Effect of Some Natural Products Either Alone or in Combination on Gastritis Induced in Experimental Rats

Abstract

Gastritis, an inflammatory state in gastric mucosa, can be induced experimentally in various ways. The present study considered the iodoacetamide model (Iodo). Omega-3 fatty acids (fish oil), black seed oil, and curcuminoids (natural products) in addition to omeprazole (synthetic proton-pump inhibitor) were tested. Supplementation of 0.1% iodoacetamide to drinking water of experimental rats for two consecutive weeks resulted in: (i) increased serum nitric oxide (NO) and gastrin, and decreased pepsinogen, (ii) depletion of gastric mucosal glutathione (GSH), and (iii) increased gastric mucosal lipid peroxidation (MDA), but failed to affect gastric mucosal myeloperoxidase (MPO) activity. Histological examination showed marked neutrophilic infiltration after 1 week of iodoacetamide administration and shedding of apical cell layer with pale edematous vacuolated gastric gland cells and thickening of muscularis mucosa after 2 weeks of iodoacetamide intake. Individual administration of omega-3 fatty acids 12 mg/kg, black seed oil 50 mg/kg, and curcuminoids 50 mg/kg body weight orally daily for 3 weeks decreased MDA, gastrin, and NO, and normalized mucosal GSH but failed to affect serum pepsinogen level. Combined administration of these natural products for 3 weeks normalized MPO activity, and other effects were nearly the same as with individual use. Omeprazole administration 30 mg/kg body weight orally daily for 3 weeks induced a similar response except for an observed increase in serum gastrin and pepsinogen levels.

Colocalization of substance P with tumor necrosis factor-α in the lymphocytes and mast cells in gastritis in experimental rats

“…Experimental models of gastric mucosal damage have been developed that include various types of stress-induced gastritis [21], intragastric application of Helicobacter pylori itself [22] and iodoacetamide-induced gastritis [23]. Iodoacetamide is a sulfhydryl group blocker that depletes sulfhydryl components in the gastric mucosa, leading to gastric damage [24,25]. In the present study we show that SP is a key mediator in the pathogenesis of gastritis via activation of TNF-a.…”

Diabetic Renal Injury Induced in Experimental Rats-Role of Curcuminoids as Probable Therapeutic Agent

“…These effects are mostly attributed to an inhibition of inducible nitric oxide synthase (iNOS) [14], NF-κB, activated protein-1 (AP-1) [15] and down-regulation of the production of proinflammatory cytokines [16].…”

“…Curcumenoids as a natural product are characterized by a variety of pharmacological actions through inhibition of inducible nitric oxide synthase (iNOS) additionally its potential as radical scavenger [14]. The latter effect is mediated through multiple mechanisms involving inhibition of the activation of various transcription factors such as nuclear factor kappa B (NFκB), activated protein-1 (AP-1) and peroxisome proliferator activated receptor-ϒ (PPAR-ϒ ) [15].…”

Role of Natural Antioxidants in Gastritis

“…Certain polyphenolics can exert a preventive action on gastric injury in rats. Research topics her have focussed on the antiulcer activity of polyphenol from grape seed (Saito et al, 1998), cacao liquor (Osakabe et al, 1998), curcuminoids and Black seed oil (Elseweidy et al, 2008) or from Opuntia ficus indica (Galati et al, 2003). This activity was mainly explained by the strong antioxidant power and/or by some other factors, such as strong protein-binding capacity (Saito et al, 1998), modulation of leukocyte function (Osakabe et al, 1998), mucus production and restoration (Galati et al, 2003).…”

“…Several investigators have also reported the antiulcerogenic activity of the ethanolic extract of the rhizome of C. longa in acute gastric mucosal lesion (Rafatullah et., 1990), but not in chronic ulcer models. More recently, it has been considered that curcumin exerts a variety of pharmacological actions through inhibition of inducible nitric oxide synthase (iNOS) as well as its potential as radical scavenger (Elseweidy et al, 2008) Thus, the previously proposed mechanisms for antiulcerogenic effect of curcumin (Yano et al, 2000), such as inhibitory effect on gastric secretion, cytoprotection, antioxidant activity and inhibition of mast-cell degranulation, need to be evaluated again. Curcumin, exerted its preventive effect on gastric lesion formation, although it possesses anti-inflammatory activity resulting from a blockade of all branches of the arachidonic acid pathway (Ammon et al, 1993).…”