Protective Effect of Prunus Dulcis Against Acetylsalicylic Acid Injury on Gastric Parietal Cells

Background: Acetylsalicylic acid is in common clinical use but has the side effect of causing gastric mucosal erosions and selective injury to parietal cells. Aim: To explore if prior treatment with Prunus dulcis (almond) had a protective effect against acetylsalicylic acid induced injury. Study design: Experimental study. Methodology: Albino mice weighing 30 to 40 grams were given two drops of almond oil without peel and 300 mg of finely ground whole almond kernel by oral gavage for sixty days followed by 400 mg/kg body weight of acetylsalicylic acid orally. Gastric mucosal damage was observed and recorded as ulcer index. The number of parietal cells/ sq. micrometer and area of parietal cells were observed and recorded under microscope in formalin fixed H and E stained sections. Data analyzed by SPSS 22.0v. Results: Mucosal damage, distortion of gastric glands and damage to parietal cells was pronounced in the positive control animals. The number of surviving parietal cells after acetylsalicylic acid insult in animals given almond oil was significantly higher when compared with positive control animals (p<0.001) and even better in animals receiving whole ground almond kernel. The area of parietal cells was also similarly larger in the treated animals. Conclusion: This study concluded Prunus dulcis offers protection against acute gastric mucosal injury and damage to the gastric parietal cells caused by acetylsalicylic acid in mice. Keywords: Prunus Dulcis, Parietal Cells, Gastric Erosions and Acetylsalicylic Acid.

Multinucleate parietal cells and cytoplasmic inclusion bodies in the gastric epithelium of callitrichids

Inclusion bodies (IBs) and multinucleate cells can be associated with viral infections; however, IBs and multinucleate cells have been described in normal tissue and with non-viral disease processes in multiple species. We examined fundic stomach from 50 callitrichids histologically for bi- and multinucleate parietal cells and cytoplasmic IBs in gastric epithelial cells. Callitrichids represented included 6 genera: Saguinus (4 spp.), Leontopithecus (1 sp.), Mico (3 spp.), Cebuella (1 sp.), Callithrix (1 sp.), Callimico (1 sp.), and 13 unspecified marmosets. Gastric epithelial IBs were present in 46 of 47 (98%) of the callitrichids from which the stomach was sufficiently well preserved to identify IBs. Cytoplasmic IBs were identified in gastric surface pit epithelial cells (43 of 44, 98%), mucous neck cells (43 of 44, 98%), parietal cells (43 of 44, 98%), and chief cells (43 of 44, 98%). The IBs were eosinophilic, ovoid, round, elongate, or variably indented, sometimes slightly refractile, and 1–6 × 1–13 µm. IBs were sometimes perinuclear and molded around the nucleus. Electron microscopy of the gastric epithelium of one marmoset indicated that IBs were composed of intermediate filaments. The IBs did not stain with immunohistochemical markers for cytokeratin AE1/AE3 or vimentin. Binucleate parietal cells were found in 49 of 50 (98%) callitrichids, and multinucleate parietal cells were observed in 40 of 49 (82%) callitrichids. Gastric epithelial cytoplasmic IBs and bi- and multinucleate parietal cells are likely a normal finding in callitrichids, and, to our knowledge, have not been reported previously.

Stomach secretes estrogen in response to blood triglyceride levels in males

The central nervous system receives body energy information and controls feeding behavior and lipogenesis1. Ghrelin, insulin, leptin and vagal afferents transmit the status of fasting, blood glucose, body fat, and food intake, respectively2-5. Estrogen, which is secreted from adipocytes and gastric parietal cells and from the ovaries in females, also acts upon the central nervous system and liver to inhibit feeding behavior and lipogenesis6-9. How blood triglyceride levels are monitored and how estrogen levels are regulated from the perspective of the lipid homeostasis is not well understood. Using male rats, we show that gastric parietal cells secrete estrogen in response to blood triglyceride levels. Parietal cells predominantly use fatty acid as an energy source. When male rats are administered olive oil or glucose, blood estrogen levels increase as the blood triglyceride, but not glucose, levels rise. Estrogen levels in stomach tissues increase as the blood triglyceride levels rise, and blood triglyceride level-dependent increases of blood estrogen levels are cancelled in gastrectomized rats. We therefore propose that in males, parietal cells in the stomach act as a sensor for the blood triglyceride levels and can secrete estrogen to inhibit the hepatic lipogenesis and feeding behavior when blood triglyceride levels are high.

Modeling acute ethanol-induced impairment with gastric organoids

Background: Ethanol has been linked to atrophic gastritis and gastric carcinoma. Although it is well known that ethanol can result in hypochlorhydria, the molecular mechanisms underlying this phenomenon remain poorly understood.Results: Here we used gastric organoids to show that ethanol permeabilized the apical membrane of gastric parietal cells and induced ezrin hypochlorhydria. The functional consequences of ethanol on parietal cell physiology were studied using organoids. Gastric organoids were pre-incubated in the basic medium or with EGTA or E64 , and incubated at 37℃ in either medium alone, or medium containing 6% ethanol. We assessed ezrin proteolysis. Ethanol permeabilization induced activation of calpainⅠand subsequent proteolysis of ezrin, which resulted in the liberation of ezrin from the apical membrane of the parietal cells. Significantly, expression of calpain-resistant ezrin restored the functional activity of parietal cells in the presence of ethanol.Conclusion: Taken together, our data indicated that ethanol disrupted the apical membrane-cytoskeleton interactions in gastric parietal cells and thereby caused hypochlorhydria.

Modeling Acute Ethanol-Induced Impairment with Gastric Organoids

Background: Ethanol have been linked to atrophic gastritis and gastric carcinoma. Although it is well known that ethanol can result in hypochlorhydria, the molecular mechanisms underlying this phenomenon remain poorly understood.Results: Here we used gastric organoids to show that ethanol permeabilized the apical membrane of gastric parietal cells and induced ezrin hypochlorhydria. The functional consequences of ethanol on parietal cell physiology were studied using organoids. Gastric organoids were pre-incubated in the basic medium or with EGTA or E64 , and incubated at 37℃ in either medium alone, or medium containing 6% ethanol. We assessed ezrin proteolysis. Ethanol permeabilization induced activation of calpainⅠand subsequent proteolysis of ezrin, which resulted in the liberation of ezrin from the apical membrane of the parietal cells. Significantly, expression of calpain-resistant ezrin restored the functional activity of parietal cells in the presence of ethanol.Conclusion: Taken together, our data indicated that ethanol disrupted the apical membrane-cytoskeletal interactions in gastric parietal cells and thereby caused hypochlorhydria.