxate barrier and luminal clearance mechanism results in prolonged contact of refluxate to esophageal mucosa and appears to be responsible for the morphological changes in the esophageal membrane of GERD patients [4,5]. Proton pump inhibitors (PPI) and histaminergic - 2 (H-2) blockers are the first line therapies in clinical management of GERD. Due to relapsing nature of disease, clinical management of GERD is difficult and require prolonged therapy [6]. Weak inhibitory activity in early phase and less effectiveness of therapy within initial hours of dosing are additional causes for therapeutic relapse in GERD [7]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
