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paniculata (C.B. Clarke) Munir Leaves on Various Gastric Aggressive Factors
Published in Parimelazhagan Thangaraj, Phytomedicine, 2020
P. S. Sreeja, K. Arunachalam, Parimelazhagan Thangaraj
Gastric acid secretion occurs in parietal cells and consist of fluid mucus, electrolytes, HCO3−, pepsinogen, intrinsic factor, peptides, and HCl (the main constituent) (Konturek et al. 2004). The gastric secretion is a complex process with three distinct phases: cephalic phase, gastric phase, and intestinal phase. (1) The factors, such as vision, smell, and taste of food, stimulate secretion, which is the cephalic phase and is partially regulated by the hypothalamus and mediated by the vagus nerve; (2) in the gastric phase, the contact of food in the gastric lumen stimulates the secretion, as well as the stomach distension, which entails the activation of the sensory receptors of the body and gastric antrum, with the activation of the vagal reflexes; and (3) the intestinal phase is the mechanical distension and the presence of amino acids and peptides from the chyme stimulate gastric fluid secretion (Goo et al. 2010). HCl has a protective role to the stomach/gastric mucosa through avoiding anti-microbial action, i.e., the growth of microbes from ingested food and water (Schubert and Peura 2008).
Anti-ulcerogenic effect of methanol fraction of Ocimum gratissimum leaves extract and honey on indomethacin-induced gastric ulcer in rats
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Aanuoluwa James Salemcity, Blessing Oluwagbamila Omolaso, Oghenefega Sheila Ogegere, Victoria Olasumbo Oluokun
The disease could be associated with mucosal damage caused by hyper-secretion of acid from the parietal cell of the intestinal tracts as well as environment-induced, lifestyle, diet and stress – either physiological or physical. Other causal factors of peptic ulcer are H. pylori, cigarettes, alcohol consumption, the use of non-steroidal anti-inflammatory drugs (NSAIDs) and Zollinger–Ellison syndrome [3]. However, only few people exposed to the major causative agents develop ulcer, partly because of predisposition or proneness as a result of genetic or environmental factors. Genetic polymorphisms in various inflammatory cytokine genes are related to peptic ulcer. For instance, IL-1β polymorphisms could influence the mucosal synthesis of the cytokine, which could play role in pathogenesis of H. pylori-induced gastro-duodenal ulceration [4]. An understanding of these events might be of utmost relevance in designing new antiulcer drugs.