Possible contribution of nitric oxide and prostaglandin in the protective effect of angiotensin (1-7) against stress induced gastric ulceration in adult male albino rats

Abstract

To assess the gastro-protective potential of the angiotensin (Ang-) (1-7) on the gastric secretion and ulceration induced by cold restraint stress (CRS) in adult male rats and the possible contribution of nitric oxide and prostaglandin E 2 . Rats were pylorically ligated and divided randomly into the following groups (8 rats each): control, cold-restraint stressed (CRS), stressed Ang-(1-7) treated, stressed L-NNA-Ang-(1-7) treated, stressed Indo-Ang-(1-7) treated groups. Our results revealed that Ang-(1-7) pre-treatment proved to be protective against development of ulcerative lesions in CRS model as evidenced by histological examination and the reduction of the ulcer index and this could be mediated through reduction of free and total acidity and pepsin concentration of gastric secretion with signifi cantly decreased lipid peroxidation and increased the gastric protective nitric oxide and prostaglandin E 2 levels. Furthermore, Ang-(1-7) pre-treatment has anti-apoptotic effect, evident by its down-regulation of the CRS induced over-expression of the gastric caspase 3. In addition, the gastro-protective effects of Ang-(1-7) were signifi cantly attenuated by co-administration with L-NNA or indomethacin. In conclusion, Ang-(1-7) can be considered a potential therapeutic agent to protect against the major clinical challenge of gastric injury resulting from stress. Nitric oxide and prostaglandin E 2 seem to contribute to the Ang-(1-7)'s gastro-protective effect (Tab. 2, Fig. 5, Ref. 35). Text in PDF www.elis.sk.

1-Deoxynojirimycin (DNJ) Ameliorates Indomethacin-Induced Gastric Ulcer in Mice by Affecting NF-kappaB Signaling Pathway

“…The remarkable increase in ulcer index and gastric volume following indomethacin-induced GU in mice, may attribute to ROS formation or prostaglandin decrease. Low-level prostaglandin level has been attributed to gastric injury and is associated with the etiology of GU, which is accordant with an earlier report ( Hassan et al, 2016 ). PGE2 can regulate the activities of various cells, the production of inflammatory cytokines and have strong inhibition on cAMP-dependent modulation of NF-κB activity.…”