Abstract
Zinc is a naturally occurring element with roles in wound healing and rescuing tissue integrity, particularly in the gastrointestinal system, where it can be detected in the mucosal and submucosal layers. Zinc chelates are known to have beneficial effects on the gastrointestinal mucosa and in cases of gastric ulcer. We synthesized complexes of zinc featuring a heterocyclic amine binding amino acids then investigated their ability to enhance the gastric self-repair. Zinc-morpholine complex, Zn(L)SCN, namely showed strong free-radical scavenging, promotion of the DNA and RNA polymerases reconstruction and suppression of cell damage. The complex’s mode of action is proposed to involve hydrogen bond formation via its bis(thiocyanato-k)zinc moiety. Zn(L)SCN complex had potent effects on gastric enzymatic activity both in vitro and in vivo. The complex disrupted the ulcerative process as demonstrated by changes in the intermediate metabolites of the oxidative pathway – specifically, reduction in the MDA levels and elevation of reduced glutathione together with an attenuation of oxidative DNA damage. Additionally, Zn(L)SCN restored the gastric mucosa, inhibited the production of pro-inflammatory cytokines (IL-6, TNF and the caspases), and preserved the gastric mucous balance. Zn(L)SCN thus exhibited anti-oxidative, anti-inflammatory and anti-apoptotic activities, all of which have cytoprotective effects on the gastric lining.
Highlights
Human health and longevity are closely linked to the balance of the digestive system
The ideal way of restoring the balance between the proteolytic capacity of the stomach and the protective capacity of the mucin layer is to induce the stomach to secrete mucus at a rate sufficient to coat the lining during the critical digestive periods
New gastroprotective agents based on elements like zinc are usually considered less noxious, with fewer severe side effects than proton pumps and H2 receptor antagonists, which act by reducing hydrochloric acid production
Summary
Gastric Ulcers in a Rat Model received: 09 October 2015 accepted: 08 June 2016 Published: 27 July 2016. The different doses of Zn(L)SCN given to the animals strongly reduced the level of MDA compared to the ulcer control group, in the same way as seen for the OMP-treated groups. The PGE2 levels induced by the highest doses of Zn(L)SCN (40 and 80 mg/kg) did not differ significantly from those induced by OMP treatment, indicating that both chemicals have similar effects on the gastric tissue. Based on the results plotted, the gastric NO level was considerably lower in the stomachs of rats treated with HCl/EtOH alone compared to the normal group. Staining for the Bax protein demonstrated that HCl/EtOH induced injury and apoptosis in the stomachs of rats (IIb), while pre-treatment with Zn(L)SCN down-regulated Bax expression
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