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Fucoidan
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Ellya Sinurat, Dina Fransiska, Nurhayati, Hari Eko Irianto
According to the hepatology data, blood clots generated against providing aspirin without fucoidan (Figure 12.2B), showing that the ulcer existed in the stomach tissue. There are no blood clots in the different performances (Figure 12.2A without aspirin and Figure 12.2C with aspirin and fucoidan). It indicates that because fucoidan does not affect the stomach tissue lining, it can prevent gastric ulcers by building a barrier in the mucosa. A thick mucus coating is particularly common on the mucous membrane, synthesized by high cylindrical epithelial cells. The gastric mucosa is a polypeptide with two purposes: it lubricates food masses to facilitate transportation within the stomach and acts as a protective coating on the lining epithelium of the stomach cavity. This protective barrier protects the stomach from being digested by its protein-lysine enzymes. It can migrate from the underlying mucosa into the surface layer according to bicarbonate secretion. The acidity of the mucous layer, or hydrogen ion concentration, is balanced in the vicinity of the epithelium and becomes acidic toward the luminal layer. While gastrointestinal mucus is excluded from the surface epithelium, little pits termed foveolae gastrique can be observed with a magnifying glass (Sinurat & Rosmawaty, 2015).
Role of Lectins in Gastrointestinal Disorders
Published in Megh R. Goyal, Preeti Birwal, Durgesh Nandini Chauhan, Herbs, Spices, and Medicinal Plants for Human Gastrointestinal Disorders, 2023
Research studies have also explored the gastric mucosa in different diseases. In peptic ulcer disease, a significant difference in peanut lectin binding was observed between Helicobacter pylori—positive and Helicobacter pylori—negative patients,45 suggesting that exposure of sialic acid residues was present in gastric epithelium colonized with this specific organism. Similar studies were reported with different lectins in Helicobacter—associated gastritis in humans3,34 as well as a guinea pig animal model of this disease.34
Biochemical Parameters and Childhood Nutritional Anemia
Published in Anil Gupta, Biochemical Parameters and the Nutritional Status of Children, 2020
Intrinsic factor is a glycoprotein that is related to the cobalamin transport proteins family. It is secreted by the parietal cells of the gastric mucosa. It is essential for the absorption of vitamin B12 in the intestine. Vitamin B12 binds with the intrinsic factor through the receptor-mediated endocytosis in the mucosa of ileum and forms vitamin B12 1/n intrinsic factor complex. It enters the hepatic portal circulation (NHS 2019).
Xiaojianzhong decoction attenuates aspirin-induced gastric mucosal injury via the PI3K/AKT/mTOR/ULK1 and AMPK/ULK1 pathways
Published in Pharmaceutical Biology, 2023
Ting Chen, Shengchuan Bao, Juan Chen, Jiaxiang Zhang, Hailiang Wei, Xin Hu, Yan Liang, Jingtao Li, Shuguang Yan
Gastric mucosal injury is closely associated with excessive apoptosis of epithelial cells (Ren et al. 2020). In a healthy state, the body eliminates excess, redundant, aging and unhealthy cells through apoptosis to maintain the balance and homeostasis of its internal environment (Park et al. 2021). In normal gastric mucosa, apoptotic cells form an ‘apoptotic cell band’ on the mucosal surface to maintain mucosal integrity and resist external stimulation. In the injury stage, apoptotic cells increase dramatically, the integrity of the gastric mucosa is destroyed, and the gastric mucosal injury is further aggravated (Li et al. 2021). Salah Khalil (2015) found that aspirin can increase the apoptosis of gastric mucosal epithelial cells and induce gastric mucosal injury, while the inhibition of apoptosis can reduce gastric mucosal injury. As an upstream signal of apoptosis, autophagy can regulate cell apoptosis, and cells are stimulated by conditions such as starvation, hypoxia, endoplasmic reticulum stress and oxidative damage to induce autophagy (Huang et al. 2020). Moderate autophagy helps to maintain cellular homeostasis, thereby ensuring cell survival. However, the continuous activation of autophagy can lead to the degradation of a large number of intracellular proteins and the engulfment of anti-apoptosis-related proteins, leaving the cells unable to maintain their normal basic structures and eventually leading to cell necrosis or apoptosis (Yang et al. 2016; Gao et al. 2021). Therefore, reducing apoptosis and regulating autophagy are important strategies for alleviating gastric mucosal injury.
Protective effect of valerian extract capsule (VEC) on ethanol- and indomethacin-induced gastric mucosa injury and ameliorative effect of VEC on gastrointestinal motility disorder
Published in Pharmaceutical Biology, 2022
Yuan Feng, Wan Dai, Junyu Ke, Yong Cui, Shuang Li, Jingjing Ma, Wenfeng Guo, Gang Chen, Ning Li, Yanwu Li
Gastrointestinal (GI) diseases, such as peptic ulcer, chronic gastritis, and functional dyspepsia, are highly prevalent and generally considered to be a leading cause of the incidence of several other concomitant diseases. GI mucosal as a barrier plays a pivotal role in the protection of digestive organs and the damage of gastric mucosa is considered the early stage of gastric ulcer (Woolf and Rose 2021). Previous studies reported that gastric mucosa damage is attributable to multiple factors including chemical factors (smoking, drinking, and drugs), physical factors (improper diet), inflammation, intestinal bacterium, and phycological stress (Padol et al. 2012; Haj Kheder et al. 2018; Zhou and Zhang 2019; Woolf and Rose 2021). Among the various reasons contributing to gastric injury, non-steroidal anti-inflammatory drugs (NSAIDs) indomethacin can depress the expression of cyclooxygenases (COXs) and increase the free radical formation and excessive generation of inflammatory mediators, thus inducing gastric mucosal damage or gastric ulcer (Abd EI-Rady et al. 2021). In addition, alcohol is another common risk factor for GI disease. Excessive drinking may cause the appearance of bleeding or stomach ulcers by rupturing the gastric mucosa barrier and inducing inflammatory cell infiltration (Ostaff et al. 2015). Recently, the animal models of gastric injuries induced by indomethacin and ethanol have been widely used to investigate the underlying pathophysiological and evaluate the protective effects of herbal medicines against gastric ulcers and gastritis (Dejban et al. 2020).
Spirulina supplements: an approach moderating aspirin persuaded histological and ultra-structural alterations in albino rats gastric mucosa
Published in Ultrastructural Pathology, 2022
Sherif A. Kamar, Ahmed H. Bayoumi, Hagar Yousry Rady
Gastric ulcer is a common multifactorial disease that is defined as a disruption in gastric mucosa and penetration along muscularized mucosa.6 About 10% of the world population are suffering from gastrointestinal tract (GIT) disorder in the form of gastric ulcers, which makes it a major field of research to investigate different mechanisms of protection and treatment.7 According to different previous studies, the gastric morbidities characterized by GIT bleeding, perforation, and erosion of the mucosal wall resulted from imbalance between aggressive insults (acid, pepsin, and Helicobacter pylori) and defensive factors (mucin, prostaglandin, bicarbonate, nitric oxide, mucosal blood flow, and growth factors).8 Non-steroidal anti-inflammatory drugs (NSAIDs), smoking, stress, chronic alcohol, altered prostaglandin E series metabolism and bad dietary habits are among many factors that can suppress defensive mucosal measures.9