Protective Effects of Gastric Mucus

Ichikawa, Takafumi; Ishihara, Kazuhíko

doi:10.5772/23951

Cited by 10 publications

(9 citation statements)

References 67 publications

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“…Gastric epithelium elaborates a variety of protective factors that act to topically neutralize or limit acid-induced damage (Figure 2). Gastric mucus provides a viscous gel matrix composed of water, mucin, electrolytes, and host and bacterial cellular components that serves to neutralize local acid production 51 . In addition to the bicarbonate and non-bicarbonate 52 buffers that are retained in the mucus network 53 and are primarily derived from the surface epithelium 45 , phospholipids within the mucus layer hinder the back diffusion of secreted protons 54 .…”

Section: Introductionmentioning

confidence: 99%

Acid and the basis for cellular plasticity and reprogramming in gastric repair and cancer

Sáenz

Mills

2018

Nat Rev Gastroenterol Hepatol

106

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Subjected to countless daily injuries, the stomach still functions as a remarkably efficient digestive organ and microbial filter. In this Review, we follow the lead of the earliest gastroenterologists who were fascinated by the antiseptic and digestive powers of gastric secretions. We propose that it is easiest to understand how the stomach responds to injury by stressing the central role of the most important gastric secretion, acid. The stomach follows two basic patterns of adaptation. The superficial response is a pattern whereby the surface epithelial cells migrate and rapidly proliferate to repair erosions induced by acid or other irritants. The stomach can also adapt through a glandular response when the source of acid is lost or compromised (that is, the process of oxyntic atrophy). We primarily review the mechanisms governing the glandular response, which is characterized by a metaplastic change in cellular differentiation known as spasmolytic polypeptide-expressing metaplasia (SPEM). We propose that the stomach, like other organs, exhibits marked cellular plasticity: the glandular response involves reprogramming mature cells to serve as auxiliary stem cells that replace lost cells. Unfortunately, such plasticity might mean that the gastric epithelium undergoes cycles of differentiation and de-differentiation that increase the risk of accumulating cancer-predisposing mutations.

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Section: Introductionmentioning

confidence: 99%

Acid and the basis for cellular plasticity and reprogramming in gastric repair and cancer

Sáenz

Mills

2018

Nat Rev Gastroenterol Hepatol

106

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“…We also showed that Na + -taurocholate resulted in extensive decrease in PAS + surface epithelial cells and gastric glands, indicating depletion of gastric mucus. The latter is an important component of the gastric mucosal barrier which retards the back-diffusion of luminal H + and thus protects the surface epithelial cells [58]. The administration of MethyB was able to prevent the Na + -taurocholate-induced depletion of gastric mucus, which could be another mechanism that underlies its gastric protective effect.…”

Section: Rosmentioning

confidence: 96%

Methylene Blue Protects against Acidified Sodium Taurocholate-Induced Gastric Mucosal Damage

Abdel-Salam

Sleem

Medhat

et al. 2019

ROS

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The effect of methylene blue (MethyB) on the development of gastric mucosal injury caused by orally given acidified sodium taurocholate (80 mM in 2 ml of 0.15 N HCI) in pylorus-ligated rats was studied. MethyB was intraperitoneally given at doses of 20 and 40 mg/kg at time of pylorus-ligation, and animals were euthanized 90 min later, when gastric secretory responses and the number and severity of mucosal lesions were determined. Lipid peroxidation (malondialdehyde), nitric oxide, reduced glutathione (GSH), and paraoxonase-1 (PON-1) activity in gastric homogenates were measured. Gastric mucosal histopathology and histochemical staining for mucopolysaccharides were also done. Results indicated that acidified sodium taurocholate (Na +taurocholate) caused severe gastric lesions. It also increased gastric malondialdehyde by 70% and decreased GSH levels by 36.4% compared with the corresponding control values. Additionally, nitric oxide decreased by 49.3% and PON-1 activity fell by 54.2% in gastric tissue of Na +-taurocholate-treated rats. The administration of MethyB reduced the number and severity of gastric mucosal lesions but had no effect on gastric acid secretion in Na +-taurocholate-treated rats. MethyB resulted in decreased malondialdehyde and increased GSH, nitric oxide, and PON-1 activity in a dose-dependent manner. Na +-taurocholate caused massive sloughing and hemorrhagic erosions of the superficial parts of gastric epithelium, lamina propria, and sloughing of gastric glands. These changes were markedly attenuated by MethyB at 40 mg/kg. MethyB also restored gastric mucus as indicated by the increase in apical epithelial cells positively stained with periodic acid Schiff. These data suggest a protective effect for MethyB against gastric mucosal damage caused by Na +-taurocholate which is likely to be due to decreased oxidative stress.

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“…Purified mucin units are curvilinear fibres with an average diameter of about 5-7 nm and a length of approximately 200 to 4000 nm [28,29]. Each macromolecular unit consists of 3 to 4 subunits with average M.wt of 4 x 10 5 Da [30]. Mucin subunits are large polypeptide chains that composed of glycosylated and non-glycosylated domains in a sequential manner where polypeptide chains in the glycosylated domain are densely covered with polysaccharide glycosylated side chains while non-glycosylated domains are cysteinerich domains that connecting glycosylated regions by intramolecular disulphide bonds [31].…”

Section: Compositions Of Intestinal Mucus and Mucin Structurementioning

confidence: 99%

Self-emulsifying drug delivery system: Mucus permeation and innovative quantification technologies

Abdulkarim

Sharma

Gumbleton

2019

Advanced Drug Delivery Reviews

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Mucus is a dynamic barrier which covers and protects the underlying mucosal epithelial membrane against bacteria and foreign particles. This protection mechanism extends to include therapeutic macromolecules and nanoparticles (NPs) through trapping of these particles. Mucus is not only a physical barrier that limiting particles movements based on their sizes but it selectively binds with particles through both hydrophilic and lipophilic interactions. Therefore, nano-carriers for mucosal delivery should be designed to eliminate entrapment by the mucus barrier. For this reason, different strategies have been approached for both solid nano-carriers and liquid core nano-carriers to synthesise muco-diffusive nano-carrier. Among these nano-strategies, Self-Emulsifying Drug Delivery System (SEDDS) was recognised as very promising nano-carrier for mucus delivery. The system was introduced to enhance the dissolution and bioavailability of orally administered insoluble drugs. SEDDS has shown high stability against intestinal enzymatic activity and more importantly, relatively rapid permeation characteristics across mucus barrier. The high diffusivity of SEDDS has been tested using various in vitro measurement techniques including both bulk and individual measurement of droplets diffusion within mucus. The selection and processing of an optimum in vitro technique is of great importance to avoid misinterpretation of the diffusivity of SEDDS through mucus barrier. In conclusion, SEDDS is a system with high capacity to diffuse through intestinal mucus even though this system has not been studied to the same extent as solid nano-carriers.

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Protective Effects of Gastric Mucus

Cited by 10 publications

References 67 publications

Acid and the basis for cellular plasticity and reprogramming in gastric repair and cancer

Acid and the basis for cellular plasticity and reprogramming in gastric repair and cancer

Methylene Blue Protects against Acidified Sodium Taurocholate-Induced Gastric Mucosal Damage

Self-emulsifying drug delivery system: Mucus permeation and innovative quantification technologies

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