Prodigiosins from a marine sponge- associated actinomycete attenuate HCl/ ethanol-induced gastric lesion via antioxidant and anti-inflammatory mechanisms. (2019). Mohamed S. Abdelfattah, Mohammed I. Y. Elmallah, Hassan Y. Ebrahim, Rafa S. Almeer.

Journal Article

2019

Published in: https://pubmed.ncbi.nlm.nih.gov/31194753/

Gastric ulcer is sores that form in the stomach mucosal layer because of erosion caused by high acid secretion and excessive use of non-steroidal anti-inflammatory drugs. Prodigio- sins (PdGs) are red-pigmented secondary metabolites produced by bacteria, including acti- nomycetes. Butylcycloheptylprodigiosin (1) and undecylprodigiosin (2) were identified and isolated from a crude extract of the actinomycete RA2 isolated from the Red Sea Sponge Spheciospongia mastoidea. Chemical structure of 1 and 2 was determined by NMR and mass spectroscopy. Although their antioxidant and anti-inflammatory properties are known, their effect on gastric lesion is unknown. Therefore, this study aimed to investigate gastro- protective effects of PdGs against HCl/ethanol-induced gastric lesion in rats. Oral pretreat- ment with PdGs (100, 200, and 300 mg/kg) attenuated severity of HCl/ethanol-induced gastric mucosal injury, as evidenced by decreases in gastric lesion index scores, ulceration area, histopathologic abnormality, and neutrophil infiltration. These effects were comparable to those of omeprazole, a standard anti-gastric ulcer agent. HCl/ethanol-induced gastric ero- sions was associated with tremendous increases in lipid peroxidation, nitric oxide, and pro- inflammatory cytokines and mediators (myeloperoxidase, interleukin-1β, tumor necrosis factor-α, and cyclooxygenase-2), and with significant decreases in enzymatic and non-enzy- matic antioxidant activities. However, PdGs ameliorated gastric inflammation and oxidative stress by downregulating nuclear factor kappa B and inducible nitric oxide synthase expres- sion and upregulating heme oxygenase-1 expression. PdGs prevented gastric mucosal apoptosis by downregulating Bax and caspase-3 expression and upregulating Bcl-2 expres- sion, thereby increasing prostaglandin E2 production. Our results suggested that PdGs exerted gastroprotective effects by decreasing the levels of inflammatory mediators, apo- ptotic markers, and antioxidants.

• Volume Number: 14(6)
• Magazine \ Newspaper: PLOS ONE
• Pages: 1-20